JBR 2013-1 by office

WETTEREN 1

P 702083

Volume 96 Page 1-54

January-February

Bimonthly

–

2013

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) 00a-Couv-2013.indd 1

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

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Instructies voor abonnees Het JBR-BTR geeft 6 nummers uit per jaar. Het tarief is vatbaar voor wijzigingen zonder voorafgaand bericht, in verhouding tot de evolutie van de papierprijzen en loonkosten in de grafische nijverheid. Het abonnement van de leden van de Koninklijke Vereniging voor Radiologie is begrepen in de bijdrage van het lidgeld. De abonnementen van niet-leden zijn te onderschrijven bij de KVBMG. Jaarabonnementen of bestellingen van losse nummers moet zo snel mogelijk gebeuren, de uitgever waarborgt de levering van de vorige nummers niet voor de abonnementen die te laat werden onderschreven. De adresveranderingen moeten 60 dagen te voren gemeld worden. TARIEF: Jaarlijks Belgie 175 € Andere landen 200 € Verzendingskosten zijn inbegrepen.

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

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

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JBR-BTR ♦ 96/1 ♦ 2013 Journal Belge de ♦ Belgisch Tijdschrift voor ♦ RADIOLOGIE

Founded in 1907 A bimonthly journal devoted to diagnostic and interventional imaging, related imaging sciences, and continuing education Contents Editorial: An international consulting co-editorship in 2013 J. Pringot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Review article: Acute stroke: basic concents and use of imaging for clinicians M. Castillo, H. Alvarez . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Extravertebral gas and fluid effusions associated with vertebral collapse containing a vacuum cleft possibly result from a pumping phenomenon: a new evidence of the dynamic hydro-pneumatical nature of the so-called vacuum phenomenon B. Coulier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Postextubation pulmonary edema: an unusual cause of transient pulmonary edema K. Carels, V. Herpels, L. Cardoen, C. Lecluyse, S. Traen, J. Verschakelen . . . . . . . . . . . . . . . . . . . . .

Necrotizing colitis complicating necrotized pancreatitis: look out for intestinal pneumatosis M.A. Siddiqui, A. Jain, S.A.A. Rizvi, K. Ahmad, E. Ullah, I. Ahmad . . . . . . . . . . . . . . . . . . . . . . . . . .

Persistent stapedial artery: a congenital anomaly to know M.I. Nica, G. Cosnard . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Pregnancy-like (pseudolactational) hyperplasia: uncommon cause of microcalcifications and mass in two cases A. Koktener, B. Cakir, K. Akin, D. Kosehan, R. Bayrak, S. Yenidunya . . . . . . . . . . . . . . . . . . . . . . . . .

Sporadic supravalvular stenosis in a young man K.M. Ghodduci, M. Antic, K. Tanaka, D. Verdries, D. Kerkhove . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Periosteal chondroma of the proximal tibia mimicking Osgood-Schlatter’s disease T. Vancauwenberghe, F.M. Vanhoenacker, J. Van Doninck, H. Declercq . . . . . . . . . . . . . . . . . . . . . . .

CONTINUING EDUCATION Dual energy CT: added value in gouty arthritis J. Spermon, C. Van Dijke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

IMAGES IN CLINICAL RADIOLOGY The ‘’kissing spine’’ revisited E. De Smet, F.M. Vanhoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Fibrous dysplasia M.-A. Van Caulaert, P. Mailleux . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

B-cell malt lymphoma of the small intestine G. Koc, O. Oyar, N. Yazıcıog˘lu, S. Bener, B. Ünsal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Angioedema of the small bowel caused by angiotensin converting enzyme inhibitor B.S. Smet, I. De Kock, A.I. De Backer, K. Verstraete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cold lumbar abscesses due to tuberculous spondylitis V. Haydan, L. Médart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Port-site metastasis after explorative laparoscopy for an incidental appendiceal mucinous cystadenocarcinoma detected with FDG PET/CT G. Ceulemans, M. Keyaerts, S. Willems, Ch. Simoens, B. Ilsen, H. Everaert . . . . . . . . . . . . . . . . . .

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Coracoclavicular joint with shoulder pain I. Willekens, M. De Maeseneer, C. Boulet, F. Verhelle, J. de Mey . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Silent double aortic arch in an elderly patient S. Dekeyzer, R. Gosselin, L. Delrue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cancer of the oesophagus in achalasia S. Maeyaert, J. Pringot, J.L. Samain, L. Ghijseling, P. Matthys . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

An unusual cause of A2 pulley rupture in a 49-year-old man M. De Maeseneer, C. Boulet, M. Kichouh, F. De Ridder, M. Shahabpour . . . . . . . . . . . . . . . . . . . . .

Eagle syndrome M. Demeter, Y. De Bruecker, S. Devuysere, D. Perdieus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Osseous venous congestion simulating sclerotic bone lesions in superior vena cava syndrome L. Duquesne, P. Desclee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Secondary tumoral calcinosis with intraosseous extension L. Van Muylder, H. Declercq, F.M. Vanhoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Sacral chordoma M. Behaeghe, A. Denis, L. Jans, K. Verstraete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Decubital ischemic fasciitis L.J. Ceulemans, G. Jacomen, F.M. Vanhoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract of papers for full membership at the Royal Belgian Society of Radiology . . . . . . . . . . . . . .

Announcements from the Museum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Forthcoming Courses and Meetings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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

iii

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

cii

Advertising index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ciii

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

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Editor: J. Pringot

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

Consulting Co-Editor: M. Castillo (USA)

President: R. Hermans Vice-President: D. Henroteaux

Managing Editor: P. Seynaeve

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

General Secretaries: M. Lemort, J. Verschakelen Meeting Secretaries: M. Spinhoven, Y. Lefebvre Treasurers: D. Brisbois, A. Van Steen Coordinator of continuing education: 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

J.F. Nisolle, M. Shahabpour

Breast imaging

M. Mortier, S. Murgo

Cardiac imaging

R. Salgado, O. Ghekière

Cardiovascular and interventional radiology

S. Heye, D. Henroteaux

Chest radiology

B. Ghaye, W. De Wever

Head and neck radiology

J. Widelec, R. Hermans

Neuroradiology

M. Lemmerling, L. Tshibanda

Pediatric radiology

B. Desprechins, L. Breysem

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

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

–

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

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

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

Dynamische tomografie:

Onmiddellijk na een bolus injectie.

Vertraagde tomografie:

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

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

Imagerie dynamique

Immédiatement après l’injection en bolus

Imagerie retardée

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

Hersenen en ruggenmerg

Tot 60 minuten na toediening.

Système nerveux central

Jusqu’à 60 minutes après administration

MRA

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

ARM

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

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

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

www.bracco.com

MR Angiography with MultiHance ® :

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

MH_MRA_3-03-08ADV

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

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

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

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

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

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JBRâ&#x20AC;&#x201C;BTR, 2013, 96: 1.

EDITORIAL AN INTERNATIONAL CONSULTING CO-EDITORSHIP IN 2013 Recently, the idea enthusiastically backed by the editorial board members, of opening the board to an internationally renowned expert in Radiology has materialized. The opportunity came with the major contribution to JBR-BTR by Mauricio Castillo of a review article on neuroradiology published in the present issue (see p. 1-54). Mauricio Castillo, MD, is professor of Radiology, Chief Division of Neuroradiology, University of North Carolina School of Medicine, and his work as the editor-in-chief of the American Journal of Neuroradiology is highly admired internationally. He kindly accepted to be nominated as consulting co-editor of the JBR-BTR for the year 2013. He will contribute to two main objectives of the project focusing this year on neuroradiology. First to stimulate the publication in our journal of high quality papers in continuing education and secondly to better inform the wider radiological community of the state of the art as well as new developments in clinical diagnostic and interventional neuroradiology. Of course, JBR-BTR will remain a general journal of Radiology serving primarily the members of the Royal Belgian Society of Radiology, but with from now on, on a yearly basis, the special focus on a subspecialty in radiology, which will be this year neuroradiology. I hope very much, dear readers, that you will appreciate the initiative of the board and enjoy readingÂ the present and next issues. Jacques Pringot Editor-in-Chief

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02-voorblz-2013-1_Opmaak 1 25/02/13 15:42 Pagina 3

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JBR–BTR, 2013, 96: 3-9.

REVIEW ARTICLE ACUTE STROKE: BASIC CONCEPTS AND USE OF IMAGING FOR CLINICIANS M. Castillo, H. Alvarez1 In this article we review basic and some advanced concepts of stroke imaging. The benefits and caveats of both CT and MRI are stressed and we attempt to familiarize the reader with current concepts regarding collateral brain circulation, its nature, and its importance in acute stroke. Key-word: Brain, ischemia, collateral circulation.

Stroke is a clinical condition with varied symptoms generally related to inadequate blood flow to a part of the brain. The term “stroke” does not imply an etiology. Strokes are mostly due to ischemia (90%) or hemorrhage (5-10%) (1). Other causes such as arteriovenous malformations and tumors may occasionally (2%) cause stroke symptoms. Because treatment for intracerebral hemorrhage must occur immediately (i.e. surgical decompression) and because it precludes treatment for ischemic stroke (anticoagulation, thrombolysis), its early detection is paramount. Since CT is exquisitely sensitive for detection of hemorrhage, it is extensively used as the initial imaging study in stroke patients (2). Recent data show that intracerebral hemorrhage is more common than previously believed with about 70,000 such cases happening every year in the USA (3). Large intracerebral bleeds carry a 32% mortality rate which has remained unchanged for many decades. Intracerebral hemorrhages will not be addressed in this review. Ischemic stroke occurs in nearly 800,000 individuals per year in the USA resulting in over 140,000 deaths (4). The treatment of stroke is based on the “brain is time” paradigm which as we will see later, is not completely correct (1). Stroke has been categorized based on its temporal evolution. But since treatment needs to be instituted as fast as possible, we cannot wait for a patient’s clinical evolution to make the correct diagnosis. In the past, ischemic stroke was broadly divided into TIA (transient ischemic attack) and infarction. The traditional definition

of TIA was time-driven; that is, symptoms resolved within 24 hours. That definition is no longer used because by 24 hours, treatment of true stroke is not possible and patients may improve due to transfer of function (brain plasticity) and still have an infarct. Therefore, TIA is now a tissuedriven definition in which the patients must have normal DWI (diffusion-weighted imaging) and symptoms need to resolve within one hour of onset (5). If one images all patients with TIAs, DWI shows lacunar and small infarcts in 35-70% of them (6). These patients cannot be considered as having had a TIA and are better categorized as having small volume infarctions which generally, and regardless of treatment, have a good prognosis (7). Approximately 45% of cerebral infarctions can be categorized as minor (segmental arterial branch occlusions) and 20% as lacunar (arising from occlusion of the deep perforating arteries). These two types of infarctions carry a good prognosis and will not be discussed here. The following discussion centers on major infarctions (35%) and on the role of collateral circulation. Over one-half of major infarctions are due to occlusion of the MCA (middle cerebral artery) and most are from emboli that arise from disease at the level of the common carotid artery bifurcation in the neck (8). It is critical to mention here that timely systemic (intravenous) thrombolytic treatment transforms about 30% of major infarctions into minor ones and that intra-arterial thrombolysis in those who fail systemic treatment will transform another 30% of major into minor ones. Thus, by adequately

From: 1. Divisions of Neuroradiology and Interventional Neuroradiology, University of North Carolina School of Medicine, Chapel Hill, NC. Address for correspondence: M. Castillo, M.D., Room 3326, Old Infirmary Building, Manning Drive, Chapel Hill, NC, 27599-7510, USA. E-mail: castillo@med.unc.edu

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treating patients one could transform up to 60% of major infarcts into minor ones which have a good prognosis (R. Gilberto Gonzales, personal communication). Imaging of acute stroke Because of its extreme sensitivity and specificity in the diagnosis of acute brain hemorrhage, CT continues to play an important role in the evaluation of the acute stroke patient (1, 8). However, its ability to depict infarctions is only about 60% within the 3-6 hours that follow onset of symptoms. Thus, if used in treatment trials it is estimated that up 50% of patients are treated unnecessarily a finding that may reflect the significant success of early trials which were only CT-driven. Hemorrhage or low density in over 1/3 of the MCA territory precludes thrombolysis. The “1/3 rule” was empirically arrived at by estimating that the volume of territory supplied by the MCA is normally about 300 ml and in our opinion estimating the volume of the involved territory is difficult and impractical. Other CT signs of acute MCA infarction include the “hyperdense MCA” (reflecting intraluminal clot), blurring with low density of the gray matter in the insular cortex (“insular ribbon” sign) and basal ganglia all off which reflect cytotoxic edema, and sulcal effacement (1). The greatest revolution in stroke imaging was the advent of DWI (9). DWI is sensitive to the imbalance between extracellular and intracellular water (cytotoxic edema) and it becomes positive in most patients in less than 1 hour after stroke symptom onset. As water migrates into the complex intracellular space and the extracellular space size is reduced by cell swelling, the ability of water molecules to randomly move (called Brownian motion) decreases giving raise to restriction of the

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pparent diffusion coefficient (ADC). a Note that the diffusion coefficient is called “apparent” because its true magnitude cannot be calculated with current clinical techniques. By comparison, cytotoxic edema seen as gray matter T2 high signal intensity on conventional MR imaging is seen in less 80% of infarctions at 24 hours. The success of DWI is based on the facts that it can be rapidly obtained stopping macroscopic motion (thus it is helpful in unstable patients who cannot hold still for prolonged periods of time), it is easy to interpret, it reliable and reproducible, and its post processing is fast and easy (10). Of course, lack of intra-arterial flowrelated enhancement (signal) on MRA, intravascular high FLAIR signal, and intravascular contrast enhancement help confirm the diagnosis vessel occlusion or severe stenosis on conventional MR imaging (11). Regardless of this, no one should attempt to image acute stroke patients without DWI. It is important to remember that DWI is ideal for the acute period but that the abnormal signal depicted by it generally disappears by 10-15 days. This phenomenon does not imply that the underlying tissues revert to normal, on the contrary, they remain abnormal and this “pseudo-normalization” is considered a caveat and artifact in DWI of subacute infarctions (12). The second most important MRI advance (but equally important for CT) was the development of brain perfusion sequences (8, 13). In both modalities, perfusion imaging is based on the same principle, that is, the passage of intravascular contrast through the capillary bed produces a loss of signal intensity in the case of MRI and a gain in density in CT. Thus, the amount of signal/density is proportional to the contrast getting to a specific regions and proportional to cerebral blood flow. In order to obtain perfusion images, MR units with echo planar capability and CT with spiral capabilities are needed. A compact bolus of contrast (in MRI contrast followed by saline solution and in CT only iodinated contrast) at a rate of 3-5 ml/sec is given generally in the right antecubital vein and from an automatically generated TTP map (time-to-peak) other parametric maps such as the CVB (cerebral blood volume), MTT (mean transit time), and CBF (cerebral blood flow) can be calculated. All maps are “relative” and not quantitative in regards to the parameters being measured. In ischemic stroke, alterations in rCBF are seen in over 90% of patients

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JBR–BTR, 2013, 96 (1)

with both MR and CT perfusion. However, circulation abnormalities are more obvious and easier to visually detect on the TTP and MTT maps. Defects seen on those two maps need to be confirmed on the rCBF one. The tissue “penumbra” is defined as that part of the brain at risk for stroke due to impaired and deficient blood supply but which can still be salvage with appropriate therapy (14). By imaging, the penumbra is the perfusion defect which can be separated from the core of the infarct as seen on the DWI, that is, a perfusion/diffusion mismatch. Patients with penumbras must be acutely and even chronically treated to save those tissues. Patients without penumbra (no diffusion/perfusion mismatch) should not be treated regardless of the size of the infarct because all of the affected tissue is considered to be irreversibly damaged. The following type’s mismatches can be seen on MRI: 1. Perfusion defect> DWI abnormality: means a penumbra is present and since the core of infarct may progress to involve the entire penumbra, treatment is indicated (Figs. 1 and 2). 2. DWI abnormality with accompanying high rCBV and defect on MTT/TTP: means presence of a penumbra with collateral circulation (see below), there is a chance of core progression and acute or chronic treatment is indicated (Fig. 3). 3. Perfusion defect and normal DWI: means no infarct but tissue is at risk due to inadequate perfusion; there is a chance of future stroke and treatment must be given. 4. DWI abnormality > perfusion defect: means early and generally spontaneous re-perfusion, core may decrease in size or remain stable. No acute treatment is needed (Fig. 4). 5. DWI abnormality = perfusion defect: means there is no penumbra, no collateral circulation, and the infarct core will remain stable. No immediate treatment is needed. Susceptibility-weighted imaging (SWI) also has the ability (perhaps even earlier than DWI) of detecting acute infarctions (15). After an arterial occlusion there is always physiological dilation of veins and arteries in the ischemic territory. SWI exquisitely depicts deoxygenated venous blood in dilated veins in ischemic

C Fig. 1. — A. Frontal MRA view shows occlusion of the right middle cerebral artery (MCA, arrow). B. Axial DWI shows areas of high signal which showed restriction on ADC map (not shown) in the deep regions of the right MCA territory. C. TTP MRI map shows delayed arrival of blood in the entire MCA territory. The mismatch between the perfusion and DWI abnormalities represents the ischemic penumbra. The large volume of the penumbra in this patient indicates that treatment would be beneficial to prevent infarct core from growing.

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ACUTE STROKE — CASTILLO et al

A A

zones. In our experience the area containing these dilated veins approximates that of the penumbra seen on perfusion studies. The problem with SWI is that it takes about 5-6 minutes to obtain and many stroke patients are unstable and unable to hold still that long. Malignant infarction The concept of malignant cerebral infarction is a recent one. These are patients in whom a large volume of infarcted tissue occurs without any collateral circulation and who will develop significant edema and mass effect leading to death in most unless a decompressive craniectomy to relief the mass effect is done (Fig. 5). Its definition varies slightly but infarcts with volumes greater than 70-100 ml can be considered as

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B Fig. 2. — A. Axial DWI shows two small bright infarcts in the territory supplied by the left middle cerebral artery. B. Arterial spin label CBF map shows large defect in that same vascular territory indicating the presence of a significant ischemic penumbra.

C alignant (that is why treating pam tients with infarcts involving over 1/3 of the MCA territory is not always indicated). The volume of the infarct

Fig. 3. — A. Axial CT shows a hyperdense (arrow) left middle cerebral artery (MCA). B. Axial DWI shows only a small infarction (arrow) in posterior left insular cortex. C. TTP MRI map shows slow arrival of blood (green) in the entire left MCA territory. The diffusion/perfusion mismatch indicates a large ischemic penumbra. D. rCBV MRI map shows that blood volume is slightly increased (red) in the affected area suggesting presence of collateral circulation a fact that explains the small size of the infarct despite a large vessel occlusion. E. Frontal view from catheter angiogram shows extensive collaterals (arrows).

core must be estimated using DWI or occasionally the area of low CT attenuation may be used as some studies have shown a correlation between it and the DWI core. The treatment is usually a hemicraniectomy in patients less than 60 years of age which reliefs the mass effect caused by swelling (16). Collateral circulation As previously stated, all brain stroke treatment protocols are based on the premise that “brain is time”

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JBR–BTR, 2013, 96 (1)

Fig. 4. — Axial DWI shows infarction in the left posterior frontal region. B. rCBF MRI map shows that perfusion defect (green) is much smaller than the diffusion abnormality indicating partial reperfusion of the affected region.

Fig. 5. — A. Axial ADC map shows a large area of dark restricted diffusion in the territory of the right middle cerebral artery. B. One week later, DWI shows massive extension of the infarction which contains areas of low signal suggesting hemorrhage and significant mass effect with midline shift to the left compatible with a malignant infarction.

which is not completely true. In reality, “time is collateral circulation” and thus, to some degree, “brain is collaterals.” This means that although we want to treat stroke patients as soon as possible the window of opportunity is not entirely time dependent. It is well known that patients with initial NIHSS (National Institutes of Health Stroke Scale) scores over 15 due poorly regardless of type of therapy. The reason for this is that in them, very little or no collateral circulation is present (1). Additionally, collateral circulation seems to predict the success of treatment. In one study, the degree of collateral circulation as seen on catheter

angiography determined the rate of successful recanalization after endovascular therapy and thus the outcome (17). Broadly, collateral circulation is a subsidiary arteriole-to-arteriole network that stabilizes CBF when the primary conduits fail (18). Collateral circulation may be intracranial (primary from the circle of Willis or secondary via other intracranial anastomoses) or extracranial (from branches of the external carotid arteries). Intracranial collaterals open up first while extracranial ones take time to develop. The development of collateral arteries depends on 3 mechanisms as follows:

1. Compensatory: collaterals incited by this mechanism appear very fast and involve the circle of Willis and the leptomeningeal network; they form adapt the mechanism of arteriogenesis. 2. Hemodynamic: this mechanism leads also to the immediate formation of collaterals via arteriogenesis. The circle of Willis is also involved in their formation. 3. Metabolic: this mechanism leads to slower collateral formation via arteriogenesis and angiogenesis via some leptomeningeal arteries. 4. Neural: this mechanism is responsible for the slowest collateral formation via angiogenesis and mostly involves the deep striatal arteries. Compensatory and hemodynamic mechanisms are responsible for collateral formation in acute stroke while metabolic and neural related collaterals mostly occur in chronic ischemia such as moyamoya. Arteriogenesis refers to the enlargement of pre-existing arteries induced by physical forces such as shear stress and volume. Angiogenesis refers to the formation new arteries from preexisting ones due to chronic hypoxia. At least in animals, arteriogenesis is modulated by 3 proteins (Canq1, Civg1, and HSg1) controlled by genes located in chromosome 7 (1921). The existence and role if any of these genes in humans, is under investigation. Once brain collateral circulation has been established its integrity may be threatened by: hypotension, dehydration, clot fragmentation, hyperthermia, hyperglycemia, hyperviscosity, infections, cardiac failure, and renal and pulmonary insufficiencies and thus careful control of stroke patients in an intensive care setting is needed (22). The most important factor in the development of collaterals is however, the integrity of the circle of Willis. A complete circle of Willis is found in about 60% of the population meaning that all communicating arteries are present and functional in case of arterial occlusions (23). In the rest, the circle of Willis is incomplete and does not function adequately as an immediate source of collateral arterial circulation. As mentioned before, collaterals are formed by arteriogenesis. In this mechanism, enzymes such as metalloproteases deconstruct the arterial wall extracellular matrix and allow increased shear stress to stretch the blood vessel (24). These enzymes

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are produced as the result of ischemia in tissues surrounding arteries. The cells in the deconstructed blood vessels secrete cytokines which travel in the systemic circulation to the bone marrow stimulating it to produce endothelial precursor cells. These cells then enter the systemic circulation and find their way to the affected artery lodging in the spaces previously created between the native cells. Endothelial precursor cells then mature and become endothelial cells. Imaging has been extensively used to study collateral brain circulation including PET, SPECT, and Doppler sonography. On conventional contrast enhanced MRI 2 findings have been correlated with the presence of collateral circulation: intravascular enhancement sign and intravascular hyperintensity on FLAIR images (so called “ivy” sign). These findings generally imply slow arterial flow and because passage of blood through collaterals is slower than through native arteries, the findings imply at least some degree of collaterals. Catheter angiography, CT angiography, and MR angiography may also show arteries in territories beyond proximal arterial occlusions implying presence of collaterals (Fig. 3). The presence of leptomeningeal collaterals seen on CTA is a strong predictor of functional outcome in stroke patients with large vessels occlusion (25). On MR perfusion, prolonged transit times and delayed MTT with high rCBV in infarcted or at risk areas corresponds, to some degree, with the presence of collaterals. Arterial spin label angiography (ASL) is a new technique which may also help to identify collaterals (26, 27). This MR technique uses an inversion pulse to continuously or non-continuously label water spins in blood flowing through the arteries in the neck. After a time delay, the head is imaged recovering a very small amount of signal in the capillary bed with respect to the background brain. This sampling must be repeated about 60 times to recover a 1-2% change in signal intensity between capillaries and brain. ASL results in CBF maps which may be quantitative or not depending on the MR system being used. ASL may show what appears to be paradoxically increased perfusion in regions of ischemia (Fig. 6). This sign called “paradoxical hyperperfusion” correlates with presence of collateral circulation. The recovery of signal in these cases is greater because of the slowness of blood flow in collaterals.

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ACUTE STROKE — CASTILLO et al

C Fig. 6. – A. Base view of MRA shows occlusion of the left middle cerebral artery. B. Axial T2 MR image shows edema involving predominantly the gray matter (cytotoxic edema) in the left temporal region. C. ASL CBF maps show slightly increased (paradoxical) perfusion in the affected regions (arrows).

B Based on these observations, some investigators have attempted to treat collaterals at same time as treating the infarction (22). Stimulation of parasympathetic fibers in the sphenopalatine ganglion may increase CBF by 40% or more but data are early and controversial. Direct and indirect (partial aortic occlusion with balloons, external blood pressure cuffs) expansion of blood volume has been found to be beneficial in some patients. Chronically, statins may improve collateral formation by stimulating endothelial cell proliferation (20). Maintaining an adequate systemic blood pressure is very important in collateral formation and in preventing strokes. Hemorrhagic infarction

transformation

Most hemorrhagic transformations involve the MCA circulation and were previously thought to occur in 15% of patients but it is now known that its incidence is much less (3.5%) (28) (Fig. 7). Nowadays, the most common cause of it is previous intravenous thrombolytic treatment. B ecause hemorrhagic transformation carries a poor prognosis, several techniques have been employed in an attempt to predict which patients will undergo it. Hemorrhagic transformation is more common in patients with poor collaterals and lack

These terms refer to development of new hemorrhage in a previously ischemic region, a complication that generally occurs within 72 hours of symptoms. It is generally due to arterial reperfusion into a damaged territory (normal pressure breakthrough).

Fig. 7. – Axial CT shows large left middle cerebral artery infarction with post thrombolysis hemorrhagic transformation.

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References

Table I. – Benefits of CT and MRI in acute stroke imaging.

CT MRI

Presence of hemorrhage

Occlusion of large artery

Mapping of ischemic core

Mapping of penumbra

++ +

++ (CTA) +

+ (CTA, CTP) ++ (DWI)

+ ++

of arterial recanalization. This observation has been confirmed by a larger study of 222 patients undergoing catheter angiography as part of intra-arterial recanalization procedures (29). Permeability studies using MRI with contrast have shown that infarcted regions with increased permeability are at high risk for hem(30, 31). orrhagic transformation However, it should be noted, that petechial and small hemorrhages in an infarcted zone are generally clinically silent, generally do not affect the patients’ outcome, and do not preclude additional treatment. Practical issues Unfortunately, less than 10% of patients arrive within the allowable time window for stroke therapy to emergency departments. Early morning stroke is a common presentation and since patients do not feel pain they do not see the need a go to the hospital immediately. Since these patients do not know when the stroke occurred, MR FLAIR images may shed some light in this regard since abnormalities on FLAIR take about 3 hours to develop. Intravenous thrombolysis may be given up to 4.5 post stroke; intra-arterial thrombolysis up 6 hours, and mechanical clot retrieval employed up to 9 hours post ictus (32). These broad guidelines apply only to infarcts involving the anterior circulation and not the vertebrobasilar system. Which is the best imaging choice when the acute stroke patients arrive at the hospital is controversial and both CT and MRI have strong proponents. The advantages of CT are: it is readily available most anywhere, it is superb at detecting hemorrhage, CTA rapidly identifies patients with major vessel occlusions which may be directly stratified to intra-arterial treatments, and CT perfusion may be easily obtained to identify the penumbra. Supporters of MRI cite the following advantages: direct identifi-

castillo.indd 8

cation of infarcted core by DWI, MRA identifies major arterial occlusions, perfusion studies include the entire brain (something not possible with many CT scanners), and identification of blood with gradient echo or susceptibility-weighted sequences. The reality is that the choice of modality will be dictated by what is available, the type of trial patients are enrolled in, and personal and institutional preferences. The best imaging choice may be combination of both CT and MRI taking advantage of their benefits (Table I). The ideal combined protocol includes a noncontrast CT for detection of hemorrhage, a CTA for detection of large vessel occlusion and MRI with DWI for mapping the infarcted core and whole brain perfusion for determining the extent of the penumbra. Conclusion A cerebral infarction is composed of 3 zones: the core, the penumbra, and surrounding area of oligemia. Imaging and treatment of stroke is geared towards salvaging the penumbra and the oligemic regions and preventing the core from enlarging. Presence of hemorrhage and large size infarcts (>100 ml) preclude treatment and carry a poor prognosis. Although it is true that “brain is time”, up until now brain attack studies have not taken into consideration the presence or absence of collateral circulation and early data indicate that patients with collaterals have a better outcome regardless of treatment. The use of CT or MRI in acute stroke patients is a matter of availability, treatment protocol, and personal and institutional preferences. The most useful protocol is probably a combination of both modalities. New techniques such as ASL MRI perfusion may allow for measurement of collateral circulation detecting those patients who carry a better outcome. Genes controlling collateral circulation have been detected in mice and probably exist in men too.

1. Gonzalez R.G.: Imaging-guided acute ischemic stroke therapy: from “time is brain” to “physiology is brain.” AJNR, 2006, 27: 728-735. 2. Symons S.P., Culen S.P., Buonanno F., Gonzalez R.G., Lev M.H.: Noncontrast conventional computed tomography in the evaluation of acute stroke. Semin Roentgenol, 2002, 37: 185-191. 3. Andaluz N., Zuccarello M.: Recent trends in the treatment of spontaneous intracerebral hemorrhage: analysis of a nationwide inpatient d atabase. J Neurosurg, 2009, 110: 403-410. 4. http://www.strokecenter.org/patients/ about-stroke/stroke-statistics. 5. Easton J.D., Saver J.L., Albers G.W., Alberts M.J., et al.: AHA/ASA scientific statement. Definition and evaluation of transient ischemic attack. Stroke, 2009, 40: 2276-2293. 6. Bertrand A., Oppenheim C., Lamy C., Rodrigo S., et al.: Comparison of optimized and standard diffusion-weighted imaging at 1.5T for the detection of acute lesions in patients with transient ischemic attack. AJNR, 2008, 29: 363-365. 7. Torres-Mozqueda F., He J., Yeh I.B., Lev M.H., et al.: An acute ischemic stroke classification instrument that includes CT or MR angiography: the Boston acute stroke imaging scale. AJNR, 2008, 29: 1111-1117. 8. Cullen S.P., Symons S.R., Hunter G., Hamberg L., et al.: Dynamic contrastenhanced computed tomography f acute ischemic stroke: CTA and CTP. Semin Roentgenol, 2002, 37: 192-205. 9. Schaefer P.W., Romero J.M., Grant P.E., Wu O., et al.: Diffusion magnetic resonance imaging of acute stroke. Semin Roentgenol, 2002, 37: 219-229. 10. Wessels T., Wessels C., Ellsiepen A., Reuter I., et al.: Contribution of diffusion-weighted imaging in determination of stroke etiology. AJNR, 2006, 27: 35-39. 11. Romero J., Schaefer P.W., Schwann L., McDonald C., Gonzalez R.G.: Conventional magnetic resonance imaging in acute stroke. Semin Roentgenol, 2002, 37: 206-211. 12. Lansberg M.G., Thjis VN., O’brien M.W., Ali J.O., et al.: Evolution of apparent diffusion coefficient, diffusionweighted, and T2 signal intensity of acute stroke. AJNR, 2001, 22: 637-644. 13. Schaefer P.W., Romero J.M., Grant P.E., Ona W., et al.: Perfusion magnetic resonance imaging of acute stroke. Semin Roentgenol, 2002, 37: 230-236. 14. Schaefer P.W., Ozsunar Y., He J., Mamberg L.M., et al.: Assessing tissue viability with MR diffusion and perfusion imaging. AJNR, 2003, 24: 436-443. 15. Mittal S., Wu Z., Neelvalli J., Haacke E.M.: Susceptibility-weighted imaging: technical aspects and clini-

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cal applications, part 2. AJNR, 2009, 30: 232-252. 16. Huttner H.B., Schwab S.: Malignant middle cerebral artery infarction: clinical characteristics, treatment strategies, and future perspectives. Lancet Neurol, 2009, 8: 949-958. 17. Bang O.Y., Saver J.L., Kim G.M., Chung C.S., et al.: Collateral flow predicts response to endovascular therapy for acute ischemic stroke. Stroke, 2011, 42: 693-699. 18. Lebeskind D.S.: Collateral circulation. Stroke, 2003, 34: 2279-2284. 19. Wang S., Zhang H., Dai X., Sealock R., Faber J.E.: Genetic architecture underlying variation in extent and remodeling of the collateral circulation. Circ Res, 2010, 107: 558-568. 20. Chalothorn D., Faber J.E.: Statin- dependent variation in collateral circulatory function in mouse hindlimb. Physiol Genomics, 2010, 42: 469-479. 21. Wang S., Zhang H., Wiltshire T., Sealock R., Faber J.E.: Genetic dissection of the Canq1 locus governing variation in extent of the collateral circulation. PLoS ONE 7:e31910. doi:10.1371/journal.pone.0031910. 22. Shuaib A., Butcher K., Mohammad A.A., Saqqur M., Liebeskind D.S.: Collateral blood

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ACUTE STROKE — CASTILLO et al essels in acute ischaemic stroke: a v potential therapic target. Lancet Neurol, 2011, 10: 909-921. 23. De Silva K.R.S., Silva R., Gunasekera W.S.L., Jayesekera R.W.: Prevalence of typical circle of Willis and the variation in the anterior communicating artery: a study of a Sri Lankan population. Ann Indian Acad Neurol, 2009, 12: 157-161. 24. Van Royen N., Piek J.J., Shcpaer W., Fulton W.F.: A critical review of clinical arteriogenesis research. JACC, 2009, 55: 17-25. 25. Lima F.O., Silva G.S., Lev M.H., Camargo E.C., et al.: The pattern of leptomeningeal collaterals on CT angiography is a strong predictor of long-term functional outcome in stroke patients with large vessel intracranial occlusion. Stroke, 2010, 41: 2316-2322. 26. Van Laar P.J., van der Grond J., Hendrikse J.: Brain perfusion territory imaging: methods and clinical application of selective arterial spinelabeling MR imaging. Radiology, 2008, 246: 353-364. 27. Chng S.M., Petersen E.T., Zimine I., Sitoh Y.Y., et al.: Territorial arterial spin labeling in the assessment of collateral circulation. Stroke, 2008, 39: 3248-3254.

9 28. Mullins M.E., Lev M.H., Schellingerhout D., Gonzalez R.G., Schaefer P.W.: Intracranial hemorrhage complicating acute stroke: how common is hemorrhagic stroke on initial CT scan and how often is initial clinical diagnosis of acute stroke eventually confirmed? AJNR, 2005, 26: 2207-2212. 29. Bang O.Y., Saver J.L., Kim G.M., Chang C.S., et al.: Collateral flow averts hemorrhagic transformation after endovascular therapy for acute ischemic stroke. Stroke, 2011, 42: 2235-2239. 30. Lin K., Kazmi K.S., Las M., Babb J., et al.: Measuring elevated microvascular permeability and predicting hemorrhagic transformation in acute ischemic stroke suing first-pass dynamic perfusion CT imaging. AJNR, 2007, 28: 1292-1298. 31. Bang O.Y., Buck B.H., Saver J.L., Alger J.R., et al.: Prediction of hemorrhagic transformation after recanalization therapy using T2*-permeability magnetic resonance imaging. Annals Neurol, 2007, 62: 170-176. 32. Wechsler L.R., Jovin T.G.: Intravenous recombinant tissue-type plasminogen activator in the extended time window and the US Food and Drug Administration. Stroke, 2012, 43: 2517-2519.

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EXTRAVERTEBRAL GAS AND FLUID EFFUSIONS ASSOCIATED WITH VERTEBRAL COLLAPSE CONTAINING A VACUUM CLEFT POSSIBLY RESULT FROM A PUMPING PHENOMENON: A NEW EVIDENCE OF THE DYNAMIC HYDRO-PNEUMATICAL NATURE OF THE SO-CALLED VACUUM PHENOMENON B. Coulier1 We report two very unusual observations in which gas and fluid effusions were transiently and unexpectedly found in the extravertebral spaces of patients presenting with painful necrotic vertebral collapse containing a vacuum cleft. We hypothesize that gas and/or fluid which progressively may replace vacuum in vertebral compression fractures could be secondarily pumped through extravertebral and retroperitoneal spaces. Although being rare, these observations may represent a potential missing link in the imaging snapshots of the cyclic and dynamic vacuum phenomenon. Key-words: Spine, diseases – Spine, CT.

Although true physical-chemical experimental proofs are lacking in the literature, numerous clinical reports have shown that many radiological manifestations of the socalled “vacuum phenomenon” (VP) only represent snapshots of a complex dynamic continuum extending from true vacuum to gas and/or fluid and vice versa (1). We report two very unusual observations in which gas and fluid effusions were transiently and unexpectedly found in the extravertebral spaces of patients presenting with painful necrotic vertebral collapse containing a vacuum cleft. We hypothesize that gas and/or fluid which progressively may replace vacuum in vertebral compression fractures could be secondarily pumped through extravertebral and retroperitoneal spaces. Although being rare these observations may represent a missing link in the imaging snapshots of the cyclic and dynamic VP. Cases reports Case 1 An 81-year-old female was admitted in the geriatric department for impairment of general state and severe lumbar pain relating to a recent fall. Plain films of the lumbar spine (not illustrated) showed a classical ischemic osteoporotic collapse of the vertebra L1.

Laboratory results showed a moderate inflammatory syndrome with a CRP level at 53 mg/l. Abdominal CT was performed to rule out the hypothesis of any occult inflammatory and/or tumoral pathology. Attention was unexpectedly retained by the presence of unusual extensive bilateral retroperitoneal effusions (Fig. 1) extending from the paravertebral to the retrorenal spaces and along the psoas muscles. These effusions were also extending under both posterior hemi diaphragms and within the retrocrural spaces of the diaphragm. The epicentre of these unusual effusions was constituted by the osteoporotic collapse of the L1 vertebra in which a vacuum cleft was clearly visible. A single gas bubble was also found within the left paravertebral root of the left psoas muscle (Fig. 1). New plain films of the lumbar spine were performed in upright (Fig. 2) and supine position (Fig. 2). Moreover lateral plain films (Fig. 2) were also obtained during stress hyperextension on a log in order to appreciate the fracture reducibility. The painful instable vertebral fracture was finally treated by kyphoplasty (Fig. 2). The symptoms resolved in two days. Postoperative abdominal CT (Fig. 1) showed a complete regression of the retroperitoneal effusions.

From: Department of Diagnostic Imaging, Clinique St Luc, Bouge (Namur), Belgium. Address for correspondence: Dr B. Coulier, M.D., Department of Diagnostic Radiology, Clinique St Luc, Rue St Luc 8, B-5004 Bouge (Namur) Belgium. E-mail: bcoulier@skynet.be

Case 2 A 64-year old male was admitted at the emergency room with complaints of acute lumbar mechanical pain after a fall in his bathroom. Supine X-rays of the thoracolumbar spine were performed at admission. They were first considered being normal and the patient was discharged (not illustrated). Three days later, the patient was readmitted for confusion which was attributed to abuse of analgesics. Severe diffuse lumbar pain was still present and an inflammatory syndrome was associated. Abdominal CT (Fig. 3) reveals the presence of an intravertebral vacuum cleft within the vertebra T12 suggesting an occult but typical ischemic vertebral collapse. Gas bubbles and edematous effusions were also extensively found outside the vertebra in the retrocrural diaphragmatic spaces. On sagittal MPR views the discordance between massive intravertebral VP and a normal height of the vertebra suggested the probably spontaneous reduction of the vertebral fracture in the supine position (Fig. 3). New plain films (Fig. 4) of the lumbar spine were then carefully performed in the upright position unmasking the real amplitude of the vertebral collapse. This collapse immediately reduced on the oblique views performed in the supine position and this caused the reappearance of an acute extensive vacuum cleft (Fig. 4). The patient was first treated conservatively with lumbar corset but the prognosis of healing was considered poor because the fractured vertebra was situated in the middle of a

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Fig. 1. — Case 1: Coronal MPR CT views (A to C) show a vacuum phenomenon (white arrow) in a severely collapsed L1 vertebra. A gas bubble is also found in the adjacent root of the left psoas muscle (black arrow). More laterally extensive bilateral effusions are found in retroperitoneal paravertebral (black arrowheads), sub diaphragmatic (grey arrowhead) and retrocrural (white arrowheads) spaces. These effusions have completely disappeared two days after kyphoplasty (E, F).

stiff spine segment – due to DISH –. In this condition the fracture site could be subject to inappropriate solicitation in any movement. A new CT performed one month later showed that paravertebral gas collection had disappeared. The vertebral vacuum had reduced but was still present. The fracture lines had progressed through the posterior arch and epinous process of the vertebra (Fig. 5). It was decided to treat the patient with kyphoplasty and this treatment quickly induced a substantial reduction of the symptoms. Discussion Fick was the first to describe the “vacuum phenomenon” in 1910 while he was studying joints under traction (2). In 1937 Magnusson (3) reported the same phenomenon in intervertebral discs and postulated

that the creation of spaces, subsequently filled by gas, required a reduction of barometric pressure within a joint and/or a disc up to 1/20 th atmosphere. In current radiological practice, a vacuum is the physical state of space that is empty of matter. In a synovial joint, a vacuum is produced when the distraction of the articular surface creates a space and there is not enough intraarticular fluid to fill in this space. The negative pressure attracts gas from surrounding tissues into the joint space, creating an intraarticular distended gas pouch. This mechanism is called the vacuum phenomenon. When the distraction of the articular surfaces stops, the produced intraarticular gas may persist. Gas that forms in a disc was first analysed by Ford in 1977 (4). It contains 90-92% nitrogen combined

with oxygen, carbon dioxide and other traces of gases. This composition was confirmed in 1997 by Yoshida et al. who analysed an intraspinal gaseous cyst (5). VP and gas collections have been described in every segment of the spine including the disc space, Schmorl nodes and vertebral structures, the epidural and intradural spaces, synovial cysts and facet joints (1). They have also been described in numerous peripheral joints or ganglion cysts (6-7), but also in gallstones (8) and unicameral bone cysts (9). Since the first description by Maldague et al. (6) the presence of an intravertebral gas cleft in vertebral compression fractures – also referred to as “Kümmell disease” (10-13) – is considered indicative of osteonecrosis. It is now commonly regarded as a specific sign for ischemic vertebral

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Fig. 2. â&#x20AC;&#x201D; Case 1: Upright lateral plain film of the L1 vertebra (A) obtained just after abdominal CT: a major collapse of the vertebra is confirmed. A small vacuum cleft (white arrow) due to acute distraction of the collapse is found on the supine oblique view (B). Stress lateral plain film obtained in hyperextension on a log (C) partially reduced the vertebral collapse and induced an extensive vacuum (black arrow). Upright lateral plain film (D) obtained after kyphoplasty. At the time symptoms have disappeared.

collapse. The most important risk factors for the development of an intravertebral gas cleft are osteoporotic vertebral fractures, steroid medication, trauma, and radiation therapy (11). Thus a vertebral compression fracture seems to represent the initial event (11). It is followed by a delayed healing due to impaired vascular proliferation and then by

osteonecrosis (11, 14). The successive flexions and extensions continuously apply shearing forces to the horizontal fracture line and maintain the absence of fusion of bony fragments. Thus the vacuum cleft represents a peculiar type of vertebral pseudarthrosis. The abnormal dynamic mobility of the vertebral pseudarthrosis can be demonstrated by a more pro-

nounced gas accumulation (or VP in the acute phase) observed in extension or decompression, a condition classically obtained in the supine position. This can lead to a partial restoration of the vertebral height as illustrated in our reported cases (Fig. 2C, 4, 5C,D). The VP is not a static phenomenon. On the contrary, various reports (1, 5, 15-18) have suggested

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Fig. 3. — Case 2: A. Axial CT views, B, coronal and C, sagittal MPR views of the thoraco-lumbar junction obtained during abdominal CT. Bilateral paravertebral effusions and numerous gas bubbles are found in the paravertebral retrocrural spaces (black arrowheads). Massive intravertebral vacuum is also found in a T12 vertebra of apparently normal height (black arrows). Multilevel ankylosis of the lower thoracic spine is found with typical fatty degeneration of some intervertebral disks (white arrows).

or demonstrated that there was a dynamic physical continuum between true vacuum, gas but also fluid. This continuum seems to depend on the duration and intensity of mechanical stretching – spontaneous or induced by stress – of an anatomical cavity, the variable nature of neighbouring tissues and

the variable permeability of the cavity walls. These reported observations are based on various crosschecking clinical observations (1, 5, 15-18). Malghem et al. (16) have very recently demonstrated the possibility of directly generating intraarticular microbubbles by creating a tran-

sient VP during mechanical traction on metacarpophalangeal joints. This study confirms that the real vacuum only represents a transitory state in natural semi-permeable cavities. Gas quickly created by VP replace the transitory vacuum and may persist up to 30 a minutes in suspension in the viscous synovial fluid (16, 19). Previously Malghem et al. also described the progressive replacement of gas by fluid on plain films and MRI in patients presenting with intravertebral vacuum (15). This replacement was observed after positioning the patients in the supine position for a sufficiently long time (15). The variable duration of this replacement probably depends on several factors: the duration of the decubitus, the intensity of the traction imposed on the spine on stress views or simply by the extension resulting from the supine position and finally the variable permeability of the cleft walls. These observations have been corroborated by others (20). The same phenomenon of replacement of gas by fluid has also been described in cases of intradiscal vacuum during prolonged supine MRI studies (21). Various observations have also clearly demonstrated that gas accumulating in joints or vertebral disks could also be secondarily progressively forced outside these structures. Gas from apophyseal joints may be forced within cysts of the ligament flava (22-23). Gas from vertebral disks may also be forced within intraspinal gaseous cysts or gascontaining herniations which may produce compressive radicular symptoms. Gas may also simply migrate in the epidural space (5, 2425). In these gaseous cysts or hernias, gas is generally injected under a certain pressure which is obtained in a stepwise fashion by a “ball-valve effect” or a “valve-pump mechanism” (1, 5). Gas – mixed with synovial fluid – may also be pumped in periarticular synovial cysts (1, 6-7). In our two cases a similar mechanism could be evoked in which the VP produces an accumulation or gas/or fluid in the vertebral cleft due to the negative pressure induced by distraction of the vertebral cleft during the supine position (suction pumping mechanism). This gas/or fluid collections may be secondarily forced through the extravertebral soft tissues when positive pressure reappears in upright position (force pumping mechanism). These various but complementary studies unequivocally emphasize the

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Fig. 4. — Case 2: A, B. Upright plain films of the thoraco-lumbar junction obtained just after the abdominal CT reveal an unambiguous collapse of about 40% of the vertebra T12. Acute intravertebral vacuum spontaneously (white arrows) reappears on the oblique plain films (C, D) obtained in supine position during the same examination.

conclusion that VP is a dynamic process. Thus when synovial, discal or vertebral spaces are stretched, vacuum phenomenon may be produced acutely and transiently. This vacuum can secondarily progressively be replaced by gas which may persists some time (16). If distention persists gas may be progressively replaced by fluid. Finally there is a question which remains unanswered in cases of

ischemic vertebral collapses: where goes the vertebral gas and/or fluid – that has replaced the vacuum after prolonged supine position – when the collapsed vertebra is resubmitted to compression especially when a supine patient – with vertebral collapse – is mobilized in upright position. Probably this gas and/or fluid may be resorbed by the walls of the cleft. Nevertheless our two cases seem to illustrate that this gas and/or

fluid could also in some conditions be forced towards the extravertebral spaces. Finally some other questions remain unanswered: – Why does the extravertebral extrusion of gas and/or fluid have not, to our knowledge, been reported before? The reason could be that, in clinical practice, only “snapshots” of the dynamic VP

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EXTRAVERTEBRAL GAS AND FLUID EFFUSIONS — COULIER

Fig. 5. — Case 2: On a control CT performed one month later (A, B) extravertebral gas and fluid has disappeared but some gas persists in the vertebra. Fracture lines have progressed through the vertebral posterior arch and spinous process (black arrows). The patient was treated with percutaneous kyphoplasty (C, D).

are generally fortuitously found. Our rare and probably unpublished observations are thus probably also fortuitous. Systematic and prospective randomized dynamic studies – comprising an active mobilization of the patient – could eventually be able to depict all the sequences of this dynamic process but this condition is difficult to perform and/or justify in clinical practice.

– Does this phenomenon of extrusion of gas and/or fluid play a role in the painful symptoms presented by the two patients? We conclude that, although rare, our observations seem to represent the illustration of a missing link in the cyclical dynamic continuum of the “vacuum phenomenon”.These observations and these conclusions have to be corroborated by further studies.

References 1. Coulier B.: The spectrum of vacuum phenomenon and gas in spine. JBRBTR, 2004 , 87: 9-16. 2. Fick R.: Handbuch der Anatomie and Mechanik der Gelenke unter Verucksichtigung der bewegenden Muskeln. Vol 2 Jena G. Fisher, Ed, 1910. 3. Magnusson W.: Über die Bedingungen des Hersvortretens der Wirklichen

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JBR–BTR, 2013, 96 (1) Genlenkspalte auf den Röntgenbild. Acta Radiol., 1937, 18: 733-741. Ford L.T., Gilula L.A., Murphy W.A., Gado M.: Analysis of Gas in Vacuum Lumbar Disc. AJR, 1977, 128: 10561057. Yoshida H., Shinomiya K., Nakai O., Kurosa Y., Yamaura I.: Lumbar Nerve Root Compression Caused by Lumbar Intraspinal Gas. Report of Three Cases. Spine, 1997, 22: 348-351. Coulier B., Cloots V.: Atypical retroperitoneal extension of iliopsoas bursitis. Skeletal Radiol, 2003, 32: 298-301. Coulier B., Devyver B., Hamels J.: Imaging demonstration of fistulous gas communication between joint and ganglion of medial malleolus. Skeletal Radiol, 2002 , 31: 57-60. Delabrousse E., Bartholomot B., Narboux Y., et al.: Gas-containing gallstones: value of the "Mercedes-Benz" sign at CT examination. J Radiol, 2000, 81: 1639-1641. Jordanov M.I.: The "rising bubble" sign: a new aid in the diagnosis of unicameral bone cysts. Skeletal Radiol, 2009, 38: 597-600. Maldague B.E., Noel H.M., Malghem J.J.: The intravertebral vacuum cleft: a sign of ischemic vertebral collapse. Radiology, 1978, 129: 23-29. Libicher M., Appelt A., Berger I., et al.: The intravertebral vacuum phenomen as specific sign of osteonecrosis in vertebral compression fractures:

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results from a radiological and histological study. Eur Radiol, 2007, 17: 2248-2252. Kümmell H.: Die rarefizierrende Ostitis der Wirbelkörper. Deutsche Med 1895, 21: 180-181. Resnick D., Niwayama G., Guerra J. Jr., Vint V., Usselman J.: Spinal vacuum phenomena: anatomical study and review. Radiology, 1981, 139: 341-348. Theodorou D.J.: The intravertebral vacuum cleft sign. Radiology, 2001, 221: 787-788. Malghem J., Maldague B.E., Labaisse M.A., et al.: Intravertebral Vacuum Cleft: Changes in Content after Supine Positioning. Radiology, 1993, 187: 483-487. Malghem J., Omoumi P., Lecouvet F.E., Vande Berg B.C.: Presumed intraarticular gas microbubbles resulting from a vacuum phenomenon: visualization with ultrasonography as hyperechoic microfoci. Skeletal Radiol, 2011. [Epub ahead of print]. Mailleux P., Ghosez J.P., Booschaert P., Malbecq S., Coulier B. The large Lumbar Facet Joint Space on MRI: An Indirect Sign of Underestimated Spondylolisthesis and Canal Stenosis. JBR-BTR, 1998, 81: 283-285. Grunshaw N.D., Carey B.M.: Case Report: Gas within a Cervical Vertebral Body. Clin Radiol, 1994, 49: 653654.

19. Unsworth A., Dowson D., Wright V.: ‘Cracking joints’. A bioengineering study of cavitation in the metacarpophalangeal joint. Ann Rheum Dis, 1971, 30: 348-358. 20. Linn J., Birkenmaier C., Hoffmann R.T., Reiser M., Baur-Melnyk A.: The intravertebral cleft in acute osteoporotic fractures: fluid in magnetic resonance imaging-vacuum in computed tomography? Spine, 2009, 34: 88-93. 21. Wang H.J., Chen B.B., Yu C.W., Hsu C.Y., Shih T.T.: Alteration of disc vacuum contents during prolonged supine positioning: evaluation with MR image. Spine, 2007, 32: 2610-2615. 22. Firth R.L.: Lumbar Intraspinal Synovial Cyst Containing Gas as a Cause for Low-Back Pain. J Manipul Physiol Therap, 2000, 23: 276-278. 23. Coulier B., Ghosez J.P., Mailleux P.: CT Diagnosis of Bilateral Clinically well Tolerated Synovial Cysts of the Lumbar Spine. JBR-BTR, 1998, 81: 141-143. 24. Righini A., Lucchi S., Reganati P., Zavanone M., Bettinelli A.: Percutaneous treatment of gascontaining lumbar disc herniation. Report of two cases. J Neurosurg, 1999, 91: 133-136. 25. Giraud F., Fontana A., Mallet J., Fischer L.P., Meunier P.J.: Sciatica Caused by Epidural Gas. Four Case Reports. Joint Bone Spine, 2001, 68: 434-437.

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POSTEXTUBATION PULMONARY EDEMA: AN UNUSUAL CAUSE OF TRANSIENT PULMONARY EDEMA K. Carels1, V. Herpels1, L. Cardoen1, C. Lecluyse1, S. Traen1, J. Verschakelen2 We report a case of sudden onset of respiratory distress caused by pulmonary edema due to laryngospasm. The diagnosis was established by the clinical context and chest X-ray. A CT-scan was performed to narrow down the differential diagnosis and to confirm the diagnosis. Postextubation pulmonary edema due to laryngospasm is a rare entity with a typical clinical and radiographic presentation. Key-word: Lung, fluid.

Case report A 17-year-old, white male with gynecomastia underwent bilateral subcutaneous mastectomy combined with a liposuction of the thoracic wall. A complete medical history and physical examination was done prior to surgery and did not reveal any stigmata of cardiac or pulmonary disease. Surgery was performed under general endotracheal anesthesia and the patient was extubated in the operating room without complications. On arrival in the recovery room, the patient remained at normal oxygen saturation levels while receiving 2L of oxygen. Removal of the oxygen mask, some minutes after extubation, induced respiratory distress with vigorous inspiratory efforts. The patient didn’t develop a petechial rash nor did he suffer from an altered mental status. Imaging findings

diagnosis of pulmonary edema. No signs of pulmonary tromboembolism or pneumothorax were detected. He received 10 mg of Furosemide intravenously and the O2 administration was sustained. A new chest X-ray (Fig. 3) 2 hours later showed partial resolution of the lung opacities which almost disappeared on the last chest X-ray 13 hours later. He was kept in observation during 24 hours and was discharged on the next day. The diagnosis of postextubation pulmonary edema due to laryngospasm was made, based on the clinical and radiological signs and their evolution in time. Discussion Pulmonary edema in the postoperative setting can have a number of causes including cardiogenic and renal failure as well as lung injury (incl. aspiration, embolism, upper airway obstruction).

Postextubation pulmonary edema is recognized by development of hypoxia shortly (1-90 min) after a laryngospasm (1). It can be induced by repeated upper airway irritation from an endotracheal tube or by a difficult intubation,from the accumulation of blood or secretions into the posterior pharynx during surgery, from vomiting, from hyperactive laryngeal reaction related to chronic smoking or occult asthma, and from esophageal reflux (2, 3). The incidence of postoperative laryngospasm ranges from 0.05 -1% in patients undergoing general anesthesia (2). These patients typically had uncomplicated anesthetic and operative courses (4). There is a number of risk factors reported in literature including obesity, young male adults, upper aerodigestive tract surgery, smoking, asthma, sleep apnea or esophageal reflux (2, 4-7). The pathogenesis remains unclear but is probably related to the negative intrathoracic pressure, due to inspiration against a narrow/closed upper airway (8). Transient injury to

A portable chest X-ray was taken. It revealed bilateral hazy lung opacities, more pronounced at the right side. Heart size was within normal limits and pleural effusions were absent. The differential diagnosis of (asymmetric) pulmonary edema or fat embolism was suggested (Fig. 1). Subsequently, a CT scan of the chest was performed to exclude pulmonary tromboembolism, pneumothorax and aspiration pneumonia. The scan showed extensive areas of patchy ground-glass opacities in a lobular distribution and areas of crazy paving in the right lung and in the left upper lobe (Fig. 2A,B), findings compatible with the clinical From: 1. Department of Radiology, AZ Groeninge, Kortrijk, Belgium, 2. Department of Radiology, University Hospitals Leuven (Gasthuisberg), Leuven, Belgium. Address for correspondence: Dr K. Carels, M.D., Department of Radiology, AZ Groeninge, President Kennedylaan 4, B-8500 Kortrijk, Belgium. E-mail: kenneth.carels@gmail.com

Fig. 1. — Supine chest X-ray revealed disseminated areas of hazy increased lung attenuation particularly in the perihilar region of the right lung.

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Fig. 3. â&#x20AC;&#x201D; Supine chest X-ray 2 hours later showing partially resolved lung attenuation with residual ground glass opacities in the right lung.

B 4. Fig. 2. â&#x20AC;&#x201D; MDCT of the thorax after intravenous administration of contrast: axial (A) and coronal (B) reconstruction demonstrate the lobular distribution of patchy ground-glass opacities around the hilum in the right lung and in the left upper lobe.

the pulmonary endothelium may also play a role in the pathogenesis but is still considered controversial (9). Both mechanisms establish an augmented transcapillary fluid efflux, which results in interstitial and alveolar edema. The X-ray findings are those seen in non-cardiogenic pulmonary edema: perihilar alveolar opacities most often symmetric and bilateral (bat-wing appearance), sometimes unilateral with a wide vascular pedicle. Pleural effusions are rare and the heart size is normal. CT findings consist of thickening of the septae, peribronchial cuffing and patchy ground-glass opacities around the hilum (10). The differential diagnosis with fat embolism, based on radiographic images alone, may be difficult and therefore the diagnosis is predominantly made on clinical basis (slow

onset of dyspnea, petechial rash and an altered mental status). A CT-scan can sometimes help in the differential diagnosis when fat containing embolic lesions are present in the pulmonary arteries. When the emboli are smaller, CT findings are more subtle and show ground glass or sometimes nodular opacities in a subpleural and centrilobular distribution, with more pronounced impairment of the peripheral lung regions compared to pulmonary edema (11). Treatment is focused on the resolution of the upper airway obstruction (O2, bronchodilatator, reintubation) and administration of diuretics (4). References 1. Scarbrough F., Wittenberg J., Smith B., et al.: Pulmonary edema following postoperative laryngospasm: case

8. 9.

10.

11.

reports and review of the literature. Anesth Prog, 1997, 44: 110-116. Westreich R., Sampson I., Shaari C.M., et al.: Negative pressure pulmonary edema after routineseptorhinoplasty. Arch Facial Plast Surg, 2006, 8: 8-15. Myles R.S., Iacono G.A., Hunt J.O., et al.: Risk of respiratory complications and wound infection in patients undergoing ambulatory surgery. Anesthesiology, 2002, 97: 842-847. Mulkey Z., Yarbrough S., Guerra D., et al.: Postextubation pulmonary edema: a case series and review. Respiratory Medicine, 2008, 102: 1659-1662. Halow K.D., Ford E.G.: Pulmonary edema following post-operative laryngospasm: a case report and review of the literature. Am Surg, 1993, 59: 443-447. Lorch D.G., Sahn S.A.: Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Chest, 1986, 90: 802-805. Holmes J.R., Hensinger R.W., Wojtys E.W.: Postoperative pulmonary edema in young, athletic adults. Am J Sports Med, 1991, 19: 365-371. Timby J., Reed C., Zeilender S., et al.: Mechanical causes of pulmonary edema. Chest, 1990, 98: 973-979. Fremont R., Kallet R., Matthay M., et al.: Postobstructive pulmonary edema: a case for hydrostatic mechanisms. Chest, 2007, 131: 1742-1746. Gleucker T., Capasso P., Schnyder P., et al.: Clinical and radiologic features of pulmonary edema. Radiographics, 1999, 19: 1507-1531. Choi J., Oh Y., Kim H., et al.: Nontraumatic pulmonary fat embolism syndrome: radiologic and pathologic correlations. J Thorac Imaging, 2002, 17: 167-169.

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NECROTIZING COLITIS COMPLICATING NECROTIZED PANCREATITIS: LOOK OUT FOR INTESTINAL PNEUMATOSIS M.A. Siddiqui1, A. Jain1, S.A.A. Rizvi2, K. Ahmad3, E. Ullah1, I. Ahmad1 Acute pancreatitis is a common cause of acute abdominal pain and is associated with a wide variety of complications. Pancreatic necrosis is one of the most important complications and is considered to be the most important indicator of disease severity as the increased frequency of death in acute pancreatitis is directly correlated with the development and extent of pancreatic necrosis. In addition to pancreatic necrosis, wide spectrums of colonic complications have been described, including functional and mechanical ileus, ischemic necrosis and fistula formation. In acute pancreatitis bowel ischemia usually involves the transverse colon or the hepatic and splenic flexures and may range in severity from mild superficial mural involvement totransmural colonic necrosis. This article reports a case of large bowel infarction as a complication of severe necrotizing pancreatitis in a 35-year-old male patient. Key-word: Pancreatitis.

Bowel ischemia is a devastating disease process encompassing a wide spectrum of clinical and radiological findings, ranging from a mild self-limiting form to bowel infarction and perforation. The conditions most frequently leading to bowel ischemia include vascular occlusion due to arterial or venous disease and hypoperfusion associated with nonocclusive vascular causes. Many other diseases may also cause such vascular changes, including abdominal inflammatory conditions such as

pancreatitis, appendicitis, diverticulitis, and peritonitis. Pancreatitis is associated with wide spectrum of colon lesions, including ileus, ischemic necrosis and fistula formation, the reported incidence being 1-15% among adult cases (1). In one series, 27% of patients with acute pancreatitis were complicated by ischemic enterocolitis (2). Early recognition of this particular complication of acute pancreatitis is important, as it is associated with very high morbidity and mortality. Here

we report a patient who developed colonic infarction as a complication of acute pancreatitis. Case report A 35-year-old man presented to the emergency department with 1day history of sudden onset of severe epigastric pain and profuse vomiting. On admission his vitals were stable. He had no previous hospital admissions and no previous similar episodes, but confessed hav-

Fig. 1. â&#x20AC;&#x201D; A. Frontal CT scout view shows focal dilatation of transverse colon with paucity of proximal and distal gas shadows consistent with colon cut-off sign (black arrows). An ill define speckled gas shadow was also present in right hypochonFrom: 1. Department of Radiodiagnosis, 2. Department of Surgery, Jawaharlal Nehru drium (white arrow). B. CT scan with lung Medical College, A.M.U. Aligarh, India, 3. Department of Radiodiagnosis, B.P. Koirala window confirmed these speckled gas Institute of Health Sciences, Dharan, Nepal. shadow to be mural air within wall of Address for correspondence: Dr. M.A. Siddiqui, MD, House No.7, Lane B, Hamza ascending colon consistent with pneuColony, New Sir Syed Nagar, Civil Lines, Aligarh, India-202002. matosis intestinalis. E-mail: drazfarsiddiqui@gmail.com

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Fig. 2. — A. CT scan at the level of pancreas showed necrosis in head and neck region along with peripancreatic fluid (black arrows). Bowel wall thickening along with mural air can be seen within ascending colon and hepatic flexure (white arrows). B. CT scan at the level of lung base revealed bilateral pleural effusion with basal atelectasis (white arrows).

ing binged on alcohol 3 days back. Physical examination revealed abdominal distention with mild right-sided tenderness but no evidence of peritonism. However patient appeared dehydrated. Laboratory examinations including urine analysis, complete blood count, liver and renal functions were within normal range except for mild leucocytosis (WBC count28,300/mm3). Serum amylase [1614 U/L (normal value < 220 U/L)] and serum lipase [815 U/L (normal value < 30 U/L)] were elevated. C reactive protein was also elevated at 314 mg/L. On erect chest radiograph, there was no free gas under diaphragm. However small bilateral pleural effusion was present. Supine Abdominal radiograph revealed focal dilatation of transverse colon with paucity of proximal and distal gas shadows (Fig. 1A). An ill define speckled gas shadow was present in right hypochondrium just below liver in the region of hepatic flexure. Ultrasonography of the abdomen demonstrated absence of gallstones and any dilatation of intrahepatic bile ducts or common duct. Pancreas and adjacent region was not visualized due to excessive bowel gas. Computed tomography (CT) of the abdomen showed heterogeneous diffusely enlarged pancreas with surrounding fat streakiness and free fluid (Fig. 2A). Non-enhancing area consistent with necrosis was seen in the head and neck region of pancreas. Circumferential thickening

of ascending colon extending up to the level of hepatic flexure was also present. There was evidence of water halo sign along with air within bowel wall suggestive of pneumatosis intestinalis (Fig. 1B). Bilateral small pleural effusion was also present (Fig. 2B). These findings were consistent with diagnosis of severe acute pancreatitis with necrotizing colitis. Patient’s condition was relatively stable considering the severity of radiologic findings and conservative management was advised. Patient was shifted to intensive care unit and was monitored closely. Prophylactic intravenous antibiotics and fluids were started. Three days after admission, the patient’s condition remained stable. A feeding tube was placed and enteral feeding started. Physiologic and biochemical parameters continued to improve and white cell count returned normal. A repeat CT seven days after admission showed resdiual pancreatic necrosis without significant peripancreatic fluid collections. The pneumatosisintestinalis had completely resolved notwithstanding some residual thickening of the wall of the ascending colon and hepatic flexure. On day 10 oral feeding was started and patient was discharged on day 18. Patient remained asymptomatic at follow-up 2 months later. Discussion Acute pancreatitis is an acute inflammatory process that is followed by complete restoration of

structural and functional normalcy after the attack subsides, provided that no part of pancreas has been destroyed by necrosis. A number of conditions are responsible for this, the most common being choledocholithiasis and alcohol abuse. Most patients present with nausea, vomiting and abdominal pain. The diagnosis is usually established by the detection of elevated levels of pancreatic enzymes in the blood, urine, or both. Once the diagnosis is established, the treatment of the patients is based on the assessment of disease stage and severity. CT is used not only to confirm the initial diagnosis but also to assess the severity of attack, and detect any complications. Modified CT severity index is a very useful scoring system that grades the severity of pancreatitis into mild, moderate and severe. In this index patients are given an even number from 0-10 on the basis of presence or absence of acute fluid collections, pancreatic parenchymal necrosis and extrapancreatic findings such as pleural fluid, ascites, extrapancreatic parenchymal abnormalities, vascular complications, or involvement of the gastrointestinal tract. Patients with a score of 8-10 are labeled as having severe acute pancreatitis and have worst prognosis. A number of systemic and locoregional complications are seen in patients of acute pancreatitis. Morbidity and mortality in acute pancreatitis is directly associated with the presence or absence of

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complications. Pancreatic necrosis and colonic lesions are two such complications associated with poor clinical outcome. Colonic complications are uncommon in the patients of acute pancreatitis. A recent analysis of pooled data reports the incidence of colonic complications from acute pancreatitis and severe acute pancreatitis as 3.3 and 15%, respectively (4). Although uncommon, colonic lesions are important as they indicate an extensive underlying inflammatory process (5). Colonic abnormalities associated with acute pancreatitis are divided into the following two groups from a pathological viewpoint: (a) Pericolitisshowing lesions mainly in the serosa and subserosa, in which pancreatic inflammation has extended directly through the mesentry; (b) Ischemic colitis, i.e., ischemic changes in mucosa, subucosa and tunica muscularis, developing into colonic necrosis and perforation in severe cases (6). Ischemic colitis is considered to result from a number of underlying patho-physiological mechanisms like congestion of blood flow due to compression by severe edema in the mesentery, thrombus formation in the mesenteric vessels, disseminated intravascular coagulopathy and, decreased blood pressure (7). Aldridge et al. reported transverse colon as the most common site of involvement (63%) followed by splenic flexure

(48%), descending colon (43%), ascending colon ((23%) and sigmoid colon (13%). In our patient, the ischemic changes were most conspicuous in the ascending colon. CT revealed thickening of the colonic wall with water halo sign and pneumatosis intestinalis, findings characteristic of transmural colonic necrosis. However no evidence of hepatic portal or portomesenteric venous gas was seen. There are many causes of pneumatosis intestinalis. It ranges from infectious, inflammatory, neoplastic, or iatrogenic mucosal injury to increased intraluminal pressure and asthma. Furthermore, it is important to differentiate it from pneumatosis cystoides coli, a benign condition of idiopathic etiology. Benign pneumatosis often appears as cystlike collections of gas in the bowel submucosa, while curvilinear, more circumferential gas collections is often considered as characteristic of bowel infarction. The management of colonic complications of severe acute pancreatitis relies on a high index of suspicion because the clinical presentation is varied, nonspecific, and could occur quite late in the disease process (4). Because such cases mainly have been reported as case reports and series, there are no evidence-based guidelines for management (4). Although surgical intervention remains the choice of treatment when nonviability of the

colon is determined, resection may be difficult and complicated. Fortunately in our case patient remained stable and responded well to conservative management probably because of good general health and young age. References 1.

Aldridge M.C., Francis N.D., Glazer G., Dudley H.A.: Colonic complications of severe acute pancreatitis. Br J Surg, 1989, 76: 362-367. Gumaste V.V., Gupta R., Wasserman D., Dave P.B., Vieux U.: Colonic involvement in acute pancreatitis. Am J Gastroenterol, 1995, 90: 640-641. Takahashi Y., Fukushima J., Fukusato T., Shiga J., Tanaka F., Imamura T., Fukayama M., Inoue T., Shimizu S., Mori S.: Prevalence of ischemic enterocolitis in patients with acute pancreatitis. J Gastroenterol, 2005, 40: 827-832. Mohamed S.R., Siriwardena A.K.: Understanding the colonic complications of pancreatitis. Pancreatology, 2008, 8: 153-158. Thompson W.M., Kelvin F.M., Rice R.P.: Inflammation and necrosis of the transverse colon secondary to pancreatitis. AJR, 1977, 128: 943-948. Yamagiwa I., Obata K., Hatanaka Y., Saito H., Washio M.: Ischemic colitis complicating severe acute pancreatitis in a child. J Pediatr Gastroenterol Nutr, 1993, 16: 208-211. Wiesner W., Khurana B., Ji H., Ros P.: CT of Acute Bowel Ischemia. Radiology, 2003, 226: 635-665.

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PERSISTENT STAPEDIAL ARTERY: A CONGENITAL ANOMALY TO KNOW M.I. Nica, G. Cosnard1 Persistent stapedial artery, one of the rare arterial congenital anomalies of the middle ear, is important to know due to its possible clinical repercussions. Ignoring its existence may lead to complications during surgery of the middle ear (notably hemorrhage). Exploration of the vascular malformation is rendered possible via high-definition computed tomography (CT) imaging of the petrous bones, which reveals the frequent bilaterality of this anatomical variation as well as the presence of associated anomalies. We report on two cases of persistent stapedial artery discovered during CT scan explorations. Key-word: Arteries, abnormalities.

Case report A 36-year-old patient presented with hypoacousia of the right ear, evolving for over one year. CT imaging in fine slices with multiplanar reconstructions revealed a small tubular mass 4mm in size, exiting from the angle of the internal carotid artery and passing between the branches of the stirrup (Fig. 1) before joining the tympanic segment of the facial nerve channel (Fig. 2). There was no spiny foramen (not illustrated). A diagnosis of a persistent stapedial artery was made. Prior to cochlear implantation, a CT scan of the petrous bones was performed on a 6-year-old child. The absence of spiny foramen was bilateral (Fig. 3). A small tubular structure showing a cranial-caudal path was visible from the promontory, in front of the fenestra vestibuli, in contact with the anterior branch of the stirrup and rejoining the enlarged facial channel in a bilateral manner (Fig. 4). A diagnosis of a persistent stapedial artery was made.

Fig. 1. — CT scan of right petrous bone using oblique axial reconstructions reveals the presence of a nodular element between the two branches of the right stirrup (white arrow).

Discussion Persistent stapedial artery is a rare vascular anomaly, with a prevalence estimated to be between 0.02% and 0.05% in a surgical series (1) and slightly higher in a study focused on the temporal bone (2). This condition is often clinically unknown, as it is generally asymptomatic and discovered fortuitously. It may be revealed as a retro-tympanic beating red mass on otoscopic examination or during an imaging examination with direct visualization of the abnormal vessel.

Fig. 2. — CT scan of right petrous bone using oblique coronal slices: visualization of the stapedial artery exiting from the internal carotid artery and joining the tympanic segment of the facial channel (white arrows).

From: 1. Department of Radiology and Medical Imaging, Cliniques Universitaires SaintLuc, Brussels, Belgium. Address for correspondence: Dr M.I. Nica, M.D., Department of Radiology and Medical Imaging, Cliniques Universitaires Saint Luc, Avenue Hippocrate 10, B-1200 Bruxelles, Belgium. E-mail: nicairina2003@yahoo.com

The most common clinical sign is the presence of a pulsating tinnitus. More rarely, there may be a conductive deafness due to ankylosis of the stirrup. At times, this anomaly is

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Fig. 3. — CT scan with transverse slices passing through the petrous bones using MIP reconstructions reveals the absence of the spiny foramen on both sides.

Fig. 4. — CT scan with axial slices passing through the petrous bones shows a persistent stapedial artery on both sides.

Fig. 5. — A: in utero, B: normal, C: persistent stapedial artery. ACP: primary carotid artery; ACI: internal carotid artery; ACE: external carotid artery; AMax: maxillary artery; AMM: meningeal middle artery; AS:stapedial artery.

detected in patients with trisomy 13, Paget’s disease, or osteosclerosis (3). This abnormality is congenital in nature and occurs in the case of abnormal regression or absent

regression of the embryonic vessels during the course of development (4, 5). Persistent stapedial artery is an abnormal vessel issuing from the intra-petrous internal

carotid artery that crosses the middle ear by passing through the branches of the stirrup. The artery terminates as a middle meningeal artery. The anomaly may occur solely or be associated with an aberrant crossing of the internal carotid artery in the middle ear (6). To better comprehend this particular anatomical pathway, one needs to understand the modifications of embryonic development leading to this anomaly. The stapedial artery is normally present in the embryo. It derives from the intra-petrous portion of the internal carotid artery and divides, naturally, into two branches, namely a superior branch that becomes the middle meningeal artery and an inferior branch that becomes the maxillary artery, which exits the cranial cavity via the spiny foramen. In the rare cases when it does not regress, the stapedial artery becomes, in the adult, the middle meningeal artery without the spiny foramen (Fig. 5). CT scan with fine slices and multiplanar reconstructions permits the diagnosis (7) via a direct visualization of the artery in the form of a hypodense tubular structure of 1 to 2mm in diameter, presenting at the level of the promontory and stirrup. Two key indirect signs are: the absence of the spiny foramen and the enlargement of the tympanic segment of the facial channel.

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Conclusion Persistent stapedial artery is a rare congenital anomaly, often asymptomatic and of unknown existence. Its identification is crucial in order to prevent hemorrhagic complications during surgery of the internal ear. During the analysis of a CT scan of the petrous bones, a systematic examination of the spiny foramen should be performed. References 1. David G.D.: Persistent stapedial artery: a temporal bone report.

J Laryngol Otol, 1967, 81: 649-660 Medline. 2. Moreano E.H., Paparella M.M., Zelterman D., Goycoolea M.V. (1994). Prevalence of facial canal dehiscence and of persistent stapedial artery in the human middle ear, a report of 1000 temporal bones. The Laryngoscope, 104 (3 Pt 1): 309-320. 3. Boscia R., Knox R.D., Adkins W.Y., Holgate R.C.: Persistent stapedial artery supplying a glomus tympanicum tumor. Arch Otolaryngol Head Neck Surg, 1990, 116: 852854. 4. Altmann F.: Anomalies of the internal carotid artery and its

branches: their embryological and comparative anatomical significance. Report of a new case of persistent stapedial artery in man. Laryngoscope, 1974, 57: 313-319. 5. Hog I.D., Stephens C.B., Arnold G.E.: Theorical anomalies of the stapedial artery. Ann Otol Rhinol Laryngol, 1978, 81: 860870. 6. Silbergleit R., Quint D.J., Mehta B.A., et al.: The persistent stapedial artery. AJNR, 21: 572577 7. Thiers F., Sakai O., Poe D., Curtin H.: Persistent stapedial artery: C.T. findings. AJNR, 2000, 21: 1551-1554.

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PREGNANCY-LIKE (PSEUDOLACTATIONAL) HYPERPLASIA: UNCOMMON CAUSE OF MICROCALCIFICATIONS AND MASS IN TWO CASES A. Koktener1, B. Cakir1, K. Akin1, D. Kosehan1, R. Bayrak2, S. Yenidunya2 Pregnancy-like (pseudolactational) hyperplasia (PLH) is an uncommon lactational change occurring independently from pregnancy and lactation. PLH has been incidentally found during breast biopsies. We report two different cases of PLH with their clinical, radiologic, and pathologic findings. Key-word: Breast.

Pregnancy-like (pseudolactational) hyperplasia (PLH) is not a common lactational change in hyperplastic duct. PLH has been determined as an incidental finding in surgical breast biopsies for benign and malignant cases. The frequency of PLH is approximately 3% among reported autopsy and surgical series (1-3). Pathologic features have been reported in the literature. However, radiologic findings have not been previously demonstrated. Herein, we report two different cases of PLH with their clinical, radiologic, and pathologic findings. Case reports

Fig. 1. — Craniocaudal mammogram of the left breast shows cluster of microcalcifications.

Case 1 A 45-year-old woman with a family history of breast cancer underwent a screening mammogram. According to the American College of Radiology Breast Imaging and Reporting Data Systems (BIRADS), suspicious microcalcifications (category IV) were detected in the upper quadrant of the left breast (Fig. 1). Ultrasound examination did not show any abnormality. Physical examination was normal. Stereotactic vacuum-assisted biopsy was achieved via 10-gauge Vacura on a prone mammography biopsy table (Fig. 2). Histopathologic examination showed pseudolactational hyperplasia including acini containing intraluminal calcification with a laminated appearance, hypersecretory cells with vesicular nuclei and vacuolated cytoplasm. Case 2 A 75-year-old woman was admitted for screening mammogram. Mammograms showed retroareolar

Fig. 2. — Mammogram of the specimen obtained by stereotactic vacuum-assisted biopsy shows microcalcifications.

localized microlobulated mass (BIRADS category IV) measuring 15 × 12 mm (Fig. 3). Ultrasound examination confirmed a hypoechoic mass in the same location

From: Department of 1. Radiology, 2. Pathology, School of Medicine, Fatih University, Ankara, Turkey. Address for correspondence: Dr A. Koktener, M.D., Department of Radiology, School of Medicine, Fatih University, Alparslan Turkes Cad. No: 57 06510 Emek-Ankara, Turkey. E-mail: akoktener@yahoo.com

(Fig. 4). Physical examination was normal. She had been taking an antihypertensive drug including besarten and hydrochlorthiazide Ultrasound guided 14-gauge trucut biopsy was performed. Pathologic examination revealed hyperplastic secretory changes with pregnancy like changes including acinar cells with vacuolated eosinophilic cytoplasm and cystic hyperplasic ductus in multipl adenosis foci.

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Fig. 4. — Ultrasonographic examination shows a hypoechoic lobulated breast mass (arrows).

References

Fig. 3. — Craniocaudal mammogram of the left breast determines retroareolar localized microlobulated mass.

Discussion Pregnancy-like changes in nonpregnant women were described by Moran in 1935 (4). PLH is a pregnancy-like change in hyperplastic epithelium which occurs independently from pregnancy and lactation. PLH is often associated with intraluminal secretions and laminated microcalcifications detected on mammography (5). Shin et al.reported the pathologic features of PLH including microcalcifications or breast masses detected on mammography (6). In one of the cases, we observed microcalcifications and in the other, a breast mass on mammography. PLH was often seen many years after pregnancy and lactation. Hormonal status and history of parity were not important in the occurrence of PLH. Some patients had no history of pregnancy or hormonal use. It was concluded that PLH in nonlactating, nonpregnant women was the result of selective

susceptibility to estrogen as a nonpathologic variation of normal female breast (2). On the other hand, antipsychotic and antihypertensive drugs, high dose estrogen for advanced breast carcinoma and prostatic carcinoma were reported to correlate with PLH (7-9). Both of our cases had a history of pregnancy and lactation. One of them with breast mass has been taking antihypertensive drug including besarten and hydrochlorthiazide. Microcalcifications and breast masses detected by mammography could be the result of PLH. In the differential diagnosis, this uncommon entity should be kept in mind by the radiologists and surgeons. Pathologic examination is necessary for accurate diagnosis. PLH without atypia is often considered a physiologic abnormality and not a precancerous sign. Whenever PLH is associated with atypia or cystic hypersecretory hyperplasia, surgical excision is recommended (6, 10).

1. Frantz V.K., Pickren J.W., Melcher G.W., Auchincloss H. Jr.: Incidence of chronic cystic disease in so-called normal breasts. A Study based on 225 postmortem examinations. Cancer, 1951, 4: 762-783. 2. Kiaer H.W., Andersen J.A.: Focal pregnancy-like changes in the breast. Acta Pathol Microbiol Scand, 1977, 85: 931-941. 3. Sandison A.T.: An autopsy study of the adult human breast. Natl Cancer Inst Monogr, 1962, 8: 58-59. 4. Moran C.S.: Fibro-adenoma of the breast during pregnancy and lactation. Arch Surg, 1935, 31: 688-708. 5. Rosen P.P.: Rosen’s Breast Pathology. 2nd ed. Philadelphia: Lippincott Williams and Wilkins. 2001: Chapter 1, Anatomy and physiologic morphology. 6. Shin J.S., Rosen P.P.: Pregnancy-like (pseudolactational) hyperplasia: a primary diagnosis in mammographically detected lesions of the breast and relationship to cystic hypersecretory hyperplasia. Am J Surg Pathol, 2000, 24: 1670-1674. 7. Huseby R.A., Thomas L.B.: Histological and histochemical alterations in the normal breast tissues of patients with advanced breast cancer being treated with estrogenic hormones. Cancer, 1954, 7: 54-74. 8. Schwartz I.S., Wilens S.L.: The formation of acinar tissue in gynecomastia. Am J Pathol, 1963, 43: 797-807. 9. Tavassoli F.A., Yeh I.T.: Lactational ad clear cell changes of the breast in nonlactating, nonpregnant women. Am J Clin Pathol, 1987, 87: 23-29. 10. Shin J.S., Rosen P.P.: Carcinoma arising from preexisting pregnancylike and cystic hyprsecretory hyperplasia lesions of the breast: a clinicopathologic study of 9 patients. Am J Surg Pathol, 2004, 28: 789-793.

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SPORADIC SUPRAVALVULAR STENOSIS IN A YOUNG MAN K.M. Ghodduci1, M. Antic1, K. Tanaka1, D. Verdries1, D. Kerkhove2 Supravalvar aortic stenosis (SVAS) is a form of congenital left ventricular outflow tract (LVOT) obstruction that occurs as a localized or diffuse narrowing of the ascending aorta beyond the superior margin of the sinuses of Valsalva. SVAS is a rare progressive congenital heart defect with a higher risk of sudden cardiac death. Our patient was a 30-yearold man referred by his GP for an incidental finding of heart murmur. Echocardiography showed a hypertrophic left ventricle with an increased pressure gradient. CT and MRI angiography and eventual arteriography confirmed the diagnosis by showing a narrowing of the aorta at the sinotubular junction with significant accelerated flow. This stenosis was eventually surgically corrected with no complications. Key-word: Aorta, stenosis or obstruction.

Supravalvular aortic stenosis (SVAS) is an uncommon but well characterized congenital narrowing of the ascending aorta above the level of the coronary arteries. It can be a familial disorder, can occur sporadically, or be associated with Williams syndrome (WS) which is a neurodevelopmental disorder affecting connective tissue and the central nervous system. Sudden cardiac death has a higher prevalence in patients with congenital supravalvular aortic stenosis. Case presentation A 30-year-old man was referred by his GP for an incidental finding of a heart murmur. Physical examination showed a mid-systolic murmur without further abnormalities. ECG showed sinus rhythm with signs of inferior and lateral strain. Genetic evaluation was normal. Transthoracic echocardiography showed a hypertrophic left ventricle with a septal thickness of 20 mm and accelerated flow above the aortic valve with a pressure gradient of 89mmHg. Supravalvular aortic stenosis was suspected. Further cardiac MRI angiography confirmed a concentric hypertrophic left ventricle (Fig. 1) without signs of delayed enhancement (Fig. 2). MRI angiography showed a supravalvular aortic stenosis (Fig. 3) with accelerated flow above the aortic valve (Fig. 4). Conventional angiography confirmed the presence of an aortic stenosis at the sinotubular junction with a maximum diameter of 18 mm and normal coronaries (Fig. 5). No

Fig. 1. — Short axis view showing concentric left ventriclular hypertrophy.

Fig. 2. — Image after contrast administration: absence of delayed enhancement.

other vascular abnormalities were found. The stenotic lesion was surgically corrected (Fig. 6). Discussion Supravalvar aortic stenosis is the rarest lesion of the left ventricular outflow tract obstruction abnormalities (LVOTOs).The majority of cases of congenital SVAS are associated with Williams-Beuren syndrome (WS). WS has an incidence of approximately 1:20,000 live births (1). Sudden death occurs at a rate higher than in the general population, both in patients with congenital supravalvular aortic stenosis associated with WS and nonsyndromic SVAS. WBS was first described in 1961 as a combination of stenoses of the large- and medium-sized arteries combined with facial dysmorphic

From : 1. Department of Radiology, 2. Department of Cardiology, UZ Brussel, Brussels, Belgium. Address for correspondence : Dr K.M. Ghodduci, Department of Radiology, UZ Brussel, Laerbeeklaan 101, B-1090 Brussels, Belgium. E-mail : kghodduci@yahoo.com

Fig. 3. — Three chamber view showing supravalvular aortic stenosis.

signs, short stature, failure to thrive and mild to moderate mental retardation. Associated features include transient hypercalcaemia in infancy, small teeth, joint stiffness, scoliosis, sensorineural hearing loss, hyperreflexia, problems of visio-spatial processing and anxiety. The syndrome is caused by heterozygous microdeletion of the ‘WBS critical

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Fig. 4. — Left ventricular outlet view showing turbulent flow at the level of stenosis.

Fig. 6. — Correction of the stenosis after surgery.

Fig. 5. — Confirmation of supravalvular aortic stenosis at angiography.

region’ on the long arm of chromosome 7 (2). The vascular features of congenital SVAS are due to an elastin arteriopathy. A large quantity of elastin is normally present in the media of the great vessels, whereas smooth muscle and collagen are the primary components of smaller arteries. Smooth muscle cells from patients with isolated SVAS produce only 50% of the elastin produced by normal cells, whereas smooth muscle cells from patients with WS produce only 15% of the normal quantity of elastin (3). The reduced net deposition of arterial wall elastin leads to increased proliferation of arterial wall smooth muscle cells resulting in multilayer thickening of the media of large arteries and subsequent development of obstructive hyperplastic intimal lesions. As a result, a characteristic hourglass narrowing of the aorta develops at the sinotubular junction. In approximately 30% of cases, there is diffuse tubular narrowing of the ascending aorta, often extending to the arch and the origin of the brachiocephalic vessels (4). In approximately 40% of WS patients, there is severe pulmonary stenosis and right ventricular pressure overload on top of the LV pressure overload and hypertrophy (5). The aortic valve may also be involved in SVAS. The elastin arteriopathy may involve the coronary arteries in a diffuse pattern whereas a thickened aortic wall can directly narrow the coronary ostia (6). There may also be stenosis in the renal and mesenteric arteries. The diagnosis of SVAS can be made by multiple imaging modali-

ties. CT and MR imaging allow visualization of the entire aorta and are the modalities of choice to demonstrate the extent of the SVAS (7). If an ECG-gated technique is used, associated findings such as left ventricular myocardial hypertrophy and BAV can be depicted. Cardiac magnetic resonance imaging and computer tomography are capable of showing ventricular hypertrophy, wall motion abnormalities, myocardial tissue characteristics, associated vascular anomalies. In addition they are able to diagnose obstructive coronary disease. Transthoracic Doppler echocardiography is useful in deriving peak instantaneous and mean pressure gradients. However, the full extent of the ascending aorta is difficult to visualize in adults with transthoracic echocardiography; transesophageal echocardiography is superior. Echocardiography is useful in assessing ventricular hypertrophy, ventricular outflow tract gradients, and wall motion abnormalities but is an insensitive method for evaluating coronary blood flow. Cardiac catheterization with coronary and aortic angiography remains the “gold standard” for delineation of aortic leaflet tethering and assessment of coronary artery lumen calibre (1). Obviously, cardiac catheterization carries its own risks in these patients. Surgical correction of the narrowing is indicated in symptomatic patients (ie, those with angina, dyspnea, syncope) or those with a mean

pressure gradient of greater than or equal to 50 mm Hg. Balloon angioplasty is not useful. Patients with SVAS and Williams syndrome show regression of stenosis without intervention, and overall survival after treatment is excellent (94% at 10 years) (7). Conclusion SVAS is a rare progressive congenital heart defect with a higher risk of sudden cardiac death than in the general population, emphasizing the importance of early diagnosis. Identifying those patients with congenital SVAS at risk for myocardial ischemia is challenging, and each patient has to be monitored closely. Cardiac imaging modalities, including multislice computed tomography and magnetic resonance imaging, show increasing promise as noninvasive imaging modalities to detect SVAS. These noninvasive modalities also can correctly identify other cardiac, aortic and pulmonary vascular abnormalities in the same session. References 1.

Burch T.M., McGowan F.X. Jr., Kussman B.D., Powell A.J., DiNardo J.A.: Congenital supravalvular Aortic Stenosis and Sudden Death Associated with Anesthesia: What s the Mystery? Anesth Analg, 2008, 107: 1848-1854. 2. Gimpel C., Schaefer F.: WilliamsBeuren syndrome-stretching to learn big lessons from small patients. Nephrol Dial Transplant, 2010, 25: 339341. 3. Urban Z., Zhang J., Davis E.C., Maeda G.K., Kumar A., Stalker H.,

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SPORADIC SUPRAVALVULAR STENOSIS â&#x20AC;&#x201D; GHODDUCI et al Belmont J.W., Boyd C.D., Wallace M.R.: Supravalvular aortic stenosis: genetic and molecular dissection of a complex mutation in the elastin gene. Hum Genet, 2001, 109: 512-520. 4. Stamm C., Li J., Ho S.Y., Redington A.N., Anderson R.H.: The aortic root in supravalvular aortic stenosis: the potential surgical relevance of morphologic findings. J

Thorac Cardiovasc Surg, 1997, 114: 1624. 5. Stamm C., Friehs I., Ho S.Y., Moran A.M., Jonas R.A., del Nido P.J.: Congenital supravalvar aortic stenosis: a simple lesion? Eur J Cardiothorac Surg, 2001, 19: 195-202. 6. Matsuda H., Miyamoto Y., Takahashi T., Kadoba K., Nakano S., Sano T.: Extended aortic and left main coronary angioplasty with a single peri-

cardial patch in a patient with Williams syndrome. Ann Thorac Surg, 1991, 52: 1331-1333. Kimura-Hayama E., Melendez G., Mendizabal A., Meave-Gonzalez A., Zambrana G., Corona-Villalobos C.: Uncommon Congenital and Aquired Aortic Diseases: Role of Multidetector CT angiography. Radiographics, 2010, 30: 79-98.

ANNOUNCEMENTS FROM THE MUSEUM

War and peace in Radiology Exhibition and meeting Date: April 20,2013 at 3.00 PM Venue: Military Hospital Brussels The exhibition shows the military events on the Yser front line during WWI and stresses the positive repercussions of the conflict by showing the evolution of Radiology from the pioneers to present-day medical imaging.

Information: info@radiology-museum.be

Symposium on Military Radiology during the Great War Date: April 26, 2013 Venue: Military Hospital, Bruynstreet 20, B-1120 Brussels Information: info@radiology-museum.be A new publication:

Radiology in a Trench Coat Military radiology on the Western front during the Great War by R. Van Tiggelen 220 p., 30.00 â&#x201A;Ź ISBN 9789038219394 Information and orders: www.academiapress.be

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PERIOSTEAL CHONDROMA OF THE PROXIMAL TIBIA MIMICKING OSGOODSCHLATTER’S DISEASE T. Vancauwenberghe1, F.M. Vanhoenacker2,3,4, J. Van Doninck5, H. Declercq6 We report a case of a periosteal chondroma of the proximal tibia in an 11-year-old girl, which was initially misdiagnosed as Osgood-Schlatter’s disease. The absence of pain and meticulous analysis of the imaging findings on initial and follow-up plain radiographs, ultrasound and MRI allowed to suggest the diagnosis of a periosteal chondroma, which was confirmed after biopsy. Besides the difficulty in the imaging diagnosis of the lesion, determination of the optimal treatment strategy may be challenging as well. Given the localization of this lesion close to the growth plate, decision has to be made whether the lesion will be treated surgically or a waitful watching policy will be implemented in order to prevent interference with the normal growth of the bone.

Periosteal or juxtacortical chondroma is an uncommon benign cartilaginous neoplasm, affecting children and adolescents. When the lesion is located at the proximal tibia adjacent to the unfused apophysis of tibial tuberosity (TT), the diagnosis can be particularly challenging, because of its radiological resemblance to Osgood-Schlatter’s disease. The purpose of this paper is to report the distinctive clinical and imaging features allowing a correct diagnosis of this unusual lesion in order to initiate appropriate treatment. Case report An 11-year-old healthy girl presented with a painless firm swelling at the anterior aspect of the left proximal tibia. There was no history of trauma and there were no signs of inflammation. Standard radiographs of the left knee showed a subtle softtissue swelling with intralesional calcifications adjacent to the left tibial tuberosity (Fig. 1). The lesion was initially interpreted as OsgoodSchlatter’s disease and relative rest was recommended. Nine months later, she was readmitted with a slightly grown swelling. Repeated lateral radiograph revealed a marked cortical remodelling distal to the TT, with cortical scalloping, endosteal sclerosis, and abundant superficial cartilaginous calcifications. The lesion also demonstrated thickening of the cortex at its proximal and distal margins, in keeping with a “cortical buttress sign” (Fig. 2). On

Fig. 1. — Initial lateral radiograph of the left knee. Note the presence of a soft-tissue swelling with intralesional calcifications distal to the tibial tuberosity (arrow), mimicking OsgoodSchlatter’s disease. The lesion is – however – located distal to the apophysis. Moreover, cortical thickening of the adjacent anterior tibia is unusual for Osgood-Schlatter’s disease.

ultrasound, there was – however – no thickening of the distal patellar tendon (Fig. 3). These findings argue against the diagnosis of OsgoodSchlatter and rather suggest a

From: 1. Department of Radiology and Imaging, H.H. Ziekenhuis, Lier, Belgium, 2. Department of Radiology, AZ Sint-Maarten, Duffel-Mechelen, 3. Department of Radiology, Antwerp University Hospital, University of Antwerp, Edegem, 4. Faculty of Medicine and Health Sciences, University of Ghent, 5. Department of Orthopedic Surgery, AZ Sint-Maarten, Duffel-Mechelen, 6. Department of Radiology, AZ SintBlasius, Dendermonde. Address for correspondence: Prof. Dr. F.M. Vanhoenacker, Dept. of Radiology, AZ SintMaarten, Duffel-Mechelen, Rooienberg, 25, B-2570 Duffel, Belgium.

tumoral lesion of the bone. Magnetic resonance imaging (MRI) was performed for further lesion characterization, which revealed a juxtacortical cartilaginous mass, adjacent to the growth plate of the TT (Fig. 4). After multidisciplinary discussion, the decision was made to remove the lesion surgically. A local resection with curettage of the adjacent cortex was performed. Histologically, the diagnosis of periosteal chondroma was made. Postoperative recovery was uneventful and there has been no recurrence for 3 years.

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Discussion

Fig. 2. — Follow-up lateral radiograph of the left knee shows abundant superficial cartilaginous calcifications (curved arrow) and thickening of the cortex at its proximal and distal margins (arrowheads), in keeping with a “cortical buttress sign”.

B Fig. 3. — Ultrasound of the left knee. Axial (A) image showing a hypo-echogenic lesion to the tibial tuberosity (curved arrow), with multiple intralesional reflections causing a retro-acoustic shadowing (arrowheads) in keeping with calcifications. Longitudinal (B) image showing a normal reflectivity and thickness of the patellar tendon (arrowheads).

Periosteal (juxtacortical) chondroma is a slowly growing, benign tumoral lesion of cartilaginous origin, originally described by Lichtenstein and Hall in 1952 (1). It must be distinguished from an osteocartilaginous exostosis and from a solitary enchondroma, as it arises between the cortical bone and the periosteum of tubular bones, leaving the medullary cavity unaffected. Although it can occur at any age, this tumor predominantly occurs in children or young adults, with a male predilection. Periosteal chondroma usually arises at the osseous insertions of tendons and ligaments or at the metaphyseal region of the long tubular bones, such as the femur and humerus. The bones of the hand and feet are also frequently affected (2). Clinically, it most often presents as a painless swelling with progressive onset. Frequently, it is an incidental radiographic finding. Plain radiographic features include a cortically based, radiolucent soft tissue mass, scalloping or remodelling of the adjacent underlying bony cortex with an endosteal border of sclerosis, matrix calcifications (occurring in approximately 50% of patients) and a “cortical buttress sign” (3). Irregularity of the osseous surface may be misinterpreted as a malignant tumor (3). On CT, cortical scalloping and intralesional matrix calcifications may be appreciated more in detail. On MR imaging the typical features of a water-rich cartilaginous tumour are found, consisting of a matrix of hyperintense signal relative to fat on T2-weighted images (WI), and of hypo- to isointense signal relative to muscle on T1-WI. Intralesional calcifications can be seen as areas of low signal intensity on both pulse sequences. The lesion is typically well delineated and often bordered by a hypointense rim on T2-WI. No bone marrow edema nor soft tissue edema is seen. Contrast enhancement is observed predominantly at the periphery of the cartilage nodules (ring-and-arc enhancement). Radiographically, differentiation has to be made with other benign and malignant tumor and tumor-like conditions, such as a osteocartilaginous exostosis (osteochondroma), in which there is continuity of both the cortical and the medullary bone. Differentiation has also to be made with an enchondroma, which is located in the medullary cavity, and

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A C

B Fig. 4. â&#x20AC;&#x201D; MR imaging of the left knee. Axial (A) and sagittal (B) fat-suppressed T2-WI, sagittal spin-echo (SE) T1-WI( C) and axial fat-suppressed T1-WI after intravenous administration of gadolinium contrast (D). Note a well-delineated juxtacortical lesion (arrow) measuring 2.5 cm, adjacent to the growth plate of the tibial tuberosity. Heterogeneity with foci of hypo-intense signal on both non-enhanced T1- and T2-WI, and peripheral ring-and-arc enhancement pattern (arrowheads) after intravenous administration of gadolinium contrast.

with a Ewing's sarcoma. The latter is a fast growing osteolytic lesion causing an unsharp margination of the cortical bone. A huge soft tissue extension is the rule. Of particular interest is the differential diagnosis with a periosteal chondrosarcoma. As a periosteal chondrosarcoma represents a relatively slow-growing malignancy, reactive sclerosis and scalloping may be seen, very similar to the radiological appearance of a

periosteal chondroma. However, a periosteal chondrosarcoma is generally larger, occurs in an older population, and tends to permeate the underlying bone with formation of bony spicules extending out from the cortex (4). A periosteal chondroma occurring at the TT in skeletally immature patients, such as in our case, may mimic a chronic avulsive lesion at the insertion of the patellar tendon

into the TT (Osgood-Schlatterâ&#x20AC;&#x2122;s disease). Clinically, Osgood-Schlatter is characterized by focal pain at the TT. On plain radiographs, fragmentation involves the TT itself, instead of the cortical bone underneath the TT. Moreover, on ultrasound, the distal patellar tendon is widened, hypoechoic and there may be hypervascularity around the fragmented TT on power Doppler imaging. MR imaging may demonstrate an

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associated infrapatellar bursitis, marrow edema within the proximal tibia, and thickened cartilage anterior to the tibial tubercle (5). Histologically, periosteal chondroma is characterized by lobulated immature cartilaginous tissue, covered by a fibrous periosteal capsule. Pathologic differentiation with a low-grade chondrosarcoma may be difficult. Medullary invasion is the most valuable differentiating finding on histopathology, as this never occurs in a periosteal chondroma. The preferred treatment for asymptomatic lesions consist of waitful watching (6), especially when excision can affect subsequent growth in children. For painful lesions, local excision, with curettage of the adjacent saucerized cortical bone is curative (7). However, when clinical and radiographic findings are inconclusive, a pre-operative excisional biopsy is mandatory. Although the recurrence rate is low, some advo-

cate adjuvant cryotherapy in order to avoid local recurrence. Conclusion When located at the tibial tuberosity, a periosteal chondroma may mimic Osgood-Schlatterâ&#x20AC;&#x2122;s disease. Awareness of this uncommon lesion, correct interpretation of clinical (absence of pain, progressive growth), imaging features and demonstration of the cartilaginous matrix on MRI may help to avoid misdiagnosis. References 1.

Lichtenstein L., Hall J.E.: Periosteal chondroma: a distinctive benign cartilage tumor. J Bone Joint Surg, 1952, 34-A: 691-697. 2. Kirchner S.G., Pavlov H., Heller R.M., Kaye J.J: Periosteal chondromas of the anterior tibial tubercle: Two Cases. AJR Am J Roentgenol, 1978, 131: 1088-1089.

3. Resnick D.: Tumors and tumor-like lesions of bone: Imaging and pathology of specific lesions. In: Diagnosis of bone and joint disorders. Edited by Resnick D. Printed by W.B. Saunders, Philadelphia, 2002, pp 3763-4128. 4. Robinson P., White L..M., Sundaram M., et al.: Periosteal chondroid tumors: radiologic evaluation with pathologic correlation. AJR Am J Roentgenol, 2001, 177: 11831188. 5. Gottsegen C.J., Eyer B.A., White E.A., Learch T.J., Forrester D.: Avulsion fractures of the knee: imaging findings and clinical significance. RadioGraphics, 2008, 28: 1755-1770. 6. Dhammi I.K., Maheshwari A.W., Jain A.K., Gulati D..: Subtrochanteric periosteal chondroma: A case report and tumor overview. Ind J Radiol Imag, 2006, 16: 329-332. 7. Brien E.W., Mirra J.M., Luck J.V.: Benign and malignant cartilage tumors of bone and joint: their anatomic and theoretical basis with an emphasis on radiology, pathology and clinical biology. II. Juxtacortical cartilage tumors. Skeletal Radiol, 1999, 28: 1-20.

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Continuing Education Dual Energy CT: added value in gouty arthritis* J. Spermon, C.F. Van Dijke1 Gouty arthritis is an inflammatory reaction as a result of monosodium urate crystal deposition in synovial fluid and periarticular soft tissue. It is the most common form of inflammatory arthritis with an estimated prevalence of 5 per 1000 in the USA. Clinical diagnosis is difficult and definite diagnosis with positive urate crystal aspiration often is made late in the disease process. Dual energy computer tomography (DECT) is a relative new non-invasive imaging modality that is able to distinguish urate crystals from calcium in soft tissue and synovial fluid. In this case report we describe the potential of DECT in gout by clarifying the technical background and present two cases in which DECT confirms the clinical diagnosis and shows the extend of the disease. Although more extensive studies should be done to validate DECT in diagnosing gout, the preliminary results in diagnosing gout, determining the extensiveness and monitoring therapy are promising. Key-word: Gout.

Gout is the most common form of inflammatory arthritis. In about 90% it presents as monoarticular arthritis, often starting at the first metatarsophalangeal joint. Four gradually stages of gout can be distinguished: first of all asymptomatic hyperuricemia, then the first presentation of acute gouty arthritis with clinical symptoms of pain and swelling. This is followed by intercritical gout with interval attacks and when left untreated it finally leads to chronic tophaceous gout with permanent joint damage and sometimes even kidney failure. Incidence rates are estimated to 5 per 1000 in the US (1). This makes gout the most common form of inflammatory arthritis in adult men. The prevalence of gout is much higher in men, with peak prevalence beyond the 4th decade, than in women, who develop gout mainly in the postmenopausal period. In this case report we present two cases of gout in which DECT had a crucial role in diagnosing gout and showing the extend of the disease. The basic technical principles of DECT are outlined and the practical usefulness of DECT is presented. Gout is a disease that occurs as a response to monosodium urate crystals deposition in periarticular soft tissue, joints and subchondral bone with secondary destruction of joints

and bones. Hyperuricemia is the underlying cause, in 80-90% this is due to high level of uric acid renal re absorption. Ultimately, a period of elevated serum uric acid leads to crystallization in the form of monosodium urate (ionized extracellular uric acid). Crystal deposition in joints leads to an inflammation reaction with secondary bone lesions, peri articular soft tissue deposits results in inflamed granulomatous tissue, eventually forming tophi. In extended disease tophi can be found in kidney and even heart valves (2). Although gout is a result of hyperuricemia, only a small percentage of patients with high levels of uric acid develop the disease. Moreover, patients with clinical acute arthritis without having gout can be presented with hyperuricemia (3). To date, visualizing urate crystals in synovial fluid by polarizing micro scopy is the gold standard (4). However, crystals are frequently found in synovial fluid from their uninflamed -and thus clinically difficult to examine- joints (5). Moreover, it has been shown that on initial examination of synovial fluid in patients with acute gout, urate crystals can be absent (6). An explanation could be that in some cases the inflammation starts with deposition of urate crystals in the periarticular soft tissue instead of synovium fluid. With a sensitivity of

From: 1. Department of Radiology, Alkmaar Medical Centre, Alkmaar, The Netherlands. Address of correspondence: Drs J. Spermon, resident radiology, M.D., Arthur van Schendelstraat 153, NL-3511 MB Utrecht, The Netherlands. E-mail: j.spermon@mca.nl *The paper was successfully presented on the joined section meeting bone and joints KBVR-NvvR, held in Mechelen, March 2012.

spermon-.indd 34

85%, the reliability of the analyses has been questioned (7, 8). Imaging modalities like ultrasound, MRI and CT can be of additional value in clinical suspected gout, but are not sufficient to differentiate gout from clinical similar diseases like rheumatic arthritis or pseudo gout (9). Unlike the standard imaging modalities, which demonstrate the anatomic structures, DECT, a relatively new modality, is able to demonstrate uric acid crystals in synovial fluid and periarticular tissue. Material end methods Dual energy CT (DECT) Tissue attenuation depends on the level of X-ray absorption during CT scanning. Absorption of X-ray depends on photon energy from defined kV of the X-ray beam and the atomic number of the exposed tissue. Attenuation of tissue with different atomic numbers has a different energy dependence. Changing the kV setting results in an alteration of photon energy and a corresponding attenuation modification of the tissue that is scanned. However tissue attenuation not only will change by altering kV settings, it also depends on the tissue that is scanned due to difference in photoelectric effect (10). DECT from Siemens – SOMATOM definition flash® – uses two energy different X-ray sources, 80-140 kV, running simultaneously. Tissue with a high atomic number shows a higher attenuation change between 80 kV and 140 kV compared to tissue with lower atomic number. The provided attenuation data are loaded in post processing software. In gout post processing protocol soft tissue is

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B Fig. 1. — Gout right hand. A. Radiograph showing non- calcified soft tissue mass at the MCP-1 joint without any osseous changes. B. DECT demonstrating large deposition of uric acid crystals at MCP-I and small deposition PIP digit 2 (uric acid crystals in green).

Case 2

used as baseline to differentiate uric acid crystals form calcium. Calcium is made out of elements with high atomic numbers and therefore show high attenuation difference, while uric acid crystals are made of elements with low atomic numbers (H,C,N,O) thus showing low attenuation difference. The results are then plotted in a figure, showing tissue with high attenuation difference above the soft-tissue baseline and tissue with low attenuation difference below this line. Scan parameters in our institution are: 1 sec rotation time and 0,7 pitch, two tubes (80 kV-250 mAs; 140 kV125 mAs), collimation 40 × 0,6 2 mm thickness with 2 mm increment reconstructed to 0,75 mm with 0,4 increment. After reconstruction three series of data are given (80 kV, 140 kV and mixed 50/50%), the latter only for viewing purposes.

spermon-.indd 35

Results Case 1 65-year-old male without history of arthritis presented at the emergency department with a swollen right thumb due to a progressive mass at the metatarsophalangeal joint. Medical history reveals hypercholesterolemia, high intake of purine and alcohol. Laboratorial analyses revealed normal uric acid level of 0.4mmol/l. Radiograph of the right hand showed a non-calcified soft tissue mass at the MCP-1 joint without any osseous changes (Fig. 1A). DECT revealed evident deposition of uric acid crystals at the MCP-1 as well as at the PIP digit 2 (Fig. 1B). Aspiration of joint fluid demonstrated uric acid crystals, no bacterial species were identified.

58-year-old male with a previous gout attack in 2006, suffering several years of painful swollen toes of the feet and hand. He was presented at the rheumatologist office with a right foot that had been painful for several weeks, especially the second and third digits. At physical examinations a large palpable mass of 5 to 3 cm at the MTP joint of both feet was observed. On clinical grounds the diagnosis of recurrent gout was made. Radiograph of the right foot showed erosive changes of the bone of the MTP-1 with a large soft tissue mass (Fig. 2A). DECT was performed to determine the extensiveness of the gout which displayed a large deposition of uric acid crystals at MTP1, but, though smaller, also at the PIP and DIP of digit 1,2, 3 and 5 and also at the ankle joint (Fig. 2B, uric acid depositions in green). No blood samples were analyzed, but aspiration of the tophi demonstrated uric acid crystals, which confirmed the diagnosis. Discussion Definite and early diagnosis of gout is obligatory not only to exclude

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B Fig. 2. — Extended gout of both feet and ankles. A. Radiograph showing erosive changes with soft tissue mass at MTP-I left foot. B. DECT revealing extensive gouty disease with multiple depositions of uric acid crystals in both feet and ankles (uric acid crystals in green).

A alternative diagnosis but also to start with the necessary medication in the earliest stage of the disease in order to prevent serious side effects of the possibly wrong medications and functional impairment of gouty arthritis and tophy. To date, demonstrating uric acid crystals in synovial fluid or topheous tissue is the gold standard in the diagnosis of gout disease. However, more extensive studies should be performed to determine the reliability of the synovial analysis. Besides, one should be skilled at joint aspiration because demonstrating of uric acid crystals in synovial fluid can be challenging and not always feasible (11). In this case report we demonstrated the potential additional value of a non-invasive imaging modality-to display uric acid crystals in joints and surrounding soft tissue as well as the extent of the gouty arthritis. Untreated patients with nonproven

spermon-.indd 36

gout will almost all have uric acid crystals during the intercritical period in previously inflamed joints (12). In this context DECT could have a beneficial value evaluating uric acid crystal depositions before clinical symptoms are apparent and even been used for late establishment of the diagnosis. Chronic hyperuricemia can lead to uric acid stones in the urinary tract resulting in nephrolithiasis. Additionally, uric acid crystal deposition can be found in renal medullary interstitium forming tophi and eventually, though rare, this may lead to chronic urate nephropathy (13). DECT is able to distinguish gouty nephrolithiasis from other forms of nephrolithiasis and also to identify renal (micro-)tophy before nephropathy is apparent (14). Tophus regression is considered mandatory in the treatment of gout, but despite adequate treatment to-

phi still can contribute to chrondolysis (15). Monitoring of therapy effect on tophi number and volume would be worthwhile and different methods of tophus assessment have been reviewed (16). Using DECT for quantification of tophi is possible and has been reported (17, 18). Extensive studies should be performed to assess the reliability of this relatively new imaging to diagnose gout. Recent attempts to study the diagnostic accuracy have recently been published. In a retrospective study 31 patients were selected and a total accuracy of DECT versus aspiration proved to be 94%. However sample size was small and selection bias appeared to be a real limitation of study (19). As this study shows, radiologists should be trained to learn about the artifacts in order to maximize the observer reliability. But of the most importance should be to determine the cutoff point for the detection of uric acid crystals by DECT before extensive prospective studies are performed. In a recent published prospective validation study 6 out of 40 (15%) proven gout patients had false negative scans, potentially due to urine lowering therapy (20). How about the radiation dose? When scanning two peripheral joints in our institution the amount of

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DUAL ENERGY CT — SPERMON et al

r adiation did not exceed the 0,5 mSv pro person – in contrast, an average person in the U.S. receives an effective dose of about 3 mSv. This is in agreement with recent published data (20). Finally, with future research one should take into account the costbenefit ratio of DECT in gouty arthritis. Conclusion DECT is a promising non-invasive imaging modality that can be applied in the diagnosis of acute and intercritical gout and to determine the extent of the disease, but could also play a role in monitoring the disease in treated patients and evaluating nephrogenic complications. However, more and extensive research should be performed to determine the reliability, accuracy and cost-benefit ratio of DECT in gouty arthritis. References 1. Weaver L.: Epidemiology of gout. Clev Clin J Med. 2008;75:S9-12. 2. Iacobellis G.: A rare and symptomatic case of mitral valve tophus associated with severe gouthy arthritis. J Endocrinol Invest, 2004, 27: 965-966. 3. Andersson H., Leden I.: Increased serum uric acid – a marker of nongouty widespread pain? A study of female patients with inflammatory and non-inflammatory pain. Scand J Rheumatol, 2006, 35: 261-267. 4. Chen L., Schumacher H.: Gout: an evidence-based review. J Clin Rheumatol, 2008, 14: S55-S62.

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5. Rouault T., Caldwell D., Holmes E.: Aspiration of the asymptomatic metatarsophalangeal joint in gout patients and hyperuricemic controls. Arthritis Rheum, 1982, 25: 209-212. 6. Schumacher H., Jimenez S., Gibson T., Pascual E., Traycof R., Dorward B., et al.: Acute gouty arthritis without urate crystals identified on initial examination of synovial fluid. Arthritis & Rheumatism, 1975, 18: 603-612. 7. Zhang W., Doherty M., Pascual E., Bardin T., Barskova V., Conaghan P., et al.: EULAR Standing Committee for International Clinical Studies Including Therapeutics. Extended report EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the standing committee for international clinical studies including therapeutics (ESCISIT). Ann Rheum Dis, 2006, 65: 1301-1311. 8. Swan A., Amer H., Dieppe P.: The value of synovial fluid assays in the diagnosis of joint disease: a literature survey. Ann Rheum Dis, 2002, 61: 493-498. 9. Perez Ruiz F., Naredo E.: Imaging modalities and monitoring measures of gout. Curr Opin Rheumatol, 2007, 19: 128-133. 10. Coursey C., Nelson R., Boll D., Paulson E., Ho L., Neville A., et al.: Dual-energy multidetector CT: how does it work, what can it tell us, and when can we use it in abdominopelvic imaging? Radiographics. 2010, 30: 1037-1055. 11. Mader R.: Repeated synovial fluid analysis may be needed to find crystals in gout. Clin Rheumatol, 1998, 17: 549-550. 12. Pascual E., Battle-Gualda E., Martinez A., Rosas J., Vela P.: Synovial fluid analysis for diagnosis for intercritical gout. Ann Intern Med 1999, 131: 756-759.

37 13. Iseki K., Ikemiya Y., Inoue T., Iseki C., Kinjo K., Takishita S.: Significance of hyperuricemia as a risk factor for developing ESRD in a screened cohort. Am J Kidney Dis, 2004, 44: 642-650. 14. Graser A., Johnson T., Bader M., Staehler M., Haseke N., Nikolaou K., et al.: Dual energy CT charactersation of urinary calculi: initialin vitro and clinical experience. Invest Radiol 2008, 43,112-119. 15. McCarthy G., Barthelemy C., Veum J., Wortmann R.: Influence of antihyperuricemic therapy on the clinical and radiographic progression of gout. Arthritis Rheum, 1991, 34: 14891494. 16. Dalbeth N., Schauer C., Macdonald P., Perez-Ruiz F., Schumacher H., Hamburger S., et al.: Methods of tophus assessment in clinical trials of chronic gout: a systematic literature review and pictorial reference guide. Ann Rheum Dis, 2011, 70: 597-604. 17. Choi H., Al-Arfaj A., Eftekhari A., Munk P, Shojania K, Reid G., et al.: Dual energy computed tomography in tophaceous gout. Ann Rheum Dis, 2009, 68: 1609-1612. 18. Nicolaou S., Yong-Hing C., Galea- Soler S., Hou D., Louis L., Munk P.: Dual-energy CT as a potential new diagnostic tool in the management of gout in the acute setting. Am J Roentgenol, 2010, 194: 1072-1078. 19. Glazebrook K., Guimaraes L., Murthy N., Black D., Bongartz T., Manek N., et al.: Identification of Intra-articular and Peri-articular Uric Acid Crystals with Dual Energy Computed Tomography: Initial Evaluation. Radiology 2011, 261: 516-524. 20. Choi K., Burns L., Sjojania K., Koenig N., Reid G., Abufayyah M., et al.: Dual energy CT in gout: a prospective validation study. Ann Rheum Dis 2012, 71: 1466-1471.

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JBR–BTR, 2013, 96: 38.

IMAGES IN CLINICAL RADIOLOGY The ‘’kissing spine’’ revisited E. De Smet1,2, F.M. Vanhoenacker1,2,3 A 46-year-old woman presented to our department with persistent low back pain, which increased by back flexion and was released by flexion. On clinical examination, localized midline lumbar tenderness was noted. MRI showed a soft tissue lesion between the adjacent spinous processes of L3 and L4. The lesion was of low signal intensity on T1-weighted images (WI) (Fig. A, arrow), and hyperintense on the T2-WI (Fig. B, arrow) and fatsuppressed (FS) T2images (Fig. C). FS T2-WI revealed also bone marrow edemaat the opposing faces of the spinous processes (Fig. C, asterisk). Based on these imaging findings, the diagnosis of Baastrup’s disease was made. The patient was treated with nonsteroidal analgetics. Comment

Baastrup’s disease,also known as ‘’kissing spine’’, is characterised by approximation and contact of adjacent spinous processes. It is part of the spectrum of degenerative changes of the lumbar spine: degeneration of the intervertebral discs and interspinal ligaments allows approximation and contact of adjacent spinous processes. The resulting microtraumata cause eburnation and flattening of the contact surfaces with the formation of a de novo bursa between the adjacent spinous processes (‘Baastrup’s bursa’). Rarely, thisbursa can become very large, extending anteriorly in the interspinous space and causing compression of the dural sac. The condition is most frequently encountered in the elderly, with almost 80% of patients older than 80. When found in young patients, the presence of predisposing factors, e.g. hyperlordosis or repetitive hyperextension (gymnasts) should be suspected. Clinical presentation consists of localised low back pain, typically aggravated by extension. However, it remains unclear whether this pain is caused by bone contact, surrounding inflammation or associated degenerative changes in these (mostly elderly) patients. The diagnosis of Baastrup’s disease can be made based on plain radiography or Computed Tomography (CT) of the lumbar spine. The lateral view shows severe narrowing of the interspinal space with sclerotic transformation and flattening of the contact surfaces. The advantage of MRI is direct evaluation of associated soft tissue changes (such as Baastrup’s bursa) and reactive bone marrow changes at the spinous processes. Particularly, FST2-WI are useful for precise assessment of these changes. On fluorodeoxyglucose-Positron Emission Tomography (FDG-PET), FDG-uptake between the processes can be seen as a result of the surrounding inflammation. Conservative treatment with analgetics is usually sufficient. When this therapy fails, interspinous infiltration with corticoids may offer pain-free intervals. The outcome of surgical removal of the affected spinous processes is variable and therefore, conservative treatment is the preferred treatment option. Complications are rare. Some authors have reported fractures of the spinous processes following continuous stress or hyperextension injury. Reference

1. Kwong Y., Rao N., Latief K.: MDCT Findings in Baastrup Disease: Disease or Normal Feature of the Aging Spine. AJR, 2011, 196: 1156-1159.

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

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JBR–BTR, 2013, 96: 39.

IMAGES IN CLINICAL RADIOLOGY Fibrous dysplasia M.-A. Van Caulaert, P. Mailleux1

A 45-year-old man presented to the emergency room for left leg pain following after a fall. Standard X-Rays showed no fracture but revealed, at the distal extremity of the tibial diaphysis, a 3 cm long, ovoid intramedullary lesion with thinning the cortex on the lateral side. There was no focal calcification or septation (A). The patient was referred to an oncologist. Technetium-99m–MDP bone scintigraphy and magnetic resonance imaging (MRI) were performed. The scintigraphy showed the lesion to be hypermetabolic (B). The MRI (C1: T1, TR 598/TE 14, 3M; C2: T1FS, TR 610/TE 14, 3M; C3: TSE, TR 3300/TE 28) showed a sharply delineated homogeneous lesion, hypointense on T1WI and hyperintense on T2WI, enhancing after injection of Gadolinium. There was no fluid-fluid level and no soft tissue mass outside the bone. No specific diagnosis could be proposed on this basis and the patient underwent a ct scan for a better analysis of the bony structure. It showed an ovoid lesion with a “ground glass” pattern, which is a relatively hypodense area compared to the cortex, hyperdense to the fatty medulla, without trabeculation. Slightly sclerotic borders indicated a benign lesion (D). On the basis of those findings, the diagnosis of fibrous dysplasia was proposed. Comment

Fibrous dysplasia is a congenital non-inherited benign bone lesion in which normal bone marrow is replaced by fibro-osseous tissue. It accounts for 2.5% of bone disease and for 5 to 7% of benign bone lesions, but the real incidence might be higher, C3 D as most of the patients are asymptomatic. Most of the lesions are discovered between 5 and 30 years. It’s a slowly growing lesion located in the diaphysis or metaphysis and able to extend into the epiphysis only after fusion. Malignant transformations into osteosarcoma, fibrosarcoma and chondrosarcoma can occur in rare cases. The diagnostic is based on radiological imaging. Plain radiographs are the first-line study and are often sufficient to lead to the diagnosis when characteristic features are present. In complex lesion or site, CT-scanning might reveal “ground-glass pattern”, specific to the diagnosis. MRI is not indicated when fibrous dysplasia is suspected, as it may reveal unspecific or even misleading like in our case. Nuclear imaging is not specific either. In conclusion, fibrous dysplasia is a benign lesion for which conventional X-rays and CT are sufficient to assess the diagnosis. MRI and scintigraphy are not specific. Reference 1.

Shah Z.K., Peh W.C., Kog W.L., Shek T.W.: Magnetic resonance imaging appearances of fibrous dysplasia. Br J Radiol, 2005, 78: 936.

1. Department of imaging, Clinique St Luc, Bouge, Belgium.

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JBR–BTR, 2013, 96: 40.

IMAGES IN CLINICAL RADIOLOGY B-cell malt lymphoma of the small intestine G. Koc1, O. Oyar1, N. Yazıcıog˘lu2, S. Bener3, B. Ünsal2 A 67-year-old male patient was admitted to the gastroenterology department with complaints of rectal bleeding for 5-6 months and weight loss in suspicion of inflamatory bowel disease. Anemia, increasing rates of lymphocytes (16.2%) and monocytes (30.7%) were revealed in routine heamotological tests. During enteroscopy examination a nodular mucosal pattern and ulcerations with exudate in jejunum were also detected. The barium follow through examination of small intestine showed aneurysmal expansion, loss of peristaltic activity, mucosal oedema in nearly 20-25 cm of jejunum. In the absence of significant stenosis, aneurysmal expansion of the jejunum was suspicious for lymphomatous involvement of the intestine. Long segment concentric wall thickening of the jejunum, presence of mesenteric lymph nodes and after intravenous gadolinium administration a significant contrast enhancement of entire wall of involved jejunum were also seen on MR enterography examination. For the unprevented rectal bleeding the patient underwent a surgical procedure and during the operation a concentric wall thickening up to about 2 cm. of distal jejunum was encountered, the segmental resection of involved intestine and adjacent mesenteric lymph nodes were made. Jejunal and also nodal B cell malt lymphomatous involvement was histopathologically proven.

Comment Primary lymphomas comprise of 1-10% of malignant tumours of digestive tract (1). The most common site of primer gastrointestinal lymphomas in Western countries is the stomach (approximately 35-75%), followed by the small intestine (30%) and large intestine (10%). Extranodal marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue (MALT) accounts for 7-8% of non-Hodgkin lymphomas. The stomach is the most common site of involvement. The distal small bowel, particularly the ileocaecal region, is a more frequent site of involvement than the proximal small intestine or colon. B cell MALT lymphoma is regarded as an indolent disease, but it sometimes progresses to a more aggressive histopathogenesis and shows resistance to therapy. The length of presenting history varies widely, the most common symptoms are abdominal pain, weight loss, diarrhea, small-bowel perforation or obstruction and palpabl abdominal mass. Intestinal barium follow through examination in lymphoma vary; if it C is presented as nodular lesions can be variable in size and irregularly distributed. Polypoid lesions seem to be smooth surfaced and may cause intussusception. As in the current case, circumferential infiltration of a small bowel segment results in a variable length of thickening and effacement of folds. Widening of the lumen rather than narrowing is detected because infiltration of muscularis layer with destruction of the myenteric plexus leads to aneurysmal dilatation (Fig. A). MR enterography examination may also show a sausage-shaped loop of bowel that is of relatively homogeneous to tissue intensity. In coronal FIESTA image, aneurysmal dilatation of affected segment, asymmetric wall thickening of usually more than 2 cm are detected and accompanied by abdominal lymphadenopathy (Fig. B). After intravenous contrast administration the wall thickening segment enhances diffusely on axial FLASH image (Fig. C). Final diagnosis is made histopathologically. Typically, tumors express pan-B antigens (CD19, CD20, CD22, CD79a), but they lack CD5, CD10, CD23, and Bcl-1 expression (Fig. D). Surgical excision is the primary treatment (and in most cases is required to make the diagnosis). When the tumor is incompletely excised, radiotherapy may be appropriate. In a minority of patients presenting with a more widespread disease, systemic chemotherapy is effective.

Reference 1.

Ha C.S., Cho M.J., Allen P.K.: Primary non-Hodgkin lymphoma of the small bowel. Radiology, 1999, 211: 183-187.

1. Department of Radiology, 2. Department of Gastroenterology, 3. Department of Pathology, Ataturk Research and Training Hospital, Izmir,Turkey.

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JBR–BTR, 2013, 96: 41.

IMAGES IN CLINICAL RADIOLOGY Angioedema of the small bowel caused by angiotensin converting enzyme inhibitor B.S. Smet1,2, I. De Kock1,2, A.I. De Backer1, K. Verstraete2 A 69-year-old male with a previous history of atrial fibrillation and hypertension was admitted to the emergency department because of acute onset of abdominal pain, accompanied by distension, nausea and diarrhea. Physical examination was unremarkable except for diffuse abdominal tenderness on palpation without rebound or guarding. Normoactive bowel sounds were noted. Routine blood analysis showed A elevated C-reactive protein 12.8 mg/dl (normal values 0.1-1.0) and INR of 3.1 (normal values 0.9-1.2 – therapeutic values 2.0-3.0). Patient was treated for atrial fibrillation with anticoagulation therapy. Hypertension was treated with beta-blocker and angiotensin-converting enzyme inhibitor Lisinopril SandozR for 10 days. Plain film of the abdomen demonstrated slightly dilated small bowel loops with air-fluid levels. CT scan of the abdomen after Iodinated contrast injection showed segmental small bowel wall thickening resulting in a stacked-coin appearance (Fig. A, B). Thickening of the small-bowel wall and mucosa was characterized by increased contrast enhancement and depiction of more layers of the small-bowel wall than normal. A striking contrast between the edematous submucosa of low attenuation separating the outer muscular layers and serosa from brightly enhancing thickened mucosa was noted. Some fluid accumulation within the small-bowel loops and prominent mesenteric vessels were also present. There was no ascites. Angiotensin-converting enzyme inhibitor therapy for hypertension was discontinued at the time of admission and abdominal complaints subsided within the next two days. The patient was discharged in good general condition and remained free of abdominal symptoms since the B moment angiotensin-converting enzyme inhibitor was discontinued. Repeated CT scan of the abdomen seven days later demonstrated complete resolution of abnormalities (Fig. C). Angiotensin-converting enzyme inhibitors are drugs used to treat hypertension and congestive heart failure. Visceral angioedema is a known rare adverse effect of angiotensin-converting enzyme inhibitors. An onset of less than 7 days after initiation of treatment is mostly seen, although more chronic forms may be possible. The frequency, duration, and severity of attacks may vary, but most cases are mild and resolve within 24-48 hr after discontinuation of the drug. A temporal relation between the initiation or discontinuation of medication and angioedema should be valuable as a diagnostic criterion. Angioedema is caused by a vascular leakage of serum from small vessels in mucous membranes. Visceral angioedema results in a layering C of the small bowel wall (small bowel target sign) caused by edematous low attenuating submucosa with fluid density, surrounded by higher attenuating outer muscular layer and brightly enhancing thickened mucosa. Fluid accumulation in the small bowel or together in the small bowel and the colon, prominent mesenteric vessels and some ascites may be noted. Findings are segmental and transient and only seen during an acute episode with return to normal after an attack. In the patient described, follow-up CT examination was performed 7 days after discontinuation of angiotensin-converting enzyme inhibitor therapy and showed a complete resolution of abnormalities. The differential diagnosis based on CT findings (target-like bowel wall thickening) include ischemia, shock bowel, radiation, vasculitis (e.g. Henoch-Schönlein purpura), intramural bleeding from trauma or anticoagulation therapy, hemophilia, nephrotic syndrome, infectious enteritis, inflammatory bowel disease (Crohn’s disease) and medication (e.g. angiotensin converting enzyme inhibitor). Reference 1.

De Backer A.I., De Schepper A.M., Vandevenne J.E., et al.: CT of angioedema of the small bowel. AJR, 2001, 176: 649-652.

1. Department of Radiology, General Hospital Sint-Lucas, Ghent, 2. Department of Radiology, University Hospital Ghent, Ghent, Belgium.

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JBR–BTR, 2013, 96: 42.

IMAGES IN CLINICAL RADIOLOGY Cold lumbar abscesses due to tuberculous spondylitis V. Haydan1, L. Médart2

A 33-year-old man, originating from Morocco, came to the hospital with a one-month history of right paralumbar mass. His general condition was good except for some weight loss. He had no fever. Blood tests showed a moderate inflammatory syndrome. Sonography revealed a huge heterogeneous cystic mass with thickened and nodular walls bulging under the skin in right flank (Fig. A). The abdominal CT scanner that completed the exploration showed extensive paravertebral collections spreading into both psoas muscles with subcutaneous extension on the right side (Fig. B, C). It also revealed irregular osteolytic lesions of several vertebral bodies from T10 to L5 (Fig. D). However, there was no formal evidence of intervertebral disc involvement. A CT-guided aspiration of 300 ml of fluid was performed and microbiologic analyses allowed identification of Mycobacterium Tuberculosis DNA, which led to the diagnosis of cold abscesses associated with tuberculous spondylitis. Antituberculous drug treatment was initiated with an excellent clinical and radiological response (Fig. E) after six weeks already with complete disappearance of collections. Comment In recent years, there has been a resurgence of tuberculosis in both developing and developed countries. Risk factors include human immunodeficiency virus epidemy, poor nutritional status, outbreaks in congregate settings, appearance of drug-resistant strains of Mycobacterium tuberculosis and an increase in migration from developing countries. Approximately 3% of tuberculosis cases involve the skeleton. Nearly 50% of those cases affect vertebrae (Pott’s disease) with paraspinal abscesses in another 75%. Haematogenous dissemination from a primary focus in the lungs or the lymph nodes is the most common means of spread. Cold abscess occurs mainly associated with osteomyelitis due to tuberculosis or actinomycosis. It develops slowly, without local redness, heat, pain or fever and can lead to a huge abscess with risk of fistula formation. The diagnosis is often delayed because of both non-specific symptoms and subacute presentation of the disease. CT and MRI are the most useful tests to establish the diagnosis and to clarify extension of the disease. Two distinct patterns of spinal tuberculosis have been identified: the first involves intervertebral disc and adjacent vertebral bodies; the second is characterized by destruction of one or more vertebrae without discitis. Aspiration of collection under imaging guidance allows adequate sampling for microbiologic analysis. The differential diagnosis of spinal tuberculosis includes subacute or chronic infections caused by bacteria or fungi and noninfectious causes, such as metastatic disease. Percutaneous drainage of the abscess is advocated by some authors in association with antituberculous drug treatment with a low induced morbidity. Surgery will be kept for the cases of ineffective drug treatment, spinal instability or deformity and neurological complications. Reference 1.

Sanal H.T., Kocaoglu M., Sehirlioglu A., Bulakbasi N.: A rare cause of flank mass: psoas abscess due to extensive primary thoracolumbar tuberculous spondylodiskitis. AJNR, 2006, 27: 1735-1737.

1. Medical student, University of Liège, 4th Master, 2. Department of Radiology, CHR Citadelle, Liège, Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2013, 96: 43.

IMAGES IN CLINICAL RADIOLOGY Port-site metastasis after explorative laparoscopy for an incidental appendiceal mucinous cystadenocarcinoma detected with FDG PET/CT G. Ceulemans1, M. Keyaerts1, S. Willems2, Ch. Simoens2, B. Ilsen3, H. Everaert1

A 62-year old female with a history of appendix carcinoma came to our department for an 18 F FDG PET/CT to further characterize a subcutaneous fixed small mass in the right fosse detected at clinical examination. Fourteen months earlier, she had undergone a right hemicolectomy because of an appendiceal mucinous cystadenocarcinoma. Since the diagnosis of appendicitis was presumed before she went into surgery, an explorative laparoscopy was performed. An inflammatory mass with loss of all anatomical references was found; hence the laparoscopy was reverted to a laparotomy. 18 F FDG PET demonstrated a hypermetabolic focus in the muscle layer of the right lower abdominal wall, in the scar where a trocar had been inserted. It is well known that scar tissue can be 18F FDG positive in the active healing phase up to 8 weeks, due to the unspecific associated inflammatory reaction. In this case however, the surgical procedure was performed 14 months ago. Further more, the metabolic activity was focal and corresponded with a heterogeneous nodular lesion that showed peripheral contrast enhancement on CT (Fig. A). The patient was referred for surgery and the port-metastasis was resected. To our best knowledge, this is the first case reporting a port-site recurrence of an appendiceal mucinous cystadenocarcinoma in a trocar scar after explorative laparoscopy. Comment

Primary appendiceal cancer is rare and accounts for 0,5% of all intestinal malignancies. The mucinous cystadenocarcinoma is the second most prevalent subgroup. The understanding of the etiology of port-site metastasis development has decreased the incidence over time from 21% to 1%, which is comparable to the incidence of scar metastases after open surgery. Port-site metastases often occur in the presence of advanced disease, but it is not exceptional for them to occur in isolation. The metabolic information obtained by 18 F FDG PET has a high positive predictive value for the detection of abdominal wall metastasis, once the acute healing phase (up to 8 weeks) has passed. Hybrid imaging with 18 F FDG PET/CT will allow detection, characterization and anatomical localization of occult lesions, as well as potential additional concomitant lesions. Reference 1.

Goshen E., Davidson T., Aderka D., Zwas S.T.: PET/CT detects abdominal wall and port-site metastases of colorectal carcinoma. Br J Radiol, 2006, 79: 572-577.

Department of 1. Nuclear Medicine, 2. Abdominal Surgery, 3. Radiology, UZ Brussel, Brussels, Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2013, 96: 44.

IMAGES IN CLINICAL RADIOLOGY Coracoclavicular joint with shoulder pain I. Willekens, M. De Maeseneer, C. Boulet, F. Verhelle, J. de Mey1 A 53-year old man presented with chronic left shoulder pain, unresponsive to anti-inflammatory treatment. There was no history of injury or chronic overuse. Radiography showed degenerative changes of the acromioclavicular joint, an acromion type 1, and the presence of coracoclavicular joint. CT scan confirmed the presence of a joint between the clavicle and the coracoid process with degenerative changes (Fig. A, B). Comment

There are many disorders that may cause shoulder pain. Most of these entities are accompanied by typical signs and symptoms. In our patient, the coracoclavicular joint caused shoulder pain. A coracoclavicular joint is a diarthrotic synovial joint that occasionally is present between the conoid tubercle of the clavicle and the superior surface of the horizontal part of the coracoid process. It was first described by Gruber at the end of the 19th century. A coracoclavicular joint represents an uncommon anatomical variant. It is considered by some authors to be genetically determined. Nevertheless cadaveric studies have not revealed a coracoclavicular joint in neonates and young children, suggesting a non-congenital cause. Aging has been implicated to play a role in its development. The coracoclavicular joint is a true synovial joint with articular cartilage and intracapsular synovial fluid, and usually, but not always, it is unilateral. Most reports are from patients of Asian origin, with sporadic occurrence in people of European or African descent. The clinical significance of the coracoclavicular joint is not entirely clear. The coracoclavicular joint has been associated with humeral head fracture, cervicobrachial syndrome, decrease in shoulder motion, thoracic outlet syndrome, and degenerative changes in adjacent joints. Osteoarthritis of the coracoclavicular joint may occur. The mean age of presentation of shoulder pain related to the coracoclavicular joint is 42 years, with a male to female ratio of 1.4:1. Brachial plexus involvement is the most common pathophysiological explanation provided. The firstline treatment is conservative, but this has an extremely low success rate of 5.9%. Surgical excision of the anomalous joint is always curative. Reference 1.

Gumina S., Salvatore M., DeSantis R., et al.: Coracoclavicular joint: osteologic study of 1020 human clavicles. J Anat, 2002, 201: 513-519.

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

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JBR–BTR, 2013, 96: 45.

IMAGES IN CLINICAL RADIOLOGY Silent double aortic arch in an elderly patient S. Dekeyzer, R. Gosselin, L. Delrue1 A 63-year-old woman with COPD presented to our hospital with complaints of breathlessness on exertion, productive cough and weight loss. Chest X-ray showed a bright silhouette extending from the aortic knob in the right paratracheal area on the PA-view and a posterior indentation of the tracheal air column on the lateral view. No other abnormalities were observed. Further work-out consisted of a contrast enhanced CT of the chest which revealed bilateral aortic arches, both of which arising from the ascending aorta anterior to the trachea. Each arch gave origin to the common carotid artery and the subclavian artery, and joined the right posterior ward to form the descending aorta. The left arch was the larger of the two arches. The trachea and esophagus were placed in the middle of the aortic ring. No abnormal compression of the trachea or the esophagus was observed.

Comment Congenital anomalies of the aortic arch represent less than 1% of all congenital cardiac defects. Double aortic arch is a splitting of the ascending aorta into two segments, which pass on either side of the esophagus and trachea and join together as a single descending aorta. Double aortic arch is the most common form of a complete vascular ring, a class of congenital anomalies of the aortic arch system in which the trachea and esophagus are completely B encircled by connected segments of the aortic arch and its branches. In the most common variation of double aortic arch, both aortic arch segments are patent, the right segment is larger than the left segment and the ductus arteriosus and descending aorta are left sided (75% of cases). A left dominant double aortic arch with a right descending aorta, as was observed in our patient, is less common and constitutes 18% of cases. In the codominant or balanced type, seen in 7% of cases, both arches are of equal diameter. In an uncommon variation of the double aortic arch, one of both arches may be atretic and may be represented by only a cord. Double aortic arch is a congenital anomaly which arises because of persistence of the fourth right pharyngeal arch artery. Embryologically, the ventral and dorsal aortas are connected by aortic arches which persist or involute to give rise to the normal aortic arch, its branches and the minor arteries of the head. The right fourth pharyngeal arch normally involutes at about 36 to 38 days. The remnant of the right pharyngeal arch becomes the right innominate artery. The left fourth pharyngeal arch persists and gives rise to the normal left aortic arch. Failure of dissolution of the right fourth pharyngeal arch artery and persistence of the left pharyngeal arch produces a vascular ring consisting of two aortic arches and encircling the trachea and esophagus. Although the defect is most frequently seen as an isolated defect in an otherwise normal individual, it has occasionally been associated with tetralC ogy of Fallot, transposition of the great arteries, pulmonary atresia defects, ventricular septal defects and 22q11.2 deletion syndrome. In most cases, this abnormality is diagnosed in infancy and patients present with symptoms related to esophageal or tracheal obstruction such as stridor, respiratory distress, recurrent upper respiratory tract infection or pneumonia, dysphagia or feeding difficulties. The severity and onset of symptoms depends on the space between the aortic segments. Sporadically, patients have been reported in whom diagnosis was delayed until childhood or even adulthood. Presentation in these patients usually consists of progressive or persistent dyspnea, dysphagia or asthma-like symptoms. The symptoms in adult patients can be atypical and misleading, as illustrated by case reports of double aortic arches detected in adulthood after long-term treatment for assumed reactive airway-disease. Case reports of elderly patients are rare, especially symptom-free cases. In our patient a double aortic arch was discovered incidentally when imaging studies were conducted for ruling out pulmonary infection and/or malignancy. As the trachea and esophagus were placed in the middle of the aortic ring and no compression of the trachea could be observed, our patients complaints of breathlessness were attributed to a non-infectious COPD exacerbation and she quickly improved under optimal inhalation therapy and corticosteroids. No satisfactory explanation for the weight loss was found. Reference 1.

Türkvatan A., Büyükbayraktar F.G., Olçer T., Cumhur T.: Congenital anomalies of the aortic arch: evaluation with the use of multidetector computed tomography. Korean J Radiol, 2009, 10: 176-184. 1. Deparment of Radiology and Medical Imaging, UZ Gent, Ghent, Belgium.

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JBR–BTR, 2013, 96: 46.

IMAGES IN CLINICAL RADIOLOGY Cancer of the oesophagus in achalasia S. Maeyaert1, J. Pringot2, J.L. Samain1, L. Ghijseling2, P. Matthys2 A 54-year old man was admitted to the emergency department for chronic dysphagia for solid as well for liquids of several years duration, with increasing severity for two weeks. The patient also had shortness of breath grade III for two weeks. The medical history of the patient was uneventful, except for surgery on the oesophagus 26 years previously, probably for achalasia. No follow-up was performed. At the time of admission, the patient doesn’t take any medication. He doesn’t smoke and consumes one or two alcohol units a day. Clinical examination fails to reveal any specific findings. Blood analysis showed a decrease of the hemoglobin level (10.4 g/dL), a slightly elevated leukocytosis (10400/µL) and elevated C-reactive protein level (127 mg/L), as well as hyponatriemia and hypochloremia. Chest X-ray shows cardiomegaly and a dilated proximal oesophagus with a marked decrease in the diameter distally. Fibroscopy shows an ulcerated tumoral lesion of 6 cm at 40 cm, biopsies showing an infiltrating epidermoid carcinoma. Bronchoscopy was negative. PET-scan confirms the presence of a large, irregular, hypermetabolic mass in the lower oesophagus and enlarged hypermetabolic mediastinal lymph nodes. Barium X-ray confirms the predominantly enlarged upper oesophagus (4 cm) with stasis of liquids and absence of peristalsis. The distal part of the oesophagus is narrowed showing a pattern compatible with treated achalasia (Fg. A). On the right posterior border of the distal one third of the oesophagus the large ulcerated lesion of approximately 8 cm with typical neoplastic pattern is demonstrated on the lateral view (Fig. B). Contrast enhanced computerized tomography of the thorax confirms the presence of the ulcerated mass and shows an enlarged lymph node in the mediastinum and the right hilus (Fig. C). Treatment consisted of radio-chemotherapy.

Comment Achalasia is a primary oesphageal motility disorder affecting mainly adults of both sexes equally and predominantly presenting with dysphagia, sometimes with regurgitation. The treatment of achalasia is symptomatic and designed to improve the oesophageal emptying. The most effective treatments are pneumatic balloon dilatation and cardiomyotomy, follow-up being based on X-ray and manometry. Late complications are related to recurrent dysphagia after treatment. Perihiatal scarring, peptic stricture or obstructing tumors can all cause recurrent symptoms. The most important late complication is the occurrence of oesophageal cancer, patients having similar symptoms in recurring achalasia and in oesophageal cancer. Therefore, mostly cancers are diagnosed in an advanced stage. The relationship between achalasia and cancer was first described in 1872 by Fagge. An increased risk of developing oesophageal carcinoma in patients with long standing achalasia has been reported by several authors, with incidences varying widely from 1.7 to 20%. It has been established that the consumption of alcohol and tobacco increases the risk of developing esophageal cancers due to the content of carcinogens in alcohol and tobacco. Achalasia is known to cause retention and increased bacterial growth and chemical irritation from the continuous composition of food that culminates in chronic oesophagitis. This is supposed to provoke cancer or make the epithelium more sensitive to carcinogens. In achalasia, either adenocarcinoma or squamous cell carcinoma may develop. Squamous cell carcinoma is the most frequent (85% of the cases) and situated in over half the cases in the middle third of the esophagus due to stasis. Adenocarcinomas are most often situated in the distal third of the oesophagus due to Barett oesophagitis, consequent to gastrointestinal reflux. Due to the localisation in the enlarged, dilated oesophagus, tumors are mostly very large at time of diagnosis. The classical imaging technique for following treated achalasia and recurrence or complications on the oesophagus is barium X-ray study. As demonstrated in the reported case, it is important to examine the entire oesophagus in many incidences to investigate the whole circumference of the dilated oesophagus. Otherwise, even an advanced lesion may remain undetected. In this example, the very large carcinoma is poorly visible on the AP incidence, but well demonstrated on the lateral view. The ulceriform cancer of the oesophagus is characterized by an ulceration surrounded by a ridge that bulges into the oesophageal lumen. In profile, the lesion creates an image of an oval niche underlined by a radiolucent band. Depending on the stage of development of the cancer, the opposite wall either remains pliable with mucosal folds, or is rigid, without any mucosal relief. Prognosis of cancers associated with achalasia is very poor due to the late stage of diagnosis. Early treatment of achalasia relieving the retention reduces the risk of oesophageal cancer. However, cancer risk continues after treatment so endoscopic or radiological follow-up is necessary, even after treatment.

Reference 1.

Aggestrup S., Holm J.C., Sørensen H.R.: Does achalasie predispose to cancer of the esophagus? Chest, 1992, 102: 1013-1016.

1. Department of Radiology, University Hospital Leuven, Leuven, Belgium, 2. Department of Radiology, Sint Elisabeth Hospital, Brussels, Belgium.

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IMAGES IN CLINICAL RADIOLOGY An unusual cause of A2 pulley rupture in a 49-year-old man M. De Maeseneer, C. Boulet, M. Kichouh, F. De Ridder, M. Shahabpour1 A 49-year-old man presented to his family physician with pain in the third finger that occurred after he tried to grasp a falling heavy object. His finger was forcefully extended from a semi-flexed position. On clinical examination extension was normal. However, flexion was slightly limited and extremely painful at the end point of flexion. Ultrasound of the finger was performed and showed that the flexor tendons at the level of the proximal phalanx were at an abnormally increased distance from the bone (Fig. A, B). Both the superficial and deep flexor were also markedly thickened. The normal slips at the side of the tendon representing the A2 pulley were replaced by a heterogeneous mainly hypoechoic area. Fluid was seen deep to the tendons in between the latter and the bone. MR imaging was performed using a dedicated wrist coil on 3 T (Fig. C-D). On transverse and sagittal proton density weighted images the flexor tendons were seen to be located at some distance from the bone at the midlevel of the proximal phalanx. The ulnar attachment of the A2 pulley could not be visualized, and the radial attachment was thickened, elongated and exhibited high signal intensity on the transverse images. Fluid sensitive sequences showed fluid in the synovial sheath and also in between the tendons and the bone.

Comment

Injuries of the flexor pulleys have been typically described in rock climbers. In our experience, the injury may also occur in less athletic contexts such as holding on to or trying to grab a falling object. Also situations with deformities of the fingers may lead to bowstring-like abnormalities of the fingers. Anatomically there are different pulleys including A and C pulleys. It is essentially the A pulleys that are mechanically important and they are named A1 to A5 from proximal to distal. Bowstringing especially occurs with ruptures of the A2 and A4 pulleys, located respectively at the level of the proximal and middle phalanx. The A1 C (and A0) pulley are typically thickened in trigger finger. The diagnosis of pulley ruptures can usually be made with ultrasound showing the increased distance of the tendon to the bone, designated bowstring injury. A disadvantage of ultrasound is that the finger can not be imaged in flexion, and it is in this position that the distance becomes more prominent. This imaging in forced flexed position is actually most easily done with CT, but is possible with MR also. Our patient had some associated findings that were better appreciated on 3T MR and that have not been emphasized in the literature. These included marked thickening of the tendons, synovial sheath fluid, and fluid between the tendons and the bone, likely related to avulsion of the synovial sheath from the bone in this location. Different surgical proecedures have been described to reconstruct the pulleys some using palmaris longus grafts. In conclusion, we describe a patient with an unusual mechanism of injury leading to an A2 pulley rupture of the finger. This abnormality was diagnosed by ultrasound, but more details of the injury could be appreciated on 3T MR images. Reference 1.

Hauger O., Chung C.B., Lektrakul N., et al.: Pulley system in the fingers: normal anatomy and simulated lesions in cadavers at MR imaging, CT, and US with and without contrast material distention of the tendon sheath. Radiology, 2000, 217: 201-212.

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

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JBR–BTR, 2013, 96: 48.

IMAGES IN CLINICAL RADIOLOGY Eagle syndrome M. Demeter, Y. De Bruecker, S. Devuysere, D. Perdieus1 A thirty-eight-year-old male patient was referred by the general practitioner to our department for recurrent throat pain radiating to head and neck for a few months. The pain was more prominent on the left side, especially during swallowing, and sometimes accompanied by a creaking noise and sensation of a ‘click’. Physical examination showed a slightly hard bulge on the left upper neck. Previous medical history was not helpful and laboratory findings were normal. Ultrasound of the neck, as a first investigation, showed no abnormalities. In addition, enhanced computed tomography of the neck was performed. Coronal reconstruction, as shown in Fig. A, revealed total ossification of the stylohyoid ligaments, from the origin on the styloid process to the insertion on the lesser horn of the hyoid bone, as well as enlargement of both styloid processes, more pronounced on the left. Pseudo-articulation between the left stylohyoid ligament and styloid process, also shown in Fig. A and more in detail on the three-dimensional reconstruction in Fig. B, caused the local swelling in the left upper neck. These radiographic findings accompanied by the patient’s complaints, is known as “Eagle Syndrome”. Because of the minor clinical repercussions, conservative treatment was optioned.

Comment “Eagle Syndrome” was first described by Eagle in 1937. It is a clinical condition caused by elongation of the styloid process (more than three centimeters in length) and/or ossification of the stylohyoid ligament. It can present unilateral or bilateral. The pathogenesis remains not well known and many pathophysiological explanations are suggested. It can be idiopathic, congenital (due to the persistence of cartilaginous precursors of the styloid process), or acquired, for example after trauma or surgery (due to the proliferation of osseous tissue at the insertion of the stylohyoid ligament). Eagle syndrome can be classified in three types based on the medical history and pathological findings. The first type, B known as the classical Eagle syndrome, implies an elongated styloid process with neck surgery (tonsillectomy) or trauma in the patient’s history. In the second type, an elongated styloid process and ossified stylohyoid ligament is seen, without prior surgery or trauma, similar to our case. The third type, or pseudostylohyoid syndrome, contains only the classical symptoms and no clinical or radiographic abnormalities nor prior history. As regards the clinical repercussions, Eagle syndrome can be divided in two main clinical presentations. Our patient presented with the classic stylohyoid syndrome, in the form of cervicofacial pain, dysphagia and foreign body sensation, caused by impingement of lower cranial nerves (V, VII, IX, or X). The second presentation, stylocarotid syndrome, is due to compression of the carotid artery, associated with referred pain, neurological focus and even syncope, mostly induced by head movements. If this is the case, complications are reported, such as (pseudo-)aneurysm and even dissection of the carotic artery, as a consequence of the repetitive traumatic injury of the vessel wall caused by the elongated styloid process or the sharp ends of a partially ossified stylohyoid ligament. Treatment can be conservative with analgetics and steroid injections. In case of neurological deficits, surgical resection of the styloid process by transpharyngeal or more obvious extraoral approach, can lead to complete resolution of the symptoms. 3D-CT scan is certainly of added value, not only for diagnostic purposes, but also in pre-surgical evaluation. Reference 1.

Murtagh R.D., Caracciolo J.T., Fernandez G.: CT findings associated with eagle syndrome. AJNeuroradiol, 2001, 22: 1401-1402.

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

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IMAGES IN CLINICAL RADIOLOGY Osseous venous congestion simulating sclerotic bone lesions in superior vena cava syndrome L. Duquesne1, P. Desclee1 A 77 year-old patient is admitted to the Emergency Department in April 2009, complaining of a one-month persistent face oedema. No amelioration was seen after stopping the treatment with Coversyl. The case study of the patient shows a type II insulin-requiring diabetes, added to a polyneuropathy and a chronic renal insufficiency, a post-smoking emphysema, an anthracosillicosis, an acute coronary syndrome and a mild heart attack with ventricular tachycardia for which the patient benefited from the placing of an implantable cardiac defibrillator in July 2008. Clinical examination on admission shows no particularity, except from facial oedema. Blood test shows a renal insufficiency as well as a moderate increase in DDimers. Cervical venous echo-Doppler US study shows a left subclavian vein thrombosis spread as far as the internal left jugular. CT angiography of the thoracic aorta made at the same time confirms the presence of a left subclavian vein thrombosis and a left innominate vein thrombosis in the surrounding area of a pacemaker catheter, which is also partly surrounded by clots in the superior vena cava. Many venous collateral pathways are visible in the parietal, muscular and left mediastinal areas (Fig. A, B). The bone window analysis shows high density in several superior dorsal vertebrae, simulating osteo-condensing lesions (Fig. C). In the context of anthracosillicosis and masses or pulmonary pseudomasses, a follow-up by thoracic CT-scan is recommended. The areas of high bone density are visible on some of the CT scans, with density and extension varying whether an injection IV of an iodized contrast medium is given or not, as well as with the timing and also depending on the side (left or right arm) the injection was given. In June, July and August 2009, without contrast, no lesion is seen (Fig. D). In the above described case, on the scans made with injection, the venous congestion bound to superior vena cava syndrome could have been confused with a metastatic bone invasion.

Comment The superior vena cava syndrome is a frequent entity, mainly manifesting itself by a swelling of the face and of the superior limbs and complicating in almost 90% of the cases a malignant tumor of mostly bronchial origin. Investigation requires medical imaging report and Doppler US study, and also a thoracic CT-scan, looking for a stenosis or venous occlusion and also for a bronchial tumor. The metastatic bone lesions found in the bronchial carcinomas are mainly lytic lesions. However, during treatment, the lesions can condense, showing a certain osteoblastic activity level. In the above described case, on the scans made with injection, the venous congestion bound to superior vena cava syndrome could have been confused D with a metastatic bone invasion. The superior vena cava syndrome being in nearly 90% of the cases linked to the existence of a malignant tumor, it is advisable to recognize this type of image in order not to confuse them with possible metastases. In doubt, a late scan with or without contrast should allow to see the difference.

Reference 1.

Jesinger R.A., Huynh B., Gover D.: Superior Vena Cava Syndrome Resulting in Osseous Venous Congestion Simulating Sclerotic Bone Lesions. AJR, 2009, 192: 344-345.

1. Dpt of Radiology, Centre Hospitalier de Luxembourg, Luxembourg, Grand Duchy of Luxembourg. 2. Dpt of Radiology, Centre Hospitalier de Jolimont, Haine-Saint-Paul, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Secondary tumoral calcinosis with intraosseous extension L. Van Muylder1,2, H. Declercq1, F.M. Vanhoenacker3,4,5 A 97-year old Caucasian woman suffering from chronic renal insufficiency was admitted with progressive pain at the left hip when mobilized. Plain radiographs showed a large lobulated well-demarcated calcified mass adjacent to the greater trochanter of the left hip (Fig. A). On subsequent CT-scan (Fig. B, axial image; Fig. C, coronal reformatted image), the mass was heterogeneously calcified with dense and less dense areas. The lesion was located within the subgluteus medius bursa and caused cortical destruction of the greater trochanter with extension of calcifications within the adjacent medullary cavity. Based on the imaging findings and the past medical history of chronic renal failure, the diagnosis of secondary tumoral calcinosis was made. Because of the advanced age of the patient, no further therapy was installed. Comment

Tumoral calcinosis is a descriptive term used for mass-like periarticular calcific deposits, irrespective of its etiology. The peri-articular tissues of the hip, elbow, shoulder, foot and wrist are most frequently involved. The lesion is usually solitary, although multiple foci may be seen as well. The disorder can be idiopathic (primary form) or can accompany several other disorders (secondary form). On imaging and histology, these two forms are indistinguishable. The secondary form is mainly associated with chronic renal failure, having a prevalence of 0.5% to 1.2% in patients on hemodialysis. The underlying etiology is primarily believed to be due to secondary hyperparathyroidism. Clinically, as in our patient, it may interfere with joint motion. Imaging features consist of multilobulated, amorphous peri-articular calcific deposits, most often along the extensor surfaces of the joint. The internal structure may be either homogeneous or heterogeneous, containing intralesional fluid-calcium levels and/or peripheral rim calcification with a low attenuation center. Cortical destruction and intramedullary extension is rare and may be due to chronic pressure erosion. Although the lesion is readily detected on plain radiographs, CT is the preferred examination for assessment of intralesional heterogeneity and local extension. Treatment is usually conservative with phosphate depletion medication. In case of failure of this therapy, subtotal parathyroidectomy should be considered. Reference 1.

Girard C.J., Wasserman P.L., Lenchik L.: Secondary Tumoral Calcinosis with Intraosseous Penetration. Radiol Case Rep, 2009, 4: 213-224.

1. Department of Radiology, AZ Sint-Blasius, Dendermonde, 2. Department of Radiology, University Hospital Leuven (UZ Leuven), 3. Department of Radiology, AZ Sint-Maarten, Duffel-Mechelen, 4. Department of Radiology, University Hospital Antwerp (UZA), 5. Department of Radiology, University Hospital Ghent (UZ Gent), Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2013, 96: 51.

IMAGES IN CLINICAL RADIOLOGY Sacral chordoma M. Behaeghe, A. Denis, L. Jans, K. Verstraete1 A 38-year-old man was admitted to our hospital for deep sacral pain. There was no significant medical history. Physical examination revealed pressure pain of the right sacroiliac joint. MRI showed a midline mass in the sacrum (arrows), isointense on T1weighted MR images and hyperintense on T2-weighted MR images (Fig. A-B), enhancing with gadolinium. Cortical destruction was present with an extraosseous soft tissue mass (arrowheads). A well-defined lesion with similar MRI signal was seen in the left groin (asterisk) (Fig. C). Diagnosis of sacral chordoma with distant metastasis was made.

Comment Chordoma is rare tumor, accounting for 1-4% of all primary bone malignancies, and has a poor prognosis. Chordomas arise from transformed remnants of notochord and are typically encountered in the axial skeleton, with most common sites being the sacrum, the skull base and the spine. Histologically chordomas are considered to be a low-grade neoplasm, but the high rate of local recurrence and potential for distant metastasis makes their clinical progression similar to that of malignant tumors. Chordomas are indolent and slow growing and often clinically silent until late-stage disease. Imaging-related diagnostic delay may arise from overlooking lytic sacral lesions on conventional radiographs, or from CT or MRI studies of the spine not extending below S2 level. Treatment of sacral chordomas is en bloc excision with wide margins and postoperative external- beam radiation therapy. Reference 1.

Walcott B.P., Nahed B.V., Mohyeldin A., et al.: Chordoma: current concepts, management and future directions. Lancet Oncol, 2012, 13: 69-75.

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

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JBR–BTR, 2013, 96: 52.

IMAGES IN CLINICAL RADIOLOGY Decubital ischemic fasciitis L.J. Ceulemans1, G. Jacomen2, F.M. Vanhoenacker3

A 77-year-old immobilized woman presented with a hard, palpable and fixed mass over the greater trochanter. Subsequent Magnetic Resonance Imaging (MRI) revealed a subcutaneous mass lesion abutting the iliotibial band. On T1-weighted images (WI), the lesion was isointense to muscle (white arrow), with a central focus of high signal intensity (SI) (Fig. A, axial T1-WI). Fat suppressed (FS) T2-WI showed predominantly hyperintense signal (black arrowheads) with intralesional foci of low SI, adjacent to the right greater trochanter (white asterisk) (Fig. B, axial FS T2-WI). After intravenous administration of gadolinium contrast, marked enhancement was seen with small areas of non enhancement, in keeping with necrotic foci (white arrow) (Fig. C, coronal contrast-enhanced FS T1-WI.). Neither invasion of the gluteus muscles nor the bone marrow of the greater trochanter was seen. Solely based on the MRI findings, malignancy could not be excluded. Therefore, wide surgical resection of the lesion was performed. Histological examination revealed the diagnosis of ischemic fasciitis, with a central hypocellular area surrounded by a fibroblastic (white asterisk) and vascular proliferating outer zone (Fig. D). Comment

Ischemic fasciitis was previously described as ‘atypical decubital fibroplasia’ and is a rare distinctive, pseudosarcomatous fibroplasia typically occurring in the deep subcutaneous tissue over bony prominences (greater trochanter, sacrum, iliac crest, shoulders) in immobilized (bid-ridden or wheelchair-bound) elderly patients. MRI findings are usually nonspecific. The lesion is predominantly isointense to muscle on T1-WI and heterogeneously hyperintense on T2-WI images. Focal areas of high SI on T1-WI may correspond to fat necrosis, whereas low SI on T2-WI may be due to old hemorrhage. After intravenous administration of gadolinium contrast, there is marked and heterogeneous enhancement. Areas in the center which do not enhance indicate the presence of necrotic foci. The lesion may breach the fascia, but the bone, which is in close contact to the adjacent soft tissue, is not involved. Lesion heterogeneity on MRI may mimic a necrotic sarcoma or abscess. The location of the lesion in the subcutaneous tissue at pressure points is the most important clue to correct diagnosis. This is of utmost importance to avoid overtreatment and unnecessary morbidity in elderly patients with poor operative risks. Histopathological examination reveals a zonal appearance. A central area of fat necrosis is surrounded by a well vascularized fibroblastic proliferation with high cellularity. Pigmented macrophages are indicative of old hemorrhage. There are also myxoid changes, hyalinisation and edema. Reference 1.

Ilaslan H., Joyce M., Bauer T., et al.: Decubital ischemic fasciitis; clinical, pathologic and MRI features of pseudosarcoma. AJR, 2006, 187: 13381341.

Department of 1. General Surgery, 2. Pathology, 3. Radiology, AZ SintMaarten, Duffel-Mechelen, Duffel, Belgium.

JBR–BTR, 2013, 96: 53-54.

ABSTRACT OF PAPER FOR FULL MEMBERSHIP BONE AND JOINTS MR imaging of the peroneal nerve around the knee F. Van den Bergh1, 3, F.M. Vanhoenacker1, 2, 3, W. Huysse3, E. De Smet1, 2, K.L. Verstraete3 Learning objectives: The purpose of this pictorial review is twofold: to present the normal anatomy of the peroneal nerve around the knee and to review the most common pathology as encountered on MR imaging of the knee. Material and methods: Our cases were culled from the databases of a University Hospital and a major regional hospital. Twenty five cases were retrieved, 11 females and 14 males, with age ranging from 17 to 68 years. Anatomic background: The peroneal nerve can easily be identified on conventional MR imaging and has some unique anatomical features. The superficial course of the nerve around the proximal fibula and the relative paucity of epineural supporting tissue make it vulnerable. At the level of the fibular neck there is a fibro-osseous tunnel under the insertion of the peroneus longus tendon where the nerve can tethered or compressed. As it courses around the fibular neck, the peroneal nerve trifurcates in a deep, superficial and articular branch. The articular peroneal branch for the proximal tibiofibular joint has been shown to be a very common location and entrance port for intraneural ganglia. General imaging features of denervation: The muscles of the anterior and lateral compartment, innervated respectively by the deep and superficial peroneal nerve, can support a diagnosis with the typical signs of denervation. There is no typical timeframe for each phase;there is some considerable overlap with different phases occurring at the same time.In the acute phase, starting after some days and lasting 4 to 6 weeks, STIR or T2-weighted images are most suited to detect muscle edema. Atrophy and fatty replacement are best seen on T1-weighted images without fat suppression. Atrophy begins after some weeks and fatty replacement occurs in the following months to years. Spectrum of pathologic conditions: Two major patterns of peroneal nerve lesions can be identified. The first is traumatic, either direct or indirect, such as inversion of the foot putting stress on the peroneal nerve. The second pattern is compressive, either from extraneurally or intraneurally. Many traumatic knee injuries can cause damage to the peroneal nerve, ranging from a relative minor direct compressive trauma to a major fracture-dislocation. Many of them are evident clini-

papers-vd bergh-+.indd 53

cally or on EMG and will not require imaging other than conventional X-rays. Our series included several cases direct impact injury, an accidental surgical transsection, a deglovement injury (Morel-Lavallée lesion), a large compressive synovial cyst originating from a pseudarthrosis in the tibial plateau and a proximal fibular fracture (Maisonneuve). Bony lesions narrowing the osteo fibrous tunnel, such as a tug lesion at the insertion of the peroneus longus muscle can compress the common peroneal nerve. Cartilaginous exostosis is another, less common cause of extrinsic osseous compression. In our series, the most frequent soft tissue tumors causing compression of the peroneal nerve are (ganglion) cysts and neurogenic tumors. Cystic lesions around the knee, most often in a degenerative setting, can be very large and sometimes compress the common peroneal nerve. The peroneal nerve is the most common location for intraneural ganglion cysts. One should carefully look for a fine stalk originating from the proximal tibiofibular joint. Useful signs on axial imaging include the tail sign (indicating the cyst’s origin anterior to the proximal tibiofibular joint), the transverse limb sign (horizontal cyst extension in the articular branch) and the signet ring sign (cyst expansion within the common peroneal nerve, displacing the nerve to the periphery). Nerve sheath tumors originating from the peroneal nerve may be benign or malignant. Differentiation between schwannoma and neurofibroma is impossible on imaging. Size more than 5 cm, intratumoral bleeding and areas of necrosis are suggestive of a malignant nerve sheath tumor, but to differentiate with a plexiform neurofibroma biopsy is still required for a definitive diagnosis. Conclusion: The peroneal nerve has some unique anatomical features contributing to its vulnerability. A whole variety of lesions may cause potential denervation of the nerve. In our series, lesions affecting the peroneal nerve are mostly traumatic or compressive. Due to its exquisite soft tissue detail, MRI provides useful information about both the anatomy of the nerve, its innervated muscles and the etiology of nerve compression. References Z.S., 1. Donovan A., Rosenberg Cavalcanti C.F.: MR imaging of entrapment neuropathies of the lower extremity. Part 2. The knee, leg, ankle,

and foot. Radiographics, 2010, 30: 1001-1019. 2. Spinner R.J., Luthra G., Desy N.M., Anderson M.L., Amrami K.K.: The clock face guide to peroneal intra neural ganglia: critical “times” and sites for accurate diagnosis. Skeletal Radiol, 2008, 37: 1091-1099. 3. Woertler K.: Tumors and tumor-like lesions of peripheral nerves. Semin Musculoskelet Radiol, 2010, 14: 547558. 1. Department of Radiology, AZ SintMaarten Duffel-Mechelen, campus Duffel, Duffel, 2. Department of Radiology, University Hospital Antwerp, Edegem, 3. Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium.

CARDIOVASCULAR AND TIONAL RADIOLOGY

INTERVEN-

Large-bore nitinol stents for malignant vena cava superior syndrome: factors influencing outcome P. Gillardin, S. Fieuws, S. Heye, J. Vaninbroukx, K. Nackaerts, G. Maleux1 Purpose: In this presentation, we report our findings concerning the use of large-bore Zilver nitinol stents for malignant vena cava superior syndrome. Factors potentially influencing outcome were analysed. Materials and methods: From December 2004 until April 2011, 78 consecutive patients who presented with malignant superior vena cava syndrome due to malignant adenopathies (n = 16) or pri mary lung tumor (n = 62), underwent an endovascular procedure. Analyzed factors were the following: tumor type, need for additional balloon-expandable stenting and Kishi score. Overall survival was calculated until end of follow-up period or decease. Results and discussion: Technical success was obtained in all but one patient (98%). Additional balloon- expandable stenting was required in 22% of the patients, in order to complete expansion of the nitinol stent. Occlusion of the stent during follow-up occurred in 8 patients (10%). Overall survival at 6 months was 54% (n = 34) and 50% (n = 8) and at 12 months 37% (n = 21) and 21% (n = 3) for respectively patients suffering from superior vena cava syndrome related to malignant primary lung tumor and adenopathies (p = 0.376).

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54 No difference in survival rate was oted as a function of additional balloon- n expandable stenting (p = 0.35) or Kishiscore (p = 0.80). Finally, compared to other studies, no more occlusion events have been noted in patients Conlusion: Patients with stenosis of malignant adenopathic and primary

JBR–BTR, 2013, 96 (1) rigin show no statistical significance in o survival at 6 and 12 months of follow-up. Additional balloon-expandable stenting (22%) is remarkably not associated with higher thrombosis rate. Kishi-score appears not to be a prognostic factor, meaning all patients with SVC-syndrome are candidate for stenting, irrespective severity degree symptoms.

Large-bore bore nitinol stents are a safe and very effective for palliative desobstruction of malignant SVC stenosis with encouraging global survival data and low reocclusion rates, irrespective of symptoms degree. 1. Department of Radiology, UZ Gasthuisberg, KUL, Leuven.

JBR–BTR, 2013, 96: 54.

FORTHCOMING COURSES AND MEETINGS NATIONAL MEETINGS 01.03.13 BELGIAN WEEK OF GASTROENTEROLOGY Research Meeting Imaging Section Information: danse@uclouvain.be

26.03.13 RBRS-Pediatric Radiology UZ Brussels Information: brigitte.dep@hotmail.be

16.03.13 CARDIAC IMAGING COURSE AND WORKSHOP 2013 Brussels Information: www.cardiacimaging.info

20.04.13 WAR AND PEACE IN RADIOLOGY Brussels Military Hospital Information: info@radiology-museum.be

21-22.03.13 ATELIER DE COLONOSCOPIE VIRTUELLE Liège, Clinique St Joseph Information: anne-marie.mandic@chc.be

23.04.13 RBRS-Chest Radiology Brussels, Saint Luc Hospital Information: benoit.ghaye@uclouvain.be

22.03.13 RBRS-Cardiovascular and Interventional Radiology Mons, Hôpital Ambroise Paré Information: Denis.henroteaux@skynet. be, sam.heye@uzleuven.be

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22.06.13 STRATÉGIE ET DÉFIS EN IMAGERIE PÉDIATRIQUE ONCOLOGIQUE COMMENT FAIRE MIEUX AVEC MOINS D’ARGENT ET DE RAYONS Liège Organization and information; Dr L. Rausin, leon.rausin@chrcitadelle. be 12-13.09.13 ATELIER DE COLONOSCOPIE VIRTUELLE Liège, Clinique St Joseph Information: anne-marie.mandic@chc.be 10-12.10.13 HRCT OF THE LUNG Leuven Information: walter.dewever@uzleuven.be, Johny.verschakelen@uzleuven.be, www.everyoneweb.com/chestradiology

RBRS Annual Symposium 2013

RBRS – Chest Radiology 23.04.13, 10-12.10.13

RBRS – Pediatric Radiology 26.03.13

RBRS – Cardiovascular and Interventional Radiology 16.03.13, 22.03.13

RBRS – Abdominal and Digestive Imaging 28.02-02.03.13

Miscellaneous 21-22.03.13, 20.04.13, 26.04.13, 22.06.13, 12-13.09.13

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

InterNATIONAL MEETINGS 07-11.03.2013 ECR EUROPEAN CONGRESS OF RADIOLOGY Vienna, Austria Information: myESR.org

24-28.04.13 EUROPEAN ASSOCIATION FOR THE STUDY OF THE LIVER (EASL) Amsterdam, The Netherlands Information: www.easl.eu

02-06.04.13 45TH IDKD 2013 DAVOS Musculoskeletal Diseases Davos, Switzerland Information: www.idkd.org

09-12.05.13 3RD IDKD INTENSIVE COURSE IN HONG KONG Diseases of the Chest and Heart Hong Kong, China Information: www.idkd.org

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13-15.06.13 ASIAN PACIFIC DIGESTIVE WEEK – WORLD CONGRESS OF GASTROENTEROLOGY Shangai, PRChina Information: www.gastro2013.org

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