JBR 2011-2 by office

WETTEREN 1

P 702083

Volume 94 Page 59-106 March-April

Bimonthly

–

2011

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

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

JBR-BTR ♦ 94/2 ♦ 2011 Journal Belge de ♦ Belgisch Tijdschrift voor ♦ RADIOLOGIE

Founded in 1907 A bimonthly journal devoted to diagnostic and interventional imaging, related imaging sciences, and continuing education Contents Left ventricular diverticulum: incidental finding on dual source cardiac CT. Y. De Bruecker, L. Janssen, F. De Somer, K. Boeren, B. Ector, L. Janssens, D. Perdieus . . . . . . . . . . . . . . . . . . . Primary appendiceal tumors: clinical imaging and pathological findings. Report of 4 cases. A. Koktener, K. Akin, D. Kosehan, C. Dener . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Extensive neurosarcoidosis and optic nerve complications. J. El Mouedden, M.C. Duray, D. Hernalsteen, G. Cosnard . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ruptured hepatocellular carcinoma following transcatheter arterial chemoembolization. S. Bruls, J. Joskin, R. Chauveau, J. Delwaide, P. Meunier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Exceptional, potentially fatal combination of emphysematous pancreatitis and gas-forming cholecystitis: successful multidisciplinary conservative treatment supported by repeated CT-staging. N. Verbeeck, K.M. Hartmann, J. Weber, M. Max . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A rare presentation of breast cancer. A. Rappaport, A. Van Steen, C. Van Ongeval . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Malignant transformation of an abdominal inflammatory myofibroblastic tumor with distant meatstases in a child. C.W. Ernst, J. Van Der Werff Ten Bosch, B. Desprechins, J. de Mey, M. De Maeseneer . . . . . . . . . . . . . . . . . . . .

59 63 66 68

71 75

LETTER TO THE EDITOR Ultrasonography and MRI findings of cutaneous B-cell lymphoma, leg type. E. Öztürk, S. Sipahioglu, Ü. Han, C. Yücesoy, A. Dilli, B. Hekimog˘lu . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

IMAGES IN CLINICAL RADIOLOGY Posttraumatic priapism in child. N. Bottosso, T. Khuc, D. Brisbois, J. Khamis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Complicated pulmonary interstitial emphysema. C. Altay . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Tympanic plate fracture following mandibular trauma with emphasis on 3D imaging. B. Coulier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Spinal abnormalities in vitamin B12 deficiency. F. Le Moine, P. Matthys . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Duodenal varices. L. Yi-lan, S. Wen-Ko, L. Yu-Peng . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Renal fornix rupture following diagnostic coronarography. J. Vanrusselt, K. Vander Eeckt, R. Oyen, F. Claus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Adrenal gland fusion. P. De Visschere, E. Schollaert, G. Villeirs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pulmonary arteriovenous malformation. E. Janssens, P. Leyman, T. De Beule, L. Ardies, P. D’haenens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ileo-colic hernia through the foramen of Winslow. R. Gutu, S.H. Sondji, S. Landen, J. Pringot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Round ligament varicocele. J. Heymans, F.M. Vanhoenacker, F. Vankelecom . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bilateral globus pallidus infarcts in ecstasy use. K. De Smet, M. De Maeseneer, Y.A. Talebian, T. Stadnik, J. De Mey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Focal eosinophilic hepatitis simulating a solitary metastatic lesion in FDG-PET/CT in a patient with history of head and neck cancer. G. Ceulemans, B. Ilsen, D. Verdries, J. de Mey, H. Everaert . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lipedematous scalp : a rare dermatological entity. P. Bosschaert, F.C. Deprez . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Schwannoma of the seminal vesicle. K. Boeren, Y. De Bruecker, Y. Vankan, D. Perdieus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

83 84 85 86 87 88 89 90 91 92 93

94 95 96

Agenesis of the pubic symphysis detected with SPECT-CT. G. Ceulemans, M. Keyaert, M. De Maeseneer, D. Verdries, H. Everaert . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Primary breast tuberculosis. S. Termos, E. Sbeity, M. Oweidat, Z.R. Korban, G.S. Ai Saad . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Grynfelt hernia. B. Coulier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

97 98 99

The European Day of Radiology (EDOR): summaries of presentations by D. Tack on safe imaging and P. Parizel and B. Lubocz on acute stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100 Abstracts of papers presented at the annual session of the research group on abdominal and digestive imaging organized in Liege on February 18, 2011 by section Abdominal Imaging . . . . . . . . . . . . . . . . . . . . . . 103 Abstract of papers for full membership at the Royal Belgian Society of Radiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104 Forthcoming courses and meetings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105 Classified services . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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

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

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

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JBR–BTR, 2011, 94: 59-62.

LEFT VENTRICULAR DIVERTICULUM: INCIDENTAL FINDING ON DUAL SOURCE CARDIAC CT Y. De Bruecker1, L. Janssen1, F. De Somer1, K. Boeren1, B. Ector2, L. Janssens2, D. Perdieus1 The purpose of this retrospective study is to describe the prevalence, size and location of left ventricular (LV) diverticulum-diverticuli on cardiac dual source CT. Dual source computed tomography cardiac angiography (DS CTCA) was performed in 482 patients. Where literature states their rare occurrence, this retrospective study demonstrates the fairly common finding of incidental LV diverticulum on DS CTCA examinations. LV diverticuli were found incidentally in 20 out of 482 patients (4.1%), a substantially higher incidence than previously reported. Although diverticuli were most common along the inferoseptal wall (45%) they also occurred in all parts of the left ventricular wall. Multiple diverticuli were found in 30% of patients. Dimensions of the LV diverticuli varied enormously. LV diverticuli are reported to be frequently associated with other congenital anomalies. Complications ranging from sudden death and heart failure to embolic events have been described in literature. No relevant associated anomaly or complication was present in the studied 20 patients. Our data support the hypothesis that LV diverticuli, incidentally found in adulthood, follow a benign course and can be managed conservatively. More knowledge is however required to understand history and prognosis about this condition. Key-words: Heart, ventricles – Heart, CT.

Left ventricular (LV) diverticuli are considered to be a rare congenital disorder. The prevalence of congenital ventricular diverticuli was reported to be 0.4% in an autopsy series of patients who had died as a result of cardiac disease and only 0.26% in a general population referred for cardiac catheterisation (1). Less than 100 cases have been reported in the English literature (2). Computed tomography cardiac angiography (CTCA) has emerged as a robust and accurate tool for the non-invasive evaluation of coronary artery disease (3, 4). CTCA further provides important new noninvasive insights into subtle details of cardiac morphology. A rather unexplored area is that of variants of the left ventricle. The goal of this study is to determine the prevalence, imaging characteristics and anatomic locations of LV diverticuli on dual source (DS) CTCA (Definition, Siemens Medical Solutions). The potential clinical relevance of the presence of these structures is discussed. Materials and methods ECG-gated cardiac CT imaging was performed in 542 consecutive patients for a period of 14 months and was retrospectively reviewed. All imaging was performed with a dual source CT (Definition, Siemens Medical Solutions) (330 milliseconds gantry rotation time, 83 ms temporal

Fig. 1. — MIP short axis view shows a basal inferoseptal located diverticulum (arrow). Involvement is more than half of the myocardial thickness on this diastolic image.

resolution). Image acquisition was performed during a single breath hold. Imaging parameters included a slice collimation of 64 x 0.75 mm, a tube voltage of 100-120 kV and an effective tube current of 750850 mAs. Patients were included in the study if intravenous contrast had been administered. Injection consisted of 80-110 ml of non-ionic contrast material (Iomeron 400, Bracco), administered at a rate of 5.0 mL/s by a power injector. Depending on heart rate, patients were scanned prospectively or retrospectively.

From: 1. Department of Radiology, 2. Department of Cardiology, Bonheiden Imelda Hospital, Bonheiden, Belgium. Address for correspondence: Dr Y. De Bruecker, M.D., Department of Radiology, Bonheiden Imelda Hospital, Imeldalaan 9, 2820 Bonheiden, Belgium. E-mail: yves.de.bruecker@imelda.be

Because diverticuli can be compressed during the systolic phase, search for LV diverticuli was done on diastolic images. Multiplanar reconstructions as well as maximum intensity projections were generated. Diverticuli were differentiated from trabeculations using following criterion: if involvement was less than half of the myocardial thickness on diastolic images, it was considered a trabeculation (5) (Fig. 1). Two investigators reviewed the images retrospectively via a consensus reading. Presence and size of LV diverticuli were recorded. The prevalence of LV diverticuli was calculated. They were measured in mediolateral length, anteropostior width and craniocaudal height. Ostium caliber of these diverticuli was also measured.

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Table I. â&#x20AC;&#x201D; Clinical and imaging characteristics of 20 patients with left ventricular diverticuli. age

sex

Nb.2

location

2 3

50 44

M F

1 2

4 5 6 7 8

64 22 86 81 73

F F F F M

1 1 1 1 1

10 11 12 13 14 15

48 45 67 75 53 52

F M M F F F

1 1 1 1 1 2

17 18

49 67

F F

1 2

19 20

63 57

F M

1 1

1 2 3

Mid inferoseptal Mid inferoseptal Basal inferoseptal Basal inferoseptal Basal inferoseptal Mid inferoseptal Basal inferoseptal Apical inferior Apical septal Mid anteroseptal

Dimensions1 (cm) 0.8 x 0.2 x 0.6 0.5 x 0.2 x 0.7 1.0 x 0.2 x 0.5 0.7 x 0.3 x 0.8 1.0 x 0.5 x 0.9 1.2 x 0.4 x 1.2 0.9 x 0.2 x 0.7 0.9 x 0.6 x 1.6 1.2 x 0.4 x 1.0 1.4 x 0.3 x 0.9

Ostium (cm) 0.4 0.2 0.2 0.2 0.4 0.6 0.2 0.3 0.8 0.4

Mid anteroseptal Mid anteroseptal Mid anteroseptal Basal inferoseptal Mid septal Apical septal Apical septal Basal inferoseptal Basal inferoseptal Mid anteroseptal Mid septal Basal inferoseptal

1.5 x 0.3 x 1.4 0.6 x 0.4 x 0.6 0.9 x 1.0 x 0.9 1.0 x 0.3 x 0.5 0.8 x 0.2 x 0.9 1.0 x 0.4 x 0.3 0.6 x 0.6 x 0.4 0.3 x 0.3 x 1.0 0.3 x 0.3 x 1.0 0.7 x 0.3 x 0.5 0.6 x 0.2 x 0.3 0.5 x 0.2 x 0.5

0.6 0.4 0.3 0.5 0.4 0.3 0.2 0.2 0.2 0.3 0.5 0.2

Mid anteroseptal Mid anteroseptal Mid septal Basal inferoseptal Basal lateral

1.1 x 0.4 x 1.1 0.5 x 0.2 x 0.2 0.6 x 0.2 x 0.2 0.6 x 0.3 x 0.4 1.4 x 0.3 x 0.6

1.2 0.2 0.2 0.2 0.3

Associated findings None Accessory left atrial appendage Chronic pericarditis None None None CT prior to PAVI3 implacement Obstructive lesion of the circumflex artery None None Accessory left atrial appendage Accessory left atrial appendage None None Accessory left atrial appendage Accessory left atrial appendage

Accessory left atrial appendage Accessory left atrial appendage None Accessory left atrial appendage

dimensions of diverticuli are given in mediolateral length x anteropostior width x craniocaudal height. Nb. = number of diverticuli. PAVI = percutaneous aortic valve implacement.

The examinations were evaluated for presence of any other cardiac congenital abnormality including left atrial accessory appendages, atrial septum defect, ventricular septum defect. They were also evaluated for presence of any acquired cardiac abnormality including coronary artery disease, aneurysm of the ascending aorta, pericardial disease. Results During the period from December 2008 through January 2010, 542 patients underwent DS CTCA. Indications were: assessment of coronary arteries (459/542), patency of coronary artery bypass grafts (3/542), pre- or postpulmonary vein isolation procedures (62/542) and pre-percutaneous aortic valve implacement (PAVI) (18/542). Coronary calcium score was determined if assessment of coronary

arteries was required. 60 patients presented with high calcium score levels (Agatston score of > 800). No contrast was administered in these patients because too many beam hardening artefacts could be expected to evaluate the coronary arteries. Since evaluation of LV diverticuli requires contrast administration, these patients were excluded from this study. 20 patients out of 482 (4.1%) were found to have LV diverticuli. Table I summarizes the clinical and imaging characteristics of these patients. 19 out of these 20 patients were imaged for evaluation of the coronary arteries. One patient was imaged prior to PAVI procedure. The diverticuli ranged from 0.5 to 1.4 cm in maximum dimension. Ostia of the diverticuli ranged from smaller than 0.2 cm to 1.2 cm. The patient group consisted of 12 women and 8 men between the ages of 34 and 86.

Most frequent location of these LV diverticuli is the inferoseptal part of the LV wall (9 out of 20 (45%)), but they occur in any location. Fig. 2 demonstrates a mid anteroseptal located LV diverticulum. Multiple diverticuli were present in 6 out of 20 patients (30%). 5 patients presented with 2 diverticuli and 1 patient presented with 3 diverticuli. When multiple diverticuli were found, they were grouped together except in 1 patient. Fig. 3 shows 2 diverticuli in 1 patient, located in the basal inferoseptal part. 1 patient presented with obstructive atherosclerotic coronary pathology; no significant coronary pathology was found in the other patients. 1 patient was known with chronic recurrent auto-immune pericarditis. 8 patients (40%) presented with left atrial accessory appendages. None of the patients presented with associated atrial or ventricular septal defect. None of the

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LEFT VENTRICULAR DIVERTICULUM — DE BRUECKER et al

Fig. 2. — MIP short axis view shows an mid anteroseptal located diverticulum (arrow). Fig. 3. — MIP horizontal long axis view shows 2 basal inferoseptal located diverticuli (arrows).

patients presented with enlarged ascending aorta. None of these structures revealed the presence of thrombus. Discussion The purpose of this study was to assess the prevalence, size and location of left ventricular diverticula as incidentally observed with DS CTCA. Literature consists predominantly of a modest number of case reports and clinical series. No typical or pathognomonic ECG changes are known, and specific laboratory tests for the diagnosis are not available. They are usually found incidentally during diagnostic imaging procedures performed for other reasons. LV diverticulum or diverticuli are considered to be rare (1). They have been described as a rare malformation that can occur isolated or in association with other congenital abnormalities such’s as Ebstein’s anomaly, hypertrophic cardiomyopathie, Cantrell’s syndrome (6-8). Apical diverticuli are reported to be frequently (more than 70%) associated with congenital abnormalities (9,10), but none of the 4 patients with apical diverticuli reported in this study revealed this association. None of our reported patients presented with a relevant cardiac abnormality. 8 out of the 20 patients (40%) presented with a non-significant left atrial accessory appendage. Diverticuli can either be secondary to intrinsic abnormalities in

embryogenenis or acquired in utero, e.g. viral infections or vascular accidents (11). Congenital ventricular diverticuli should be differentiated from other causes of acquired ventricular aneurysms such as those after myocardial infarction, myocardial inflammatory disease such as sarcoidosis or myocarditis, infectious endocarditis or trauma (12). Differential diagnosis with acquired ventricular aneurysms can not be made with certainty based on imaging alone. Often the distinction can only be made with knowledge of cardiac history. According to pathology findings (13), congenital diverticuli can be classified in two types: fibrous or muscular. In our study, we didn't classify the diverticula. Any localized protrusion of the ventricular lumen, with a depth more than half of the muscular wall on diastolic images, was considered to be a diverticulum as done in a similar study by Srichai et al. (5). Srichai et al. studied the prevalence of LV diverticuli in a cardiac CT population (2.2%, 15 out of 675 patients). The substantially higher prevalence in our study (4.1%) can be explained by better temporal resolution in DS CTCA as only a small percentage of patients were scanned with this technique in the Srichai's study (16.7%, 113 out of 675). Most common location of diverticuli in our study is the inferoseptal part of the LV (45% of patients (9 out of 20)). This finding corresponds to the literature (5). Our study further

shows that diverticuli can appear in any location of the LV wall. We describe the anteroseptal location of a LV diverticulum in 6 patients which is, to our knowledge, never published in literature before. Overall dimensions (from smaller than 2 mm to 1.4 cm) and dimensions of the ostia of the studied diverticuli vary enormously. The sizes of ventricular diverticula described in the literature range from as small as 0.5 cm in diameter to as large as 8-9 cm (12). Several complications have been reported in asscociation with a ventricular diverticulum. Pitol et al. reported a case of a patient with new onset of arrhythmia due to a LV diverticulum at the age of 56 (14). Handler et al. reported a 25-year-old male with heart failure and a LV diverticulum on MRI (15). Bernasconi et al. reported a case of prenatal rupture (16). Bell and Ehmke reported a child with fatal cerebral embolisation (17). Too few cases have been described to find a relation between location and symptomatology. It is generally accepted that larger diverticuli are more prone to be symptomatic (18). The management of this condition remains unclear and is primary affected by symptoms and associated malformations. Based on the possible reported complications some authors recommend aggressive surgical treatment (19). Others suggest that the clinical course may be benign and recommend a more

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conservative approach (20). All diverticuli described in this study were incidental findings and could not be related to symptomatology. They were managed conservatively with clinical follow-up. It is clear that more knowledge is required to decide upon adequate therapy. Mode of treatment has to be individually tailored and depends on clinical presentation, accompanying abnormalities and possible complications. Our study has some limitations. Pathology was not available to confirm the diagnosis. Because it was a retrospective study in an almost exclusive coronary setting (just 1 out of 20 patients with LV diverticuli was scanned for pre PAVI procedure), the results can only be related to this group and not to the general population. The potential association with other cardiac and non cardiac abnormalities is not sufficiently assessed and needs to be investigated in future studies. Male to female ratio is 1 to 1.5 in our study but too few patients are included in this study to make any conclusions. In conclusion, DS CTCA represents a unique tool to assess subtle anatomic cardiac variants. Our data show that left ventricle diverticuli can be incidentally found in more than one twenty-fifth of subjects undergoing DS CTCA. They further support the hypothesis that LV diverticuli, incidentally found in adulthood, follow a benign course. More knowledge is however required to understand prognosis about this condition. References 1. Skapinker S.: Diverticulum of the left ventricle of the heart, review of the

JBRâ&#x20AC;&#x201C;BTR, 2011, 94 (2)

literature and report of a successful removal of the diverticulum. Arch Surg, 1951, 63: 629-634. Cianciulli T.F., Del Carmen Gonzalez Colaso P., Saccheri MC., Lax J.A., Redruello H.J., Guerra J.E., Prezioso H.A., Vidal L.A.: Left ventricular diverticulum, a rare echocardiographic finding: two adult patients and review of the literature. Cardiol J, 2009, 16: 76-81. Leschka S., Alkadhi H., Plass A., Desbiolles L., GrĂźnenfelder J., Marincek B., Wildermuth S.: Accuracy of MSCT coronary angiography with 64-slice technology: first experience. Eur Heart J, 2005, 26: 14821487. Scheffel H., Alkadhi H., Plass A., Vachenauer R., Desbiolles L., Gaemperli O., Schepis T., Frauenfelder T., Schertler T., Husmann L., Grunenfelder J., Genoni M., Kaufmann P.A., Marincek B., Leschka S.: Accuracy of dual-source CT coronary angiography: First experience in a high pretest probability population without heart rate control. Eur Radiol, 2006, 16: 2739-2747. Srichai M.B., Hecht E.M., Kim D.C., Jacobs J.E.: Ventricular diverticula on cardiac CT: more common than previously thought. AJR, 2007, 189: 204208. Bashour T.T., Saalouke M., Yazji Z.I.: Apical left ventricular diverticulum with Ebstein malformation. Am Heart J, 1988, 115: 1332-1334. Maron B.J., Hauser R.G., Roberts W.C.: Hypertrophic cardiomyopathy with left ventricular apical diverticulum. Am J Cardiol, 1996, 77: 1263-1265. Cantrell J.R., Haller J.A., Ravitch M.M.: A syndrome of congenital defects involving the abdominal wall, sternum, diaphragm, pericardium, and heart. Surg Gynecol Obstet, 1958, 107: 602-614. Mady C.: Left ventricular diverticulum: analysis of two operated cases and review of the literature. Angiology, 1982, 33: 280-286.

10. Marijon E., Ou P., Fermont L., et al.: Diagnosis and outcome in congenital ventricular diverticulum and aneurysm. J Thorac Cardiovasc Surg, 2006, 131: 433-437 11. Brachlow A., Sable C., Smith S., Slack M., Martin G.: Fetal diagnosis and postnatal follow-up of an asymptomatic congenital left ventricular diverticulum. Pediatr Cardiol, 2002, 23: 658-660. 12. Ohlow M.A.: Congenital left ventricular aneurysms and diverticula: definition, pathophysiology, clinical relevance and treatment. Cardiology, 2006, 106: 63-72. 13. Wu J.M., Yu C.Y.: Isolated congenital left ventricular diverticulum. Pediatric Cardiol, 1996; 17: 254-256. 14. Pitol R., Cardoso C.O., Cardoso C.R., et al.: Congenital ventricular diverticulum associated with ventricular tachycardia. Arq Bras Cardiol, 2005, 84: 173-175. 15. Handler C.E., Walker J.M.: Congenital diverticulum of the left ventricle presenting as heart failure and diagnosed by magnetic resonance imaging. Int J Cardiol, 1989, 22: 115-119. 16. Bernasconi A., Deleziode A.L., Menez F., Vuillard E.: Prenatal rupture of a left ventricular diverticulum: A case report and review of the literature. Prenat Diagn, 2004, 24: 504-507. 17. Bell W.E., Ehmke D.A.: Diverticulum of the left ventricle in a child with fatal cerebral embolization South Med J, 1971, 64: 537-540. 18. Tandar A., Meredith K.G., Anderson J.L.: Multiple left ventricular diverticuli in an asymptomatic adult: Case report and review of the literature. Catheter Cardiovasc Interv, 2007, 69: 453-458. 19. Parthenakis F.I., Kochiadakis G.E., Patrianakos A.P., Hamilos M.I.: Peripheral arterial embolism due to a left ventricular diverticulum in a young adult. Chest, 2005, 127: 1452-1454. 20. Archbold R.A., Robinson N.M., Mills P.G.: Long-term follow-up of a true contractile left ventricular diverticulum. Am J Cardiol, 1999, 83: 810813.

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PRIMARY APPENDICEAL TUMORS: CLINICAL IMAGING AND PATHOLOGICAL FINDINGS. REPORT OF FOUR CASES A. Koktener1, K. Akin1, D. Kosehan1, C. Dener2 Primary appendiceal tumors are rare clinical and radiological entities. We report 4 cases including muscinous cystadenoma associated with pseudomyxoma peritonei, muscinous cystadenoma associated with mucocele, lowgrade muscinous neoplasia associated with appendicitis in elderly patients, and carcinoid tumor associated with appendicitis in a young adult. Key-word: Appendix, neoplasms.

Primary appendiceal neoplasms are rare clinical and pathological entities. Most common manifestation of these tumors is acute appendicitis due to the luminal obstruction. Intussusception, palpable mass, gastrointestinal bleeding, abdominal distention (because of pseudomyxoma peritonei), genitourinary symptoms may be also seen. On the other hand, they may be asymptomatic and incidentally diagnosed (1, 2). We present four primary appendiceal neoplasm with different clinical, pathological, and radiological findings. Case 1: A 75-year-old man presented with the symptoms of disuria, dyspepsia, epigastric pain. His physical examination determined abdominal distension, ascites. Laboratory investigation showed high level of CEA: 20.9 mg/ml (0-5 mg/ml), PSA: 29.4 ng/ml (0-4 ng/ml), CRP: 19 mg/L (0-8 mg/L) and low level of hemoglobin 12.8 g/dL. Abdomen ultrasonography (US) showed ascites with peritoneal thickening. Colonoscopy revealed tubuler adenoma at the rectum. Gastroscopy found eosaphageal ulcer, erythmatous gastritis, bulbitis. Abdomen computed tomography (CT) determined large amount of ascites (Fig. 1). Parasynthesis found mucinous ascites without any cell. Right hemicolectomy was performed. Final pathologic analysis reported rupture of appendiceal mucinous cystadenoma. Case 2: An asymptomatic 68-yearold man followed-up for prostate cancer admitted to the hospital for routine controls. On US examination paracecal localized a bilobulated cystic mass with 20 × 10 mm dimension and minimal peritoneal fluid

Fig. 1. — Axial contrast-enhanced CT scan shows ascites associated with pseudomyxoma peritonei.

were seen (Fig. 2). Laboratory examination including tumor markers found no abnormality. Colonoscopic examination showed colitis, diverticulosis at the sigmoid colon and tubuler adenoma at the rectum. Abdomen CT determined no abnormality except the findings on US (Fig. 3). Laparotomy including appendectomy was performed. Pathologic examination determined mucinous cystadenoma. Case 3: A 59-year-old man presented with right lower quadrant pain lasting 3 days. Physical examination showed right lower quadrant tendernes. Laboratory investigation found elevated level WBC: 17600/mL (36009600/mL), ESR: 65 mm/hr, CRP:

From: 1. Department of Radiology, 2. Department of Surgery, 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

78 mg/L. Abdomen US examination determined acute appandicitis features with peritoneal fluid (Fig. 4). Appendectomy was performed and pathology found low-grade mucinous neoplasia with peritonitis. Case 4: A 38-year-old man admitted to the hospital with the symptoms of emesis, and abdominal pain. Physical examination determined tenderness of the lower quadrants. Laboratory examination showed leukocytosis (WBC: 13800/mL). Abdomen US examination showed edema of the mesenteric fat and peritoneal fluid in the right lower quadrant. Abdomen CT determined appendicitis with mesenteric inflammation (Fig. 5). Appendectomy was performed. Pathologic examination reported the diagnosis of tubular carcinoid tumor. Discussion Primary appendix tumors are not common, and seen 0.5%-1% of

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Fig. 2. — Transabdomainl US image demonstrates a bilobulated cystic lesion-mucocele.

Fig. 4. — US image showes thick-walled, dilated appendix (A) with mesenteric inflammation (arrows).

Fig. 3. — Axial contrast enhanced CT scan demonstrates fluidfilled lesion; mucocele near the cecum (arrow).

Fig. 5. — Axial contrast-enhanced CT scan showes the retrocecal appendix with wall thickening and mesenteric inflammation (arrow).

appendectomy specimens. Epithelial tumours of the appendix include low-grade mucosal tumours as well as invasive adenocarcinoma. The other neoplasms are carcinoid tumor, lymphoma, ganglioneuroma, phechromocytoma, mesenteric tumors. Retention cysts, hyperplastic polyps, and diffuse mucosal hyperplasia are not truly neoplastic (1, 2). Of these, mucocele is the most common one. Mucocele is a mucinous distention of the appendiceal lumen caused by mucosal hyperplasia, cystadenoma, and cystadenocarcinoma (3). They are relatively asymptomatic and found incidentally during palpation or abdominal imaging. When inflammation occurs, acute appendicitis, abscess may develop. The other presentations of mucocele may be intussusception or pseudomyxoma peritonei. In the treatment, benign

tumor are cured with appendectomy, malign lesions need right hemicolectomy (1, 4). In the diagnosis of mucinous neoplasms, abdominal radiography may show a soft-tisue mass in the right lower quadrant with curvilinear mural calcification in less than 50% of cases (5). At US, a cystic mass with or without calcification is seen. The differential diagnosis includes periappendiceal abscess, duplication cyst, mesenteric cyst, and hydrosalpinx (1). Francica et al. described the features of giant mucocele of the appendix at B-mode and contrastenhanced sonographic examinations. They determined a thin hyperechoic border without either solid vegetan or sign of infiltration of surrounding tissue, a complex internal echo structure without anechoic lacunae, including curvilinear, wavy

bands of echogenic material (onion skin sign), and avascularity on contrast-enhanced sonography (6). CT shows the anatomic relation and mural calcification more sensitively. Pseudomyxoma peritonei, and intussusception may be also diagnosed by US or CT (1). CT findings of pseudomyxoma peritonei include a nonspecific ascites and a diagnostic signs of visceral scalloping which distinguishes mucinous from fluid ascites on CT (7, 8). Poorly adhesive mucin producing cells pool in the sites of relative statis like pouch of Douglas/rectovesical pouch, right and left subphrenic spaces and surface of the liver and spleen. Mucosal hyperplasia and mucinous cystadenoma may be associated with hyperplastic poylps and adenomatous polyps (9). Mucinous

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cystadenoma and colon cancer have been diagnosed with an incidence of up to 20% (10). That is why colonoscopy is needed when appendiceal mucinous cystadenoma is determined. Appendiceal neuroendocrine tumors (carcinoids), represent up to 80% of appendiceal neoplasia, are found 1/100-300 appendectomies. Peak age is within the fourth decade. Epithelial tumours are seen in the adults older than the carcinoid group. Most of the carcinoids are asymptomatic and diagnosed after pathological examination. Although it has a malign potential, metastases and carcinoid syndrome are very rare (1). Because of their small size, carcinoid tumors of the appendix are not typically diagnosed by imaging. If they are metastatic, mesenteric or liver masses may be seen (11). Rioux et al showed sonographic finding of carcinoid tumor as a distal hypoechoic mass with a normal proximal wall of appendix in two cases (12). Imaging features show the signs of obstruction and appendicitis at CT and US. Mucocele rarely develops (13). Calcification may be seen but mimics appendicolith. Appendectomy is sufficient for the tumours less than 1.5-2 cm in size. When it is greater, right hemicolectomy is warranted (2, 14). On the other hand, CT findings suggesting acute appendicitis could be seen in other inflammatory or neoplastic processes including Crohn’s disease, right sided colon cancer (15, 16). Except for carcinoid tumor, all our cases were in elderly population. Patient with mucocele was asymptomatic and incidentally diagnosed at US as a cystic mass. Patient with abdominal distention had pseudomyxoma peritonei result of the rupture of appendiceal mucinous

cystadenoma. Both the patient with low-grade mucosal neoplasia and the patient diagnosed carcinoid tumor had symptoms and imaging features of acute appendicitis. However, we could not determine the carcinoid tumor of retrocecal localized appendix. Except this, our findings were correlated with the literature. In conclusion, primary appendiceal neoplasms are rare clinical and pathological conditions. Especially in elderly group, neoplasms should be kept in mind, besides a simple obstruction and inflammation of appendix vermiformis by the radiologist and the surgeon as it may alter the surgical approach or it may give a way to diagnose the associated abnormalities (peritoneum, colon, over). After the operation the patient should be followed-up for any developing pathology including the colon, and peritoneum. References 1. Pickhardt P.J., Levy A.D., Rohrmann C.A., Kende A.I.: Primary neoplasms of the appendix: radiologic spectrum of disease with pathologic correlation. Radiographics, 2003, 23: 645-662. 2. Barry M., Collins C.G., McCawley N., McGunness J., Leahy A.L.: Synchronous appendiceal tumours. Surgeon, 2007, 5: 111-113. 3. Higa E., Rosai J., Pizzimbono C.A., Wise L.: Mucosal hyperplasia, mucinous cystadenoma and mucinous cystadenocarcinoma of the appendix. A re-evaluation of appendiceal ‘mucocele’. Cancer, 1973, 32: 15251541. 4. Rutledge R.H., Alexander J.W. Primary appendiceal malignancies: rare but important. Surgery, 1992, 111: 244-250. 5. Madwed D., Mindelzun R., Jeffrey R.B. Jr.: Mucocele of the appendix: imaging findings. AJR, 1992, 159: 69-72.

6. Francica G., Lapiccirella G., Giardiello C., Scarano F., Angelone G., De Marino F., et al.: Giant mucocele of the appendix: clinical and imaging findings in 3 cases. J Ultrasound Med, 2006, 25: 643-648. 7. Sulkin T.V., O’Neill H., Amin A.I., Moran B.: CT in pseudomyxoma peritonei: a review of 17 cases. Clin Radiol, 2002, 57: 608-613. 8. Dixit A., Robertson J.H.P., Mudan S.S., Akle C.: Appendiceal mucoceles and pseudomyxoma peritonei. World J Gastroenterol, 2007, 13: 2381-2384. 9. Qizilbash A.H.: Mucoceles of the appendix. Their relationship to hyperplastic polyps, mucinous cystadenoma, and cystadenocarcinomas. Arch Pathol Lab Med, 1975, 99: 548-55. 10. Lino H., Jass J.R., Simms L.A., Joung J., Leggett B., Ajioka Y., et al.: DNA microsatellite instabilty in hyperplastic polyps, serrated adenomas, and mixed polyps: a mild mutator pathway for colorectal cancer? J Clin Pathol, 1999, 52: 5-9. 11. Bittle M.M., Chew F.S.: Radiologic reasoning: recurrent right lower quadrant inflammatory mass. AJR, 2005, 185: S188-194. 12. Rioux M., Duchesne N., Langis P.: Carcinoid tumor of the appendix: ultrasound findings in two cases. J Clin Ultrasound, 1994, 22: 129-133. 13. Hermans J.J., Hermans A.L., Risseeuw G.A., Verhaaar J.C., Meradji M.: Appendicitis caused by carcinoid tumor. Radiology, 1993, 188: 71-72. 14. Moertel C.G., Weiland L.H., Nagomey D.M., Dockerty M.B.: Carcinoid tumor of the appendix: treatment and prognosis. N Engl J Med, 1987, 317: 1699-1701. 15. Checkoff J.K., Wechsler R.J., Nazarian L.N.: Chronic inflammatory appendiceal conditions that mimic acute appendicitis on helical CT. AJR, 2002, 179: 731-734. 16. Watchorn R.E., Poder L., Wang Z.J., Yeh B.M., Webb E.M., Coakley F.V.: Computed tomography findings mimicking appendicitis as a manifestation of colorectal cancer. Clin Imaging, 2009, 33: 430-432.

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EXTENSIVE NEUROSARCOIDOSIS AND OPTIC NERVE COMPLICATIONS J. El Mouedden, M.C. Duray, D. Hernalsteen, G. Cosnard1 We present the case of a 35-year-old patient suffering from nasal obstruction and headache for 3 years. The patient was hospitalized for a recent and progressive decline of vision of the right eye associated with afferent pupillary deficit and inferior altitudinal hemianopsia. He was diagnosed with systemic sarcoidosis involving the central nervous system as illustrated by magnetic resonance imaging (MRI) scans showing different type diffuse lesions of meningo-encephalitis. Our case is characterized by severe cerebral pachyleptomeningeal lesions complicated by optic nerve compression and cervical spinal cord damage. MRI value of diagnosis for systemic neurosarcoidosis was supported by histological examination of a biopsy of the sphenoid sinus lesions that showed epithelioid granulomas presence without caseous necrosis. Thus, MRI of the brain and spinal cord is a powerful tool method in monitoring and diagnosing aymptomatic and symptomatic neurosarcoïodosis. MRI is also a powerful tool in monitoring the neurosarcoidosis during therapeutic treatments. Key-word: Sarcoidosis.

Sarcoidosis is a granulomatous inflammatory disease that can affects almost any organ and many parts of the body. This disease is termed neurosarcoidosis when the nervous system is involved. Although sarcoidosis is well described in literature, however, the cause of the disease is still not understood. Neurosarcoidosis may be asymptomatic or present debilitating chronic condition such as headache, cranial nerve palsy, seizures, paresis and paresthesias. The prevalence of neurosarcoidosis is estimated to be one-fourth of the systemic sarcoidosis patients that have histological evidence of central nervous system involvement. Herein, we report the MR findings of a 35-year-old patient with neurosarcoidosis. The lesions were characterized by pachy- and leptomeningeal lesions complicated by optic nerve compression and cervical spinal cord damage. Case report A 35-year-old patient, who had complaints of nasal obstruction and headache for 3 years was hospitalized for a recent decline and progressive loss vision of the right eye. Clinical examination showed a grasping and behavioral disorder of frontal lobe type, afferent pupillary deficit and inferior altitudinal hemianopsia right. Lumbar puncture showed slight increase of protein and glucose concentration, and oligoclonal bands identical to those of serum. Biology showed high levels of converting enzyme angiotensin. In the year 2006, he underwent resection of cervical lymphadenopathy with the diagnosis of sarcoidosis. MR images showed thick,

Fig. 1. — Axial T1-weighted gadolinium contrast-enhanced MR image shows a thick nodular pachymeningeal lesion and leptomeningeal extension (arrows).

nodular pachymeningeal lesion and leptomeningeal extension in frontal (Fig. 1, 2) and right temporal area (Fig. 3) associated to meningeal enhancement in the hypothalamopituitary area (Fig. 2). Right optic nerve was compressed and stretched by pachymeningitis. He also had multifocal leptomeningeal enhancement of the spinal cord and cervico-dorsal myelitis. Biopsy of the sphenoid sinus lesions showed epithelioid granulomas without caseous necrosis. Discussion Neurosarcoidosis is a serious clinical affection (1.2) which manifests in 5% of cases of sarcoidosis and is observed in 14 to 27% of autopsy series (1-5). The clinical manifesta-

From: 1. Department of Medical Imaging, UCL Saint Luc, Catholic University of Louvain, Brussels, Belgium. Address for correspondence: Dr J. El Mouedden, M.D., Department of Medical Imaging, UCL Saint Luc, Catholic University of Louvain, Avenue Hippocrate 10, B-1200 Brussels, Belgium.

Fig. 2. — Sagittal T1-weighted contrastenhanced image shows basal meningeal enhancement extended to pituitary area (thin arrow), brainstem and sphenoid sinus (arraowhead). Cervical spinal cord myelo-meningitis is also observed (thick arrow).

tions are highly polymorphic, depending on the location, size of lesions and their evolution (1, 3, 6). Histologically, there is an accumulation of epithelioid granulomas without caseous necrosis affecting preferentially the leptomeninges of the skull base (2) (Fig. 1 and 2) but also pachy meninges around the brain parenchyma and cranial nerves (1, 3-7). MRI can detect neurological lesions in 10% of patients with multisystem sarcoidosis (4) and is the imaging modality of choice in the diagnosis and follow-up of nervous involvement of sarcoidosis, even if the lesions are highly polymorphic (1, 3, 4, 6-7). The finding on the imaging examinations are however nonspecific. The differential diagnosis with other diseases such as tuberculosis, Wegener's granulomatosis, fungal meningitis, lymphoma, and meningeal carcinomatosis can be difficult. In neurosarcoidosis, the clinical presentation is often of low expression or even asymptomatic, in discrepancy with the major radiolog-

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Fig. 3. — Axial T2-weighted image shows meningeal lesion associated with high signal intensity on T2 of the subcortical right frontal white matter (arrow).

ical extension lesions. The association of leptomeningeal enhancing lesions and hypothalamic-pituitary after injection of gadolinium is most suggestive of diagnosis (1) (Fig. 1 and 2). In one third of cases, there is cranial nerve damages (4.8) often symptomatic, sometimes with a wide predilection for the facial and the optic nerve (3-4, 8-9). In our case there was an excellent correlation between radiological observation and clinical symptoms. Oculomotor nerve damage is very rare and is mainly secondary to intracranial hypertension (3, 6). These lesions were observed frequently in women (4). Optic nerve damage may be primary (unilateral or bilateral) or secondary to chiasmatic lesions (6, 8). Nerve damages are of 2 types: either by perivascular lymphocytic infiltration (3) or more often, as observed in our case, compression by granulomatous pachymeningitis (Fig. 4). Involvement of the brain parenchyma himself is rarely observed. If so, lesions are caused by the extension of sarcoid granulomas from the meninges into the spaces of Virchow-Robin and present as nodular or pseudo-tumor lesions enhancing after intravenous gadolinium (1, 3-6). These tumor-like lesions, however, are the most clinically symptomatic (4). It may also present as white matter lesions, of high signal intensity on T2, and non enhancing after gadolinium injection (Fig. 3). They are either gliotic scars of deep inflammatory lesions or lesions secondary to microangiopathy sarcoidosis (10). Moreover, acute

ischemic injury in a young person without known etiology must evocate the diagnosis of neurosarcoidosis (11). Lesions of cerebral white matter are considered irreversible (2), have no clinical correlation, and do not always regress under immunosuppressive therapy (4, 9). A spine cord myelo-meningtis is classic but not systematic in a neurosarcoïodosis. It has the same radiological and histopathological features as brain damage and affects most of the entire cervical spine (3.4). A normal MRI does not exclude the diagnosis of neurosarcoidosis, especially in patients with only cranial neuropathy (3, 6) or in patients previously treated with corticosteroids (1). The imaging can assess the response to immunosuppressive therapy (3, 4). The regression of lesions on MRI is often delayed compared with clinical improvement (3, 6). Conclusion Our patient is diagnosed with neurosarcoidosis, presenting as lesions of the pachy- and leptomeninges of brain and cervical spine. Our report confirms other similar observations already described in literature by Authors using MRI. Thus, our observations support the usefulness of MRI as a powerful tool for diagnosing and monitoring symptomatic neurosarcoidosis. References 1. Pickuth D., Heywang-Köbrunner S.H.: Neurosarcoidosis: Evaluation with

10.

11.

MRI. J Neuroradiol, 2000, 27: 185188. Valeyre D., Chapelon-Abric C., Belin C., Dumas J.L.: Sarcoidosis localized in the central nervous system. Med Interne, 1998, 19: 409-414. Christoforidis G.A., Spickler E.M., Recio M.V., Mehta B.M.: MR of CNS Sarcoidosis: Correlation of Imaging Features to Clinical Symptoms and Response to Treatment. AJNR Am J Neuroradiol, 1999, 20: 655-669. Shah R., Roberson G.H., Curé J.K.: Correlation of MR Imaging Findings and Clinical Manifestations in Neurosarcoidosis. AJNR Am J Neuroradiol, 2009, 30: 953-961. Weber-Donat G., Pons-Ukkola E., Garcia C., Teriitehau C., Minvielle F., Baccialone J. : A propos d’une observation singulière de neurosarcoïdose. J Neuroradiol, 2009, 04; 004. Zyberberg F., Méary E., Cérez D., Meder J.F., Frédy D.: Aspect en irm de la sarcoïdose du système nerveux central. J Radiol, 2001, 82: 623-631. Spencer T.S., Campellone J.V., Irama M.N.H., Quaiser U., Antonio J. R.: Clinical and magnetic resonance imaging manifestations of neurosarcoidosis. Semin Arthritis Rhum, 2005, 34: 649-661. Zajicek J.P., Scolding N.J., Foster O., Rovaris M., Evanson J., Moseley I.F., et al.: Central nervous system sarcoidosis diagnosis and management. QJM, 1999, 92: 103-117. El Ouni F. , Arifa N., Souei M. , Hasni I., Elbahri F., Tlili K.: Neurosarcoidosis as the initial presentation of systemic sarcoidosis. J Neuroradiol, 2006, 33 : 274-275. Seltzr S., Mark A.S., Atlas S.W.: CNS sarcoidosis: evaluation with contrastenhanced MR imaging. AJNR Am J Neuroradiol, 1991, 12: 1227-1233. Hodge M.H.. Williams R.L, Fukui M.B.: Neurosarcoidosis Presenting as Acute Infarction on DiffusionWeighted MR Imaging: Summary of Radiologic Findings. AJNR Am J Neuroradiol, 2007, 28: 84-86.

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RUPTURED HEPATOCELLULAR CARCINOMA FOLLOWING TRANSCATHETER ARTERIAL CHEMOEMBOLIZATION S. Bruls1, J. Joskin2, R. Chauveau2, J. Delwaide3, P. Meunier2 Transcatheter arterial chemoembolization (TACE) is known to be an effective palliative treatment in unresectable hepatocellular carcinoma (HCC). Although TACE can control tumour growth and palliate the patients, complications of TACE with significant morbidity are well known and adversely affect the outcome of patients. Necrotic tumor rupture is a serious complication of TACE and has a high mortality rate. We report a case of ruptured HCC following TACE in a 78-year-old male patient who subsequently developed peritonitis and pneumoperitoneum. This case gives us the opportunity to underline the importance of such complications and demonstrates the utility of CT imaging for diagnosis and management of patients with ruptured HCC. Key-word: Liver neoplasms, therapy.

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. It is a growing public health problem and its incidence is increasing worldwide (most cases of HCC in Asia and sub-saharan Africa but recently, in western countries too (1, 2)). The presence of cirrhosis is the major risk factor, essentially due to chronic hepatitis C and hepatitis B infection or alcohol disease (1). Hepatocellular carcinoma is of poor prognosis: the five-year survival rate is less than 5 percent (2). The prognosis depends on hepatic function, tumour size, and tumour extent at the time of diagnosis. Nowadays, orthotopic liver transplantation only remains curative, but because of the shortage of organ donors, these treatments are applicable only to a small part of all patients. The majority of the patients with unresectable HCC are treated by various palliative therapies included surgical resection (partial hepatectomy), or percutaneous treatment. Despite advances in imaging techniques and follow-up programs only 20% of patients are candidates for surgery at the time of diagnosis (3, 4) due to an advanced tumor stage, comorbidities, poor hepatic functional reserve or shortage of donor livers. Case report A 78-year-old man was referred to our hospital in September 2008 for a health deterioration associated with weight loss. His medical history was

remarkable for silicosis associated with respiratory failure, type 2 diabetes and cerebrovascular accident. He had a previous history of smoking and persistent alcohol abuse was documented. On admission, his height was 165 cm and his body weight 74 kg. There was no history of hematemesis, vomiting, flushing or diarrhea. Clinical examination revealed a hepatomegaly without splenomegaly. Jaundice, ascites, peripheral oedema and other signs of chronic liver disease were not observed. The patient’s blood pressure was 120/60 mmHg and heart rate was regular to 74 beats per minute. Laboratory test revealed marked leukocytosis (18000/mm3), hemoglobin level 11g/dl and abnormal liver function tests (ALP/GGT: 125/158 IU/L). Serum tumor markers were within normal range ( -fetoprotein: 2.6 ng/ml). Other laboratory tests were also within normal range. However, glycaemia (110 mg/dl) and HbA1c (7.9%) were slightly elevated. Tests for hepatitis B and C virus markers were all negative. The patient showed a Child-Pugh score of 7 (class B). A triphasic contrast enhanced CTscan showed three hypervascular lesions, without clear wash out, suspected of malignancy. The bigger one was in segment IV (4 × 4 cm) and near to the liver capsule. The other lesions were localized in segment II and in segment VI. Ultrasound was not contributive because of patient’s corpulence. A

From: 1. Department of Surgery, 2. Department of Medical Imaging, 3. Department of Gastroenterology and Hepatology, University Hospital of Liège, Liège, Belgium. Address for correspondence: Dr P. Meunier, M.D., Department of Medical Imaging, CHU Liège, B-4000 Liège, Belgium.

CT-guided biopsy of the largest hepatic lesion (segment IV) confirmed the diagnosis of well differentiated HCC in a cirrhotic liver. The patient was medically treated. On a follow-up CT scan, a few months later, it appeared that the segment IV mass was markedly increased (6 × 5.5 × 7 cm) (Fig. 1A). The segment II and VI lesion were confirmed but stable. Additional tests did not reveal any metastasis. After multidisciplinary consensus and given the patient’s delicate clinical condition, surgical treatment was not adequate. In these conditions, the presence of multiple liver HCC nodules justified a transarterial chemoembolization (TACE). TACE was performed with no intra-operative complications. Embolization of the feeding artery was performed with small gelfoam pledgets before (to reduce the flow) and after (to achieve stases) injection of 50 mg of cisplatine (Fig. 1B and C). Postoperative and one week control CTscan (Fig. 2) didn’t show any sign of active arterial contrast extravasation and other complications. Three weeks after transarterial chemoembolization (TACE), the patient complained about a right upper abdominal pain. This led to an abdominal CT-Scan (Fig. 3) that revealed ruptured necrotic mass with associated peritonitis and pneumoperitoneum but no active bleeding. At this time, laboratory test revealed stable anemia (haemoglobin level: 10.9 g/dl), hypoalbuminemia (19 g/l), abnormal liver function tests (ALP/GGT: 359/168 IU/L) and elevated conjugated bilirubin level (5.2 mg/L). Because of the bad general state of the patient, conservative treatment was decided with discharge from hospital to palliative care. Unfortunately, the patient died two months after TACE procedure.

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Fig. 1. — A: Coronal Multi-Planar Reconstruction (MPR) of a contrast enhanced CT scan of arterial phase demonstrates a hyperenhancing lesion in segment IV. B: Hepatic angiography (arteriogram) shows an anarchic hypervascularised hepatic mass that suggests hepatocellular carcinoma with formation of arteriovenous shunts. C: Hepatic angiography after chemoembolization shows an almost complete regression of the anarchic vascularisation in the lesion.

Fig. 2. — Contrast enhanced CT scan obtained one week after TACE shows the integrity of the liver capsule.

Discussion Transarterial chemoembolization (TACE) is an efficient palliative well accepted treatment for unresectable HCC (3, 5, 6). In the presence of multiple HCC nodules, TACE remains the

treatment of choice (7). TACE combines the effect of targeted chemotherapy with the effect of ischemic necrosis induced by arterial embolization (8). The basic principles of the procedure consist of a reduction of hepatic arterial blood supply to the tumor as well as the delivery of cytostatic agents (Adryamycin, Cisplatin, or Doxorubicin) directly into the tumor. It is well known that HCC is hypervascularised (with a high propensity for vascular invasion and growth factor produce) and that this hypervascularisation is mostly dependent on the hepatic artery and its branches (9). The survival benefit of this treatment is confirmed by two metaanalyses (10, 11) and two recent randomized controlled trials (4, 12) that allowed showing a significant higher survival rate compared to a group of best supportive care after three years. However its benefice appears only in selected patients with unresectable HCC and preserved liver

function. Tumor sizes, hypovascularity on imaging and elevated INR are predictors of increased mortality after TACE therapy for HCC (13). Contraindications for TACE (19) include portal vein thrombosis, significant arteriovenous shunting and poor liver function (Child-Pugh class C). Imaging techniques and correct anatomical evaluation is essential to select those patients who may potentially benefit from the procedure. CT or MR examinations should be done prior to TACE (8). Although mean survival rates of 12 months (13) have been reported, a variety of complications have been described after TACE with significant morbidity. These complications are more often benign and include postembolization syndrome (fever, abdominal pain, nausea, and vomiting), impaired liver function, and leukocytopenia (3, 5, 14). However major complications are described. Liver failure, as well as liver abscess, splenic infarction,

Fig. 3. — Axial (A and B) and sagittal (C) contrast enhanced CT scan, in arterial phase, obtained 3 weeks after TACE shows a capsular rupture at the level of the necrotic mass with associated peritonitis and pneumoperitoneum.

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upper gastrointestinal bleeding, bile duct complications, acalculous cholecystitis, pulmonary embolism, spasm or occlusion of hepatic artery and acute renal failure are associated with significant morbidity and mortality. Rupture following TACE is uncommon and represents less than 1% of all complications (15) but it is probably the most important complication of TACE with an extremely poor prognosis (1). The mortality and morbidity rate is high because the patients usually suffer from an advanced disease. The mechanism of rupture of HCC after TACE is unclear. It is probably to be related to tumor and capsular necrosis and increased pressure inside the friable tumor after TACE. Secondary infection, vascular injury during TACE or inflammation secondary to the chemotherapeutic agents could play a role too (1). They can appear especially when there is no tumor capsule or when the lesion is located adjacent to the Glissonian liver capsule (16). Two series from Asia conclude that most patients with complications after TACE had pre-existing risk factors as large tumor size, or extracapsular extension of the tumor (15, 17). Patients with ruptured hepatocellular carcinoma present right upper abdominal pain and abdominal distension and the diagnosis is usually confirmed by US or CT-Scan. CT imaging is the most useful modality in the imaging of HCC (18) and can detect most of complications following TACE (18). In a ruptured HCC, blood or gas (as a result of necrosis) may be seen in the lesion, around the liver or within the peritoneal cavity. Bleeding may also occasionally be seen. Management of patients with rupture of HCC following TACE is difficult and remains controversial because patients have already been diagnosed as having inoperable tumor and poor liver function. The primary objective in the management of these patients is to control potential bleeding and to maintain haemodynamic parameters stables. Hemostasis can be done by surgical laparotomy, interventional or conservative methods. Battula et al (19) consider that a repeat TACE can be

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performed to stabilize the tumor. In ours opinion, emergency embolization is an efficient haemostatic treatment in case of intra-peritoneal bleeding of a ruptured HCC. In this particular situation of our patient with a bad general health and the absence of active bleeding, TACE or embolization had to be excluded. The only left solution was conservative management. Although TACE is generally a safe procedure, tumor rupture remains a potential complication. As showed in our patient, it appears to be especially important in large tumors adjacent to the liver capsule. In case of such important masses, liver rupture is a clear but relatively rare complication that may occur even in absence of TACE. This complication may appear relatively lately (several weeks) after procedure, that the reason why a precise follow-up is mandatory. References 1. Gomaa A.I., Khan S.A., Toledano M.B., et al.: Hepatocellular carcinoma: epidemiology, risk factors and pathogenis. World J Gastroenterol, 2008, 14: 4300-4308. 2. El-Serag H.B., Mason A.C.: Rising incidence of hepatocellular carcinoma in the United States. New Engl J Med, 1999, 340: 745-750. 3. Rose M.D., Chapman W.C., Brokenbrough A.T., Wright J.K., Rose A.T., Meranze S., Mazer M., Blair T., Blanke C.D., Debelak J.P., Wright-Pinson C.: Transcatheter arterial chemoembolization as primary treatment for hepatocellular carcinoma. Am J Surg, 1999, 177: 405-410. 4. Llovet J.M., Real M.I., Montana X., et al.: Arterial embolisation or chemoembolisation versus symptomatic treatment in patients with unresectable hepatocellular carcinoma: a randomised controlled trial. Lancet, 2002, 359: 1734-1739. 5. A comparison of lipiodol chemoembolization and conservative treatment for unresectable hepatocellular carcinoma. Groupe d’étude et de Traitement du Carcinome Hépatocellulaire. New Engl J Med, 1995, 332: 1256-1261. 6. Kiely J.M., Rilling W.S., Touzios J.G., Hieb R.A., Franco J., Saeian K., Quebbeman E.J., Pitt H.A.: Chemoembolization in patients at high risk: results and complications. J Vasc Inter Rad, 2006, 17: 47-53.

7. Acunas B., Rozanes I.: Hepatocellular carcinoma: treatment with transcatheter arterial chemoembolization. Eur J Radiol, 1999, 32:86-89. 8. Shin S.W.: The current practice of transarterial chemoembolization for the treatment of hepatocellular carcinoma. Korean J Radiol, 2009, 10: 425434. 9. Nakashima T., Kojiro M.: Pathologic characteristics of hepatocellular carcinoma. Semin Liver Dis, 1986, 6: 259266. 10. Llovet J.M., Bruix J.: Systematic review of randomized trials for unresectable hepatocellular carcinoma: Chemoembolization improves survival. Hepatology, 2003, 37:429-442. 11. Geschwind J.F., Ramsey D.E., Choti M.A., et al.: Chemoembolization of hepatocellular carcinoma: results of metaanalysis. Am J Clin Oncol, 2003, 26: 344-349. 12. Lo C.M., Ngam H., Tso W.K., et al.: Randomized controlled trial of lipidol chemoembolization for unresectable hepatocellular carcinoma. Hepatology, 2002, 35: 1164-1171. 13. Shen H. Agarwal D., QI R., Chalasani N.: Predictors of outcome in patients with unresectable hepatocellular carcinoma receiving transcatheter arterial chemoembolization. Aliment pharmacol Ther, 2007, 26: 393-400. 14. Jinglin X., Zhenggang R., Shenglong Y., Sharma D, Zhiying L., Yuhong G., Yi C., Zengchen M., Zhiquan W., Jia F., Lunxiu Q., Xinda Z., Zhaoyou T., Binghui Y.: Study of severe and rare complications of transarterial chemoembolization (TACE) for liver cancer. Euro J Rad, 2006, 59: 407-12. 15. Chung J.W., Park J.H., Han J.K., et al.: Hepatic Tumors: Predisposing Factors for Complications of transcatheter oily chemoembolization. Radiology, 1996, 198: 33-40. 16. Sokamoto I., Aso N., Nagaoki K., et al: Complications associated with Transcatheter arterial embolization for hepatic tumors. Radiographics, 1998, 18: 605-619. 17. Liu C.L., Ngan H., Lo C.M., et al.: Ruptured hepatocellular carcinoma as a complication of transarterial oily chemomboliation. Br J Surg, 1998, 85:612-614. 18. Kim H.C., Yang D.M., Jin W., et al.: The various manifestations of ruptured hepatocellular carcinoma: CT imaging findings. Abdom Imaging, 2008, 33: 633-642. 19. Battula N., Srinivasan P., Madanur M., et al.: Ruptured hepatocellular carcinoma following chemoembolization: a western experience. Hepatobiliary Pancreat Dis Int, 2007, 6: 49-51.

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EXCEPTIONAL, POTENTIALLY FATAL COMBINATION OF EMPHYSEMATOUS PANCREATITIS AND GAS-FORMING CHOLECYSTITIS: SUCCESSFUL MULTIDISCIPLINARY CONSERVATIVE TREATMENT SUPPORTED BY REPEATED CTSTAGING N. Verbeeck1, K.M. Hartmann1, J. Weber2, M. Max3 Usually considered as a life-threatening disease, emphysematous pancreatitis requires early diagnosis and aggressive multidisciplinary treatment including the Departments of Gastroenterology, Intensive Care Medicine, Interventional Radiology and even Surgery. The prognosis for emphysematous cholecystitis is also quite poor. It requires surgery even if a percutaneous cholecystostomy can contribute to a temporary stabilization of the patient. Computed tomography is the imaging modality of choice to detect emphysematous pancreatitis and gas-forming cholecystitis. It enables their grading and helps identify their complications. Moreover, it proves essential in the follow-up of the lesions. Key-words: Pancreatitis – Cholecystitis.

Emphysematous pancreatitis (EP) is a rare occurrence characterized by the presence, in the pancreatic parenchyma, of gas produced mainly by tissue necrosis and/or bacteria. It can also, just like in the exceptional case we are reporting, be complicated by gas-forming cholecystitis where gas appears in the lumen and even in the wall of the gallbladder. Since the rate of mortality and morbidity of EP can reach 40 and 100% respectively, this condition requires early CT diagnosis together with intensive multidisciplinary management. Nowadays, interventional techniques under endoscopic or radiological guidance supersede surgery. Emphysematous cholecystitis (EC) is also often fatal. It requires prompt diagnosis too and must be treated surgically even if the acute phase can be overcome by percutaneous cholecystostomy. Case report A 77-year-old male patient is admitted to the Emergency Department for acute abdominal pain. His laboratory data show a normal leukocytosis but the values for pancreatic amylase reach 2471 U/L (normal values: 13-53 U/L) and the lipase level reads 11856 U/L (normal values: 13-60 U/L). The requested abdominal CT scan displays peripancreatic fat stranding without associated necrosis of the pancreas (Fig. 1). Since we cannot argue in favour of a pancreatitis of exogenic origin, we suppose that a solitary

Fig. 1. — Contrast-enhanced CT image showing the peripancreatic fat stranding (arrows), without necrosis of the pancreas (Balthazar grade C, severity index 2).

stone may have migrated. The patient is then transferred to the Gastroenterology Department where a classical treatment is started, combining strict fasting and intravenous analgesics. On the next day, the levels of amylase and lipase have dropped to respectively 828 et 1385 U/L, however the pain worsens and leukocytosis rises to 15.3 G/L (normal values: 4.8-10.8 G/L). Therefore, a second CT examination is carried out and reveals, in addition to a nearly 80% necrosis of the pancreatic parenchyma, an emphysematous pancreas as well as gas in the gallbladder lumen and wall (Fig. 2). A cholecystostomy is then per-

From: Departments of 1. Radiology, 2. Gastroenterology, 3. Intensive Care Medicine, Centre Hospitalier de Luxembourg, Luxembourg. Address for correspondence: Dr N. Verbeeck, M.D., Centre Hospitalier de Luxembourg, 4, rue Barblé, L-1210 Luxembourg, Grand Duchy of Luxembourg.

formed under CT scan guidance and the patient is transferred to the Intensive Care Unit where his vital parametres are maintained. Because of the cholecystitis, antibiotics are administered. Five days later, since the case is severe and though the patient’s overall state of health has improved, he will undergo another CT examination: the slices reveal the disappearance of gas in the gallbladder wall and in the pancreas and the almost complete liquefaction of the latter (Fig. 3). A fourth CT scan is performed a fortnight later when the patient complains again of abdominal pain. It displays an enlarging pancreatic collection (Fig. 4). This collection will be double drained endoscopically via the stomach, which will prove rather tricky because of a former surgical treatment of the Billroth II type. The efficiency of the drainage, which

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Fig. 2. — Enhanced CT, one day later: emphysematous (large arrows), necrotizing (stars) pancreatitis, together with gas (long arrows) in the vesicular lumen and wall, and in some portal veins (Balthazar grade E, severity index 10).

Fig. 4. — CT demonstration of the enlarging pancreatic collection (stars).

Fig. 3. — CT slice of the pancreas necrosis (stars) with the head remaining partially vascularized (short arrows). The long arrow points to the cholecystostomy.

will yield half a litre of necrotic material, will be monitored by a fifth CT scan (Fig. 5). Since the patient’s overall state of health is improving and since his biological values have returned to normal, the cholecystostomy drainage tube is removed and he is transferred back to the Gastroenterology Department. A sixth, low-dose, CT examination, is performed two weeks later: the peripancreatic collection is receding (Fig. 6), the patient can thus be discharged. The latest CT scan, on outpatient basis three months later, will reveal the disappearance of the pancreatic collection (Fig. 7). The removal of the gastro-pancreatic drains is planned.

Fig. 5. — CT control of the drainage: oblique coronal reconstruction showing the double drain (lightning) between the remaining stomach (Billroth II, thick arrow) and the pancreatic collection (thin arrows) which begins to decrease in size.

Discussion In Europe and in North America, 80% of cases of pancreatitis are caused by cholelithiasis or alcohol abuse (1-3). The literature does not reveal any figure concerning the frequency of emphysematous transformation of pancreatic necrosis but the occurrence is considered to be rare (1, 4). The combination of EP and gas-forming cholecystitis, like the one we report here, is even more exceptional.

Up to quite recently the prognosis for EP was considered to be extremely poor (1, 2, 5). At present and for some authors this gloomy prognosis should be revised as gasforming pancreatitis no longer looks more serious but even less than non emphysematous necrosing pancreatitis (4, 6). One can wonder to which extent this change in the prognosis does not result from the improvement of the aggressive treatments applied for such gas-forming pancreatitis.

EMPHYSEMATOUS PANCREATITIS AND GAS-FORMING CHOLECYSTITIS — VERBEECK et al

Fig. 7. — The latest low-dose CT control, three months later on outpatient status, showing the disappearance of the collection (arrows). Fig. 6. — Low-dose CT control, a fortnight later: the collection still recedes.

EC remains very precarious too, with a mortality rate of 15% to be compared with the 4% lethality rate in uncomplicated cholecystitis (5). Resulting from phenomena of tissue necrosis, gas can also be produced by the fermentation of bacteria carried by the blood stream, the lymphatic channels or a biliary reflux (2, 5, 7). Escherichia coli, Klebsiella, Staphylococcus Aureus and Clostridium are the main pathogenic agents involved (3-5, 8) but tuberculous bacteria are sometimes mentioned too (9). Arteriosclerosis, diabetes, renal failure and immunocompromised condition contribute, quite logically, to the increased production of gas (2, 5). Let us remember that gas pockets can also appear in case of enteric fistula or incompetent sphincter of Oddi, even as a result of endoscopic or surgical instrumentation (2, 5). The symptomatology of pancreatitis and cholecystitis remains vague and usually associates abdominal pain, occasionally localized, nausea and vomiting (1-3). Emphysematous lesions are known to be serious and are accompanied by general signs such as agitation, tachypnea, even shock (1). In the mid seventies, in order to evaluate the prognosis of pancreatic lesions and thus to provide guidelines for their treatment, Ranson defined a series of clinical and biological criteria measured on admission and 24 hours later (10, 11). They are shown in table I. Since the advent of CT scanners, radiologists have also been able to identify severity criteria for pancreatitis. We will go back over them soon.

Table I (from Balthazar and Ranson, Radiology, 1985, 156: 768). — Early prognosis signs of acute pancreatitis. At admission or diagnosis

During initial 48 hours

Age over 55 years

Hematocrit fall greater than 10 percentage points

White blood cell count over 16 x 109/l

Blood urea nitrogen level rise more than 5 mg/dl

Blood glucose level over 200 mg/dl

Serum calcium level below 8 mg/dl

Serum lactic acid dehydrogenase level over 300 IU/l

Arterial PO2 below 60 mm HG Base deficit greater than 4 mEq/l

Serum glutamic-oxaloacetic transaminase level over 250 IU/dl

Estimated fluid sequestration more than 6 l

Standard radiological abdominal examinations remain nonspecific. They can identify the presence of calcifications, endo- or extra-luminal air, pleural effusion or associated ileus (1-3). Ultrasonography permits visualisation of gas within the gallbladder but evaluates pancreatic lesions with difficulty because of frequent air-filled digestive interpositions (1, 3, 5). CT is the imaging modality of choice in case of EP and/or gas-forming cholecystitis (3, 5, 10, 12-14). The presence of extradigestive air, even in tiny quantities, as well as of radiopaque or radiolucent stones, is readily identified. Most important, CT identifies severity signs of the pancreatic pathology which, when summed, allow for an evaluation of the prognosis. This list of criteria, whose setting-up is the result of

research works carried out by M. Hill and then E. Balthazar, is shown in Table II, A and B (10, 11, 13). As far as EC is concerned, its staging is modelled on the basis of standard radiology but its CT reading is much easier. Stage 1 is characterized by the presence of gas within the gallbladder, stage 2 by wall emphysema and stage 3 by gas within the pericholecystic spaces (5). Besides being an excellent implement for diagnosis and prognostic evaluation, CT also allows for secure aspiration and drainage whenever a percutaneous procedure is advisable. It finally facilitates the followup of the lesions. In order to reduce the irradiation level of the patients, we have chosen to carry out the follow-up examinations with lowdose CT scans unless the patient’s condition worsens or his clinical

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Table II (from Balthazar and Robinson, Radiology, 1990, 174: 331-336). A. Balthazar grade and severity index (0 to 10) CT signs (simplified)

Balthazar grade

Balthazar severity index

A B C D E

0 1 2 3 4 +2 +4 +6

Normal pancreas Enlarged pancreas Peripancreatic fat inflammation 1 fluid effusion (even in the pleural space) 2 fluid effusions (or gas in 1 or 2) < 30% pancreatic necrosis 30-50% pancreatic necrosis > 50% pancreatic necrosis

B. Correlation of CT severity index with mortality and morbidity CT severity index 0-3 4-6 7-10

mortality

morbidity

3% 6% 17%

8% 35% 92%

parametres deteriorate. In the latter case the benefit of a low dose might result in a loss of capital information. MRI, mainly since the advent of high-performance 3T machines, is slowly carving out its place in the primary evaluation as well as in the follow-up of pancreatitis (3). In the case of emphysematous lesions however, we think that its weak capability to detect gas collections remains a strong handicap. The medical treatment of pancreatitis still consists of strict fasting and intravenous analgesics since the advantage of administering somatostatin or preventive antibiotherapy has not yet been proved. Serious, largely necrotized, even emphysematous lesions must be closely monitored in the Intensive Care Unit, with hydro-electrolytic and bloodpressure control. Artificial respiration may be required but antibiotics will only be administered in case of infection. Cholecystitis is treated in a similar way but antibiotics must be administered from the very start. When necessary, percutaneous CT or US guided aspiration or drainage will be performed (3, 8, 14-16). If the definitive cure of EC does really require surgical treatment, the consensus is less broad in the case of gas-forming pancreatitis (8, 10). The present tendency is to limit necrosectomy and closed lesser sac lavage, not only because of their cost but also because of their potentially deleterious nature (6). Conclusion Basing ourselves on this exceptional combination of EP and gas-

forming cholecystitis, we confirm that CT remains the examination of choice for their diagnosis and followup. It allows for their precise staging and helps evaluate their prognosis. Finally, by monitoring the procedure it contributes to secure percutaneous therapeutic treatments. If the severity of EP is presently being reevaluated, it remains sure that such cases of gas formation in the pancreas or the gallbladder remain particularly serious and require aggressive multidisciplinary management. Up to now, only surgery is able to cure EC definitively but surgical treatment of gasforming pancreatitis is less and less plebiscited.

References 1. Dive C., Geubel A.: Gastro-entĂŠrologie Clinique (Volume 3). Louvain, Imprimerie J. Dieu-Brichart, 1993. 2. Daly J.J., Alderman D.F., Conway W.F.: General case of the day. RadioGraphics, 1995, 15: 489-492. 3. Mortele K.J., Banks P.A., Silverman S.G.: State-of-the-art imaging of acute pancreatitis. JBRBTR, 2003, 86: 193-208. 4. Wig J.D., Kochhar R., Bharathy K.G., et al.: Emphysematous pancreatitis. Radiological curiosity or a cause for concern ? JOP, 2008, 9: 160-166. 5. Grayson D.E., Abbott R.M., Levy A.D., et al.: Emphysematous infections of the abdomen and pelvis: A pictorial review. RadioGraphics, 2002, 22: 543561. 6. Kvinlaug K., Kriegler S., Moser M.: Emphysematous pancreatitis: A less aggressive form of infected pancreatic necrosis ? Pancreas, 2009, 38: 667-671.

7. Mendez G., Isikoff M.B.: Significance of intrapancreatic gas demonstrated by CT: A review of nine cases. AJR, 1979, 132: 59-62. 8. Wig J.D., Mettu S.R., Jindal R., et al.: Closed lesser sac lavage in the management of pancreatic necrosis. J ,Gastroenterol Hepatol, 2004, 19: 1010-1015. 9. Morris D.L., Wilkinson L.S., Al Mokhtar N.: Case report: Emphysematous tuberculous pancreatitis diagnosis by ultrasound and computed tomography. Clin Radiol, 1993, 48: 286-287. 10. Balthazar E.J., Ranson J.H., Naidich D.P., et al.: Acute pancreatitis: Prognostic value of CT. Radiology, 1985, 156: 767-772. 11. Balthazar E.J., Robinson D.L., Megibow A.J., et al.: Acute pancreatitis: Value of CT in establishing prognosis. Radiology, 1990, 174: 331-336. 12. Isikoff M.B., Hill M.C., Silverstein W., et al.: The clinical significance of acute pancreatic hemorrhage. AJR, 1981, 136: 679-684. 13. Hill M.C., Barkin J., Isikoff M.B., et al.: Acute pancreatitis: Clinical vs CT findings. AJR, 1982, 139: 263-269. 14. Ku Y.M., Kim H.K., Cho Y.S., et al: Medical management of emphysematous pancreatitis. J Gastroenterol Hepatol, 2007, 22: 455-456. 15. Velasco Guardado A., Prieto Vicente V., Fernandez Pordomingo A., et al.: Emphysematous pancreatitis: Conservative or surgical treatment? Gastroenterol Hepatol, 2009, 32: 605609. 16. Choi H.S., Lee Y.S., Park S.B., et al.: Simultaneous emphysematous cholecystitis and emphysematous pancreatitis: A case report. Clin Imaging, 2010, 34: 239-241.

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A RARE PRESENTATION OF BREAST CANCER A. Rappaport, A. Van Steen, C. Van Ongeval1 The case of a 67-year-old woman with a large lump in the left axillary region and the left breast is presented. Pathologic investigation of these masses in 2 hospitals was inconclusive. Further work-up in our radiologic department showed beside the presence of the two tumoral masses, abnormalities with the radiologic characteristics of granulomatous mastitis. Final pathologic analysis showed the presence of an invasive ductal carcinoma in the two masses in combination with a granulomatous stromal reaction. Key-word: Breast neoplasms, diagnosis.

Case report A 67 year-old woman with no medical history presented several open wounds in the left breast since 2007. In march 2009 the woman visited her general practitioner because she had felt a lump in the left axillary region and fluid discharge was present from the persistent open wounds in the left breast. The patient had no fever. The general practitioner sent the woman to a regional hospital, because he suspected underlying abscedation. Breast mammography and ultrasound was performed and showed a large mass in the left axilla and the left breast. Fine needle aspiration, core biopsy and incisional biopsy of the two masses showed inflammatory changes without signs of malignancy. Because of the conflict between the worrisome imaging findings and the reassuring pathology results, the patient was sent to a larger breast center for a second opinion. Repeated fine needle aspiration and core biopsy of the two masses confirmed the inflammatory changes but also a few atypical cells were found which were suspicious for malignancy. Subsequently the patient was sent to our radiologic department for a third opinion. Clinical exam showed a red oedematous left breast with a few ulcerations in the upper lateral quadrant. A large mass was palpated in the lateral part of the left breast as well as a large axillary mass with the presence of an antiseptic wick. Still a

large amount of purulent fluid was drained by this wick. Clinical exam of the right breast, right axilla and left infraclaviculary and supraclaviculary regions were negative. Culture of the fluid from the open wound in the left axilla showed the presence of Staphylococcus Aureus. Because of the swelling, edema and fluid discharge, only a mammogram of the right breast was taken, which showed no abnormalities. An ultrasound was repeated and showed a large well demarcated axillary mass. This mass was built up out of a vascularised solid component in the lower half and a liquefied component in the upper half with inlying air bubbles (Fig. 1). Diffuse breast edema was present, mainly in the outer quadrant. In the left upper outer quadrant a vertically orientated irregular mass was present (Fig. 2A). Just beneath this irregular mass, a tubular mass was present which connected two skin ulcerations (Fig. 2B). A few cystic zones were present in the tubular mass. PET-CT confirmed the imaging findings on ultrasound (Fig. 3). A core biopsy was performed of the two masses with as aim the solid component of the axillary mass and the stellar ends of the vertically orientated mass. Analysis of the core biopsies showed as well in the axillary as in the breast mass the presence of a poorly differentiated invasive ductal adenocarcinoma with a lymphoplasmocytic and granulomatous stromal reaction. Because of the extent of the tumoral mass neo-adjuvant chemo-

Fig. 1. â&#x20AC;&#x201D; Ultrasound of the left axillary mass shows the solid lower component.

therapy was started (Taxotere for 8 cycles). This was associated with Clamoxyl for 2 months because of the associated Staphylococcus Aureus infection. Three months later control mammography (Fig. 4) and ultrasound showed an evident regression of the tumoral mass in the left axilla and left breast. Shortly afterwards mastectomy in association with conventional axillary lymph node dissectionwas performed.Pathology of the resected specimen showed no residual tumor (ypT0N0). Adjuvant chemotherapy was given (Taxotere for 3 cycles), followed by radiotherapy of the left thoracic wall and tributary areas of the axillary lymph nodes. Discussion

From: 1. Department of Radiology, University Hospital of Leuven, Belgium. Address for correspondence: Dr A. Rappaport, Department of Radiology, UZ Leuven, Herestraat 49, 3000 Leuven. E-mail: annelies.rappaport@uz.kuleuven.ac.be

The presence of a granulomatous stromal reaction in combination with an invasive breast tumor is an

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B Fig. 2. — Ultrasound of the left breast mass in the upper lateral quadrant shows on A the vertical orientated, irregular demarcated mass (arrows) and on B a tubular mass connecting two skin ulcerations (arrowheads) with presence of a few cystic zones (arrow).

unusual feature. Witnesses are the few literature reports on this subject, almost exclusively in histopathologic journals. Other tumors which are frequently associated with a granulomatous stromal reaction are non-Hodgkin lymphoma, Hodgkin lymphoma, testicular seminoma, renal cell carcinoma, nasopharyngeal carcinoma and ovarian dysgerminoma (1). Granulomatous reaction is also seen in lymph nodes draining a tumor with or without the presence of metastasis and is defined as a sarcoid reaction or sarcoid-like lymphadenopathy (1). The cause of the granulomatous stromal reaction is unclear.

Fig. 3. — Axial images of contrast enhanced PET-CT show on A the partially liquefied (curved arrow) axillary mass with peripheral nodular, contrast enhancing, solid components (arrow). Notice also the present of air in the liquefied part (arrowhead). On B the tubular mass (arrow) is seen in the left upper lateral quadrant connecting skin ulcerations (curved arrow). Note also the diffuse skin thickening (edema) (arrowhead).

Some authors interpret the reaction as a T-cell mediated immune response to an antigen expression of the carcinoma acting as the local trigger (2). Others suggest it to be an idiopathic foreign body reaction to the necrotic zones in the tumor or as a part of a known systemic granulomatous disease (3). Some pathologists suggest to use the reaction as a sign of microinvasion (4). Radiologic literature doesn’t mention the radiological image of a breast tumor with a granulomatous reaction. However no correlation between this phenomenon and granulomatous mastitis is cited in literature, the resemblance on imaging in our case is striking. There is not yet enough information in literature (due to the rarity of granulomatous tumoral reaction) to suggest that these two

entities are synonyms or that they are components of the same spectrum of granulomatous reactions. As in granulomatous mastitis a tubular mass and skin sinuses were present in our case, what made us mention granulomatous mastitis in our differential diagnosis list. Granulomatous mastitis is an idiopatic granulomatous lobulitis (59). Auto-immune reaction or local damage are postulated as possible causes. In contrary to malignancy, granulomatous mastitis tends to present in a younger population (typically postpartum) but an older age at presentation is possible (5-9). Granulomatous mastitis is a known mimicker of malignancy on imaging. Mammography can be negative or it also can present as a focal mass or poorly defined asymmetry (often retro-areolar) sometimes with the presence of edema (5-7).

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A RARE PRESENTATION OF BREAST CANCER — RAPPAPORT et al

mentioning granulomatous mastitis or granulomatous reaction. When core-biopsy or fine-needle aspiration (FNA) are negative but imaging features are suspect for malignancy, as in our case, it is designated to repeat the biopsy aiming on the peripheral non-necrotic zones. This modus operandi narrows the false negative biopsies/FNA down. References 1.

Fig. 4. — Craniocaudal and oblique mammography of the left breast shows the irregular demarcated large opacity (arrow) in the axillary region which contains air (arrowhead) and the more tubular density in the left upper lateral quadrant (curved arrow) with adjacent skin retraction. Note also the residual breast edema.

On ultrasound it can present as multiple irregular, clustered, tubular hypoechoic lesions; large irregular hypoechoic mass(es) with sometimes the presence of hypoechoic linear tracks to the skin (cutaneous sinuses) or abcesses (5, 7). Edema is also frequently encountered. MR-imaging has similar findings as ultrasound but it can better depict the microabscesses as T2-hyperintense masses which have a typical rim enhancement on T1-weighted imaging (8). MRI gives also a better overview of the extend of the disease and can exclude mimickers such as fat necrosis (6, 8).

Conclusion Although no other radiologic reports on granulomatous reaction in a breast tumor are available to our knowledge, we presume that when a patient presents aside a tumoral mass, imaging characteristics of granulomatous mastitis, you can suggest this rare diagnosis. This can help your pathologist to rime the granulomatous and tumoral changes when analysing a core biopsy or cytology. On the other hand, a malignant tumoral process should be in your differential diagnostic list whenever

Bhatia A., Kumar Y., Kathpalia A.S.: Granulomatous inflammation in lymph nodes draining cancer: a coincidence or a significant association. Int J Med and Med Sc, 2009, 1: 13-16. Bässler R., Birke F.: Histopathology of tumour associated sarcoid-like stromal reaction in breast cancer. An analysis of 5 cases with immunohistochemical investigations. Virchows Arch A Pathol Anat Histopathol, 1988, 412: 231-239. Santini D., Pasquinelli G., Alberghini M., Martinelli G.N., Taffurelli M.: Invasive breast carcinoma with granulomatous response and deposition of unusual amyloid. J Clin Pathol, 1992, 45: 885-888. Coyne J., Haboubi N.Y.: Microinvasive breast carcinoma with granulomatous stromal response. Histopathology, 1992, 20: 184-185. Yilmaz E., Lebe B., Usal C., Balci P.: Mammographic and sonographic findings in the diagnosis of idiopathic granulomatous mastitis. Eur Radiol, 2001, 11: 2236-2240. Van Ongeval C., Schraepen T., Van Steen A., Baert A.L., Moerman P.: Idiopathic granulomatous mastitis. Eur Radiol, 1997, 7: 1010-1012. Hovanessian Larsen L.J., Peyvandi B., Klipfel N., Grant E., Iyengar G.: Granulomatous lobular mastitis: imaging, diagnosis, and treatment. AJR, 2009, 193: 574-581. Kocaoglu M., Somuncu I., Ors F., Bulakbasi N., Tayfun C., Ilkbahar S.: Imaging findings in idiopathic granulomatous mastitis. A review with emphasis on magnetic resonance imaging. J Comput Assist Tomogr, 2004, 28: 635-641. Memis A., Bilgen I., Ustun E.E., Ozdemir N., Erhan Y., Kapkac M.: Granulomatous mastitis: imaging findings with histopathological correlation. Clin Radiol, 2002, 57: 1001-1008.

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MALIGNANT TRANSFORMATION OF AN ABDOMINAL INFLAMMATORY MYOFIBROBLASTIC TUMOR WITH DISTANT METASTASES IN A CHILD C.W. Ernst1, J. Van Der Werff Ten Bosch1, B. Desprechins2, J. de Mey2, M. De Maeseneer2 Inflammatory myofibroblastic tumors (IMT) are lesions that mostly affect young adults and children. The tumor is made up of myofibroblasts and a mixed inflammatory infiltrate and rarely undergoes malignant transformation. We present a case of a 13-year-old boy with a pelvic mass diagnosed as IMT which underwent malignant transformation and metastasised to the liver. We report the ultrasound, computed tomography (CT) and magnetic resonance (MR) findings of this rare disorder. Key-word: Neoplasms, in infants and children.

Inflammatory myofibroblastic tumor (IMT) was initially described as a pulmonary lesion in young adults. It has subsequently been found in various anatomic locations and over a wide age range (1). IMT is a distinctive tumor of proliferating myofibroblasts with a background of an inflammatory infiltrate. The tumor rarely undergoes malignant transformation. The potential for recurrence and focal invasion are reported in oncologic, surgical, and radiological literature (2-4). Reports and radiologic imaging of malignant transformation, however, are very few (5) and to our knowledge, this is the first report that provides imaging of distant metastasis. The purpose of this article is to raise awareness of this possibly aggressive entity. Case report A 13-year-old boy presented with a 5-week history of abdominal pain, weight loss, and anorexia. On physical examination the child appeared skinny and pale. On palpation a 10-cm large suprapubic mass was evident. Medical history of the patient was positive for neurofibromatosis type 1. Hence, initially the mass was thought to represent a neurofibroma. Ultrasound showed a solid, heterogeneous multilobulated pelvic mass (Fig. 1), which measured 12 x 9.5 x 7 cm. Right hydronephrosis was also evident. On CT the mass showed mild contrast enhancement. Hydronephrosis of the right kidney and the presence of a liver nodule were also demonstrated.

MRI of the liver showed a welldemarcated lesion in the anterosuperior segment of the right liver lobe with marked contrast uptake (Fig. 2). Pelvic MRI showed a large, mildly enhancing, pelvic mass (11.3 x 8.2 x 7.6 cm) with compression of the bladder (Fig. 3). A Positron Emission Tomography scan (PET) was performed and showed marked uptake of labelled glucose in the lesion suggesting a malignant origin. No hypermetabolic foci were seen in the liver. The patient underwent exploratory laparotomy. Pathologic examination of the specimen showed a variable cellular spindle cell neoplasm with a vascular myxoid pattern and a prominent inflammatory background. Multiple histiocytoid cells with vesicular nuclei were present. The tumor cells were plump with high mitotic activity. Due to the prominent subpopulation of histiocytoid cells and the high mitotic activity the tumor was diagnosed as an IMT with malignant transformation. No efficient treatment regimen has been reported for this type of malignancy. Several case reports suggest different combinations of chemotherapy with variable results. A first attempt was made with a course of chemotherapy: fosfamide, vincristin, and actinomycin, with no results. One month after diagnosis the patient underwent surgery. The pelvic mass and liver lesion were removed. Pathology of the liver lesion confirmed the diagnosis of a metastasis. Following surgery the patient was given one cycle of doxorubicin and cisplatinum and one

From: Department of 1. Paediatric Oncology, 2. Radiology and Medical Imaging, University Hospital VUB, Brussels, Belgium. Address for correspondence: Dr M. De Maeseneer, M.D., Department of Radiology, Laarbeeklaan 101, B-1090 Jette. E-mail: michel.demaeseneer@uzbrussel.be

Fig. 1. â&#x20AC;&#x201D; Ultrasound of the abdomen showing a large pelvic mass, predominantly solid with a few small hypoechoic areas (arrows).

month later he received two cycles of high dose methotrexate (HDMTX) with a one week interval. Nevertheless a tumor recurrence was found 8 weeks postoperatively. Follow up CT showed a new pelvic mass (10 x 8.2 x 7 cm) and two lesions in the liver (6.1 x 5.9 x 5.5 cm, 3.7 x 4.9 x 3 cm). The patient underwent a resection of the pelvic mass. Intraoperatively, severe peritoneal seeding and invasion of the intestinal mucosa (rectum and sigmoid) was noted. Subtotal resection of the tumor (approximately 90%) was achieved with resection of the invaded part of the recto-sigmoid. The liver lesions were not resected. The patient received another 2 cycles of doxorubicin, cisplatinum, and high dose methotrexate. Interval CT scan after those two cycles of chemotherapy showed a significant enlargement of the liver lesions (10.8 x 9.2 x 9.9 cm, 10.2 x 8 x 9.5 cm) with almost total invasion of the liver, important subcapsular expansion

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ABDOMINAL INFLAMMATORY MYOFIBROBLASTIC TUMOR — ERNST et al

Fig. 2. — Abdominal CT demonstrates the presence of a hypodense nonenhancing liver lesion of 1.5 cm (arrow).

Fig. 4. — Interval computed tomography during second chemotherapy shows a significant enlargement of the liver lesions and the presence of two similar intra-peritoneal lesions (arrows).

Fig. 3. — Coronal post-gadolinium T1weighted fat sat image shows a large irregularly enhancing, centrally located pelvic mass (arrows).

and the presence of two new intraperitoneal masses (5.4 x 5.7 x 5.1 cm, 5.3 x 5.2 x 5.7 cm) (Fig. 4) The disease was progressive and chemotherapy was unsuccessful. The patient was given palliative care. Discussion Inflammatory myofibroblastic tumor (IMT) is a distinct tumor of proliferating myofibroblasts with an associated inflammatory infiltrate. The tumor rarely undergoes malignant transformation (1). IMTs most often are seen in the lungs of young adults, but there have been reports in children, and in various anatomic locations (6-8). Extrapulmonary IMTs in children have been described involving the mesentery (1, 9), retroperitoneum, abdominal soft tissues, liver (10), bladder (11, 12), mediasti-

num, head and neck, extremities, appendix (7), and kidneys (1, 13) with the largest tumors occurring in the abdomen and retroperitoneum (1, 14). The clinical presentation of IMT varies depending on the site where the tumor originates. Symptoms of intra-abdominal IMT include the presence of a mass, fever, pain, and weight loss. The etiologic factors responsible for development of IMT are not clearly understood. Although some investigators still believe it is a benign neoplasm, IMT is now more regarded as a true neoplasm with a wide spectrum of biologic behaviour, varying from the more frequent benign lesions to the uncommon tumors that are multifocal and prone to multiple recurrences (1, 10, 15). This latter subset of tumors may show local invasion or even metastasise (1, 2, 16). Due to the rarity of these tumors, very little is described in the medical literature regarding the management of aggressive IMTs. One positive outcome of abdominal IMT with malignant transformation (without distant metastasis) has been reported. This successful outcome was related to cisplatinum, doxorubicin, and methotrexate as an adjunct to surgical resection (1). No reports were found of a successful treatment of

IMT with malignant transformation and distant metastasis (or multifocal lesions). The radiologic features of intraabdominal IMTs are non-specific. Abdominal radiographs may show displacement of bowel segments caused by soft tissue mass and possible amorphous calcification within the tumor (6, 17). Ultrasound and CT show a solid, sometimes heterogeneous, well demarcated mass (6, 17). These imaging modalities may show infiltrative or multifocal disease. The MR findings are similar to the CT findings. Conventional barium studies can further characterize intestinal involvement (2, 9). The differential diagnosis based on imaging includes soft tissue sarcoma (rhabdomyosarcoma), lymphoma and neuroblastoma. The precise diagnosis of IMT can be made pathologically. Awareness and inclusion of IMT in the differential diagnosis of aggressive abdominal processes may have important treatment implications (2). IMT should be viewed as a tumor of low malignant potential. Rarely it shows local recurrence and metastatic spread (1). In summary, we report a case of a IMT that was locally aggressive in addition to showing metastatic spread. References 1. Dishop M.K., Warner B.W., Dehner L.P., et al.: Succesful treatment of inflammatory myofibroblastic tumor with malignant transformormation by surgical resection and chemotherapy. J Pediatr Hematol/Oncol, 2003, 25: 153-158. 2. Hedlund G.L., Navoy J.F., Galliani C.A., et al.: Aggressive manifestations of inflammatory pulmonary pseudotumor in children. Pediatr Radiol, 1999, 29: 112-116. 3. Chan J.K.C: Inflammatory pseudotumor: A family of lesions of diverse nature and etiologies. Adv Anat Pathol, 1996, 3: 156-171. 4. Bahadori M, Liebow AA: Plasma cell granulomas of the lung. Cancer, 1973, 191-208. 5. Meis J.M., Enzinger F.M.: Inflammatory fibrosarcoma of the mesentery and retroperitoneum: a tumor closely simulating inflammatory pseydotumor. Onkologie, 2001, 24: 368-372. 6. Karnak I., Senocak M.E., Ciftci A.O., et al.: Inflammatory myofibroblastic tumor in children: Diagnosis and treatment. J Pediatr Surg, 2001, 36: 908-912. 7. Bonnet J.P., Basset T., Dijoux D.: Abdominal inflammatory myofibroblastic tumors in children: report of an

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10.

JBRâ&#x20AC;&#x201C;BTR, 2011, 94 (2) appendical case and review of the literature. J Pediatr Surg, 1996, 31: 1311-1314. Pettinato G., Manivel J.C., De Rosa N., et al.: Inflammatory myofibroblastic tumor (plasma cell granuloma). Am J Clin Pathol, 1990, 94: 538-546. Day D.L., Sane S., Dehner L.P.: Inlammatory pseudotumor of the mesentery and small intestine. Pediatr Radiol, 1986, 16: 210-215. Coffin C.M., Humphrey P.A., Dehner L.P.: Extrapulmonary inflammatory myofibroblastic tumor: A clinical and pathologic survey. Semin Diagn Pathol, 1998, 15: 85-101. Albores-Saavedra J., Manivel J.C., Essenfeld H., et al.: Pseudosarcomateus myofibroblastic proliferations

in the urinary bladder of children. Cancer, 1990, 66: 1234-1241. 11. Hojo H., Newton W.A., Hamoudi A.B., et al.: Pseudosarcomatous myofibroblastic tumor of the urinary bladder in children: a study of 11 cases with review of the literature. An intergroup rhabdomyosarcoma study. Am J Surg Pathol, 1995, 19: 1224-1236. 12. Williams M.E., Longmaid H.E., Trey G., et al.: Renal failure resulting from infiltration by inflammatory myofibroblastic tumor responsive to corticosteroid therapy. Am J Kidney Dis, 1998, 31: E5. 13. Coffin C.M., Watterson J., Priest J.R., et al.: Extrapulmonary inflammatory myofibroblastic tumor (inflammatory pseudotumor). A clinicopathologic

and immunohistochemical study of 84 cases. Am J Surg Pathol, 1995, 19: 859-872. 14. Conte M., Milanaccio C., Nantron M., et al.: Multiple inflammatory fibrosarcoma of the abdominal cavity in a child. Med Pediatr Oncol, 1996, 27: 198-201. 15. Scott L., Blair G., Taylor G., et al.: Inflammatory pseudotumor in children. J Pediatr Surg, 1988, 23: 755758. 16. Kim K.A., Park C.M., Lee J.H., et al.: Inflammatory myofibroblastic tumor of the stomach with peritoneal dissemination in a young adult: imaging findings in a case report. Abdom Imag, 2003 Oct 28 (Epub ahead of print).

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JBR–BTR, 2011, 94: 81-82.

LETTER TO THE EDITOR ULTRASONOGRAPHY AND MRI FINDINGS OF CUTANEOUS B-CELL LYMPHOMA, LEG TYPE E. Öztürk1, S. Sipahioglu1, Ü. Han2, C. Yücesoy1, A. Dilli1, B. Hekimog˘lu1

We read the case report about imaging findings of cutaneous B-cell lymphoma in JBR-BTR with great interest (1). We would like to share ultrasonographic and magnetic resonance imaging (MRI) findings of our case with primary cutaneous B-cell lymphoma, leg type. Our patient (an 84-year-old woman) presented with fast progressing swelling and reddish open wounded skin lesion on her left lower leg and palpable masses occurred at the left groin and inner side of thigh without ulceration. Ultrasonography (US) showed subcutaneous edema around open wound. Sharply demarcated subcutaneous nodules, which had hyperechoic peripheral zone and hypoechoic central zone, were observed during US examination at palpable masses located in the groin and thigh (Fig. 1). T1 weighted MRI images of the calf revealed diffuse edema in subcutaneous tissue (Fig. 2). There were clearly defined nodules, which were isointense to muscle on T1 weighted images, and slightly hyperintense to muscle on fat saturated T2 weighted images in the subcutaneous inner thigh tissue (Fig. 3). Patient could not tolerate staying in the gantry, therefore contrast-enhanced examination was not completed. Histopathological examination revealed cutaneous large B-cell lymphoma that was confirmed by immunohistochemical examination. Imaging procedures did not show an evidence of nodal or extranodal focus, therefore the diagnosis of a primary cutaneous large B cell lymphoma of leg type was made. The skin lesions regressed and palpable masses disappeared within a few days after chemotherapy. Unfortunately, patient died shortly after the diagnosis.

Fig. 1. — There are sharply demarcated, nodular subcutaneus lesions which had hyperechoic periferal zone and hypoechoic santral zone. Hypoechoic bands are extending from santral echogenity to periferal zones.

Fig. 2. — T1 weighted coronal MRI squences shows there are skin infiltration/edema in left calf skin (arrows).

The term ‘‘primary cutaneous lymphoma’’ refers to cutaneous T-cell lymphomas (CTCLs) and cutaneous B-cell lymphomas (CBCLs), that present in skin with no evidence of extracutaneous disease at the time of diagnosis (2). CBCLs are most frequently presented as skin nodules or tumors without ulcerations. Primary cutaneous B-cell lymphoma, leg type (PCBCL LT) is more common in women older than age of 70 years and has a poor prognosis. It appears clinically as non-specific, reddish-

bluish skin lesions with or without palpable subcutaneus nodular masses on lower leg(s). It can mimic panniculitis/cellulitis clinically so misdiagnosis is possible (2). In their case, Vanhoenacker et al. reported a CBCL presented as a slowly growing painless cutaneous nodule on upper arm with favorable prognosis (1), whereas it appeared as a fast progressing swelling and reddish, open wounded skin lesion on lower leg and subcutaneous nodules within thigh with poor prognosis in our case. Lesion locations, disease onset and prognosis of our case are different from Vanhoenacker’s case, however patients’ ages and MRI findings were similar. As emphasized in the article of Vanhoenacker et al., MRI has a potential role in assessing the

Department of 1. Radiology, 2. Pathology, SB Ankara Dıs˛kapı YB Training and Research Hospital, Ankara, Turkey.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94 (2)

C A

Fig. 3. â&#x20AC;&#x201D; T1 weighted coronal (A) and axial (B) images of left tigh shows multiple subcutaneus well demarcated nodules (arrows) that are isointense to muscle. Fat saturated T2 weighted images (C) shows slightly hyperintense lesion (arrow) and skin edema.

exact size of lesions and local staging of disease. On the other hand 18F-fluorodeoxyglucose (FDG)positron emission tomography (PET) has value for distant staging and treatment monitoring. In our case, MRI showed extension of the disease but FDG-PET could not performed as it was not existing in our hospital.

Although a rare diagnosis, PCBCL should be included in the differential diagnosis of thickening and edema of subcutaneous tissue and multiple subcutaneus nodules with or without skin lesions detected on US and MRI. Awareness of PCBCL LT by radiologists can facilitate the differential diagnosis in patients with masses and skin lesions on leg(s).

References 1.

Vanhoenacker F.M., Baten A., Vandeputte V.: Imaging findings of a cutaneous B-cell lymphoma. JBRBTR, 2009, 92: 285-288. 2. Willemze R., Jaffe E.S., Burg G., Cerroni L., Berti E., Swerdlow S.H., et al.: WHO-EORTC classification for cutaneous lymphomas. Blood, 2005, 105: 3768-3785.

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JBR–BTR, 2011, 94: 83.

IMAGES IN CLINICAL RADIOLOGY Posttraumatic priapism in child N. Bottosso, T. Khuc, D. Brisbois, J. Khamis1

A 12-year-old-boy was admitted to our Medical Imaging Department for scrotal/perineal heamatoma and a painless partial erection after bicycle trauma. He had no other medical history. Doppler US and angiography of penile region were performed. A gray-scale US (axial view, Fig. A)) shows an irregular hypoechoic region within the echogenic cavernous tissue and cavernosal lacuna (arrows). The color Doppler US (sagittal view, Fig. B) demonstrates extravasation of blood from the lacerated cavernosal artery (arrow), in an arteriallacunar fistula with high systolic velocity and turbulent flow. The pelvic angiogram (Fig. C) shows that the fistula (arrow) in the right corpus cavernosum is fed by a right pudendal artery. Based on morphology and localization of the lesion on Doppler US and pelvic angiography, the diagnosis of posttraumatic arterial lacunar cavernous fistula was made. The patient was treated by selective embolization of the right cavernous artery, without complication. A penile Doppler evaluation after 10 days was normal and demonstrated recanalization of the embolized artery. Comment

Priapism is defined as involuntary, prolonged penile erection caused by factors other than sexual arousal. Priapism affected 1, 5 / 100000 persons / year. It is a rare occurrence in children but can occur at any age, including newborns. It is classified as either low-flow or high-flow. High-flow priapism is less common and results from unregulated arterial inflow to the corpora cavernosa usually due to an arterial-venous fistula. The most common etiology in children is perineal or penile trauma. This type of priapism frequently presents days to weeks after the traumatic event. It is usually not associated with penile ischemia: venous outflow is not compromised, tissue ischaemia does not occur and the condition remains painless. Colour Doppler US is highly sensitive and the patterns in high-flow arterial priapism are markedly increased systolic velocity flow within the corpus cavernosum or cavernosal artery, development of an arteriallacunar fistula (sensitivity 100%, specificity 73%). The gold standard for the diagnosis of AVF is digital subtraction angiography. Limitations of color Doppler US include underestimation of the number of accessory feeding vessels, which may become patent only after embolization of the main vascular supply and difficulty in recognizing vessels that feed the fistula from the opposite side. Treatment consists of super selective embolization of the torn artery with a success rate of about 90%. After embolization, penile Doppler US evaluation is recommended to assess recanalization of the embolized cavernosal artery (sensitivity 75%, specificity 100%). Complications can be pain, erectile dysfunction, and corporeal fibrosis.

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

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 84.

IMAGES IN CLINICAL RADIOLOGY Complicated pulmonary interstitial emphysema C. Altay1 A 6-year-old boy with known acute lymphocytic leukemia was referred for radiologic evaluation of his complaints of newly onset cough, high fever, dsypnea and general situation worsening. The patient underwent invasive mechanical ventilation through an endotracheal tube in the intensive care unit. The patient's symptoms resolved within 7 days of initiating therapy and he was extubated, however left axillary crepitation and left side chest pain began. HRCT examination revealed irregular-shaped air spaces along the medium sized bronchovascular sheaths noted in the apices of both lungs (pulmonary interstitial emphysema) with localised pneumothorax in the left upper thorax and subcutaneous emphysema in the left axillary region additional to the diminished patchy ground-glass opacities (Fig. A, B). Most of these free air spaces were along the bronchovascular sheaths measured less than 1 cm in diameter. Pleural effusion and pneumomediastinum was not present in limited HRCT examination. There was marked clinical improvement at three-weeks follow-up. HRCT (Fig. C) done at the time of the three-weeks follow-up visit showed significant resolution of the pulmonary opacities and free air of the interstitium and subcutaneous tissue.

Comment

Pulmonary interstitial emphysema (PIE) typically occurs as a complication of barotrauma secondary to most commonly possitive pressure mechanical ventilation. Rupture of overdistended pulmonary alveoli leads to entry of air into the pulmonary interstitium. PIE is recognized commonly in the premature newborns who have surfactant deficient disease but rarely in younger childhood. More rarely it could develop with air tapping by obstruction due to meconyum aspiration or pulmonary hypoplasia requiring high ventilatory pressure. Radiologic imaging can assist by determining the presence and dissemination of PIE. This condition may occur diffusely throughout the lung, or it may be unilateral or lobar in occurrence. The HRCT findings of PIE includes free air along the bronchovascular sheaths and occasionally complicated with pneumomediastinum, pneumothorax and subcutaneous emphysema. Radiologic C imaging is also useful in monitoring for the potential complication of pneumothorax. Interstitial changes are initially linear but may become more cystic as the air in the interstitium congregates locally. In most patients, PIE is transient, lasting only for several days and rarely, it can persist and form expanding, radiolucent masses. Rarely PIE be complicated with pneumothorax and subcutaneous emphysema. PIE results either from increased intra-alveolar pressure or from decreased interstitial pressure. As a conclusion air flows from the alveolar space into the interstitial and pleural space. In some cases PIE can lead to the development of secondary pneumothorax. This differs from primary and iatrogenic pneumothorax. Spontaneous subcutaneous emphysema is thought to result from increased pressures in the lung that cause alveoli to rupture. In spontaneous subcutaneous emphysema, air travels from the ruptured alveoli into the interstitium and along the blood vessels of the lung, into the mediastinum and from there into the tissues of axillary. In conclusion, PIE is a rarer condition in elderly ages than in newborns and HRCT findings of PIE are fairly specific. PIE should be included in the differential diagnosis of pulmonary air leak conditions especially who treated with positive-pressure mechanical ventilation. Reference 1.

Kemper A.C., Steinberg K.P., Stern E.J.: Pulmonary interstitial emphysema: CT findings. AJR, 1999, 172: 1642.

1. Department of Radiology, Izmir Ataturk Research and Training Hospital, Izmir, Turkey.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 85.

IMAGES IN CLINICAL RADIOLOGY Tympanic plate fracture following mandibular trauma with emphasis on 3D imaging B. Coulier1

A 73-year-old patient was addressed to our department of medical imaging for combined CT imaging of the head and petrous bone. The patient had fallen from his height on his mandibula and reported pain in the area of the left temporo mandibular joint. The pain was associated by external otorrhagia. At physical otoscopic exam there was some narrowing of the external auditory canal in which blood was visible. Neurootologic symptoms were absent. High definition MDCT of the left temporal bone first excluded fracture of the temporal bone. The pneumatization of the temporal bone remained normal but a small sagittal fracture of the margin of the tympanic plate bone (white arrow on fig. A, B, C) was clearly individualized. It was associated with sagittal vertical impaction of the articular surface of the condylar process (black arrow on fig. A, B, C). The anatomic landmarks of theses relatively subtle bone lesions were particularly illustrated by volume rendering views (Fig. D, E). In the absence of mandibular fractures and neuro-otologic complications, a conservative treatment was chosen and was effective improving the patientâ&#x20AC;&#x2122;s condition. Comment

Trauma to the symphysis region of the mandible may be directed posteriorly, with sufficient power to dislocate the condylar process toward the anatomic structures adjacent to the temporomandibular joint thus causing fracture of the middle cranial fossa, temporal fossa, tympanic plate and/or the mandibular condylar process itself. The tympanic plate bone forms the anterior wall, roof and posterior wall of the external auditory canal and is connected to the rest of the temporal bone by the petrotympanic and tympanomastoid fissures. Fractures may be divided into longitudinal fractures limited to the tympanic plate or those in association with fractures of the petrous part of the temporal bone. Traumatic fracture of the tympanic plate are rare and their clinical findings usually manifest immediately and include: hemorrhage of the external auditory canal (83% of cases), associated with neuro-otologic symptoms like hypoacusis, stenosis of the external auditory canal, limitation of mouth opening and an history of mandibular trauma. Hemorrhage of the external auditory canal which represents the main symptom may be a clinical feature of basilar fracture and is associated with rupture the articular cavity roof, fracture of the tympanic plate, laceration of the auditory canal anterior wall and/or rupture of the tympanic membrane. CT is the technique of choice to evaluate the fragment displacement, alterations in the shape or outline of anatomic components, widening of the petrotympanic fissure and fracture relationship with the tympanic membrane. Reference 1.

Psimopoulou N., Antoniades K., Magouti D., Karakassis D.: Tympanic plate fracture following mandibular trauma. Dentomaxillofac Radiol, 1997, 26: 344346.

1. Department of Diagnostic Radiology, Clinique St Luc, Bouge, Belgium.

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JBR–BTR, 2011, 94: 86.

IMAGES IN CLINICAL RADIOLOGY Spinal abnormalities in vitamin B12 deficiency F. Le Moine, P. Matthys1

A 25 year-old woman was hospitalized in psychiatry with progressive weight loss and diagnosis of anorexia. Her past medical history mentioned hyperthyroidism. For 3 months, she had been complaining of paresthesia of the lower limbs and ataxia without vertigo or lombosciatalgia. Neurological examination revealed considerable ataxia without motor deficit neither abnormality of the cranial nerves. Diffuse tactile hypoaesthesia of lower limbs bilaterally (most on the left side) was found. There was a vibration anesthesia and with lost position sense of lower limbs but with normal thermoalgesia. Evoked potentials showed a central origin, medullar bilateral (most on the left). No lesions were found on CT-scan of the brain. Magnetic resonance imaging (MRI) of the cervical spine, revealed focal hyperintense lesions into the dorsal spinal cord, most evident at the C4-C5 level. Hyperintense lesions on the sagittal T2 weighted /TSE (Fig. A) and STIR images (Fig. B) in the dorsal spinal cord with also a combined alteration of the bone marrow (hypo-intense signal of bone marrow on T1 and T2weighted/TSE) were seen. These hyperintense lesions were found in the dorsal spinal cord columns, more evident on the left side, on axial T2 gradient echo weighted images (Fig. C). The combination of lesions involving both the dorsal spinal cord columns and also the bone marrow, together with the clinical history of anorexia, was suggestive of deficiency alterations. Blood analysis revealed a megaloblastic anemia with vitamin B12 deficiency. Folic acid level was normal. Endoscopy demonstrated chronic atrophic gastritis with intestinal metaplasia. The patient was treated with intramuscularly injections of cobalamin with a rapid clinical recuperation and also a normalization of the signal abnormality in both cord and bone marrow (Fig. D). Comment

On MRI, the vitamin B12 deficiency, which is causing a subacute combined sclerosis or degeneration, will show most typically hyperintense lesions to the dorsal spinal cord columns. Also the alteration of the bone marrow is considered as a result of the anemia with an augmentation in hematopoesis. In the differential diagnosis of the spinal cord lesions, a large list of etiologies must be considered. Among them, inflammatory demyelization (multiple sclerosis or disseminates encephalomyelitis) is the most frequent cause. Also infectious lesion (herpes, HIV, ...), miscellaneous (sarcoidosis, ...), amyoD trophic lateral sclerosis, iatrogenic (radiation myelitis), traumatic or degenerative compressive myelopathy, vascular (ischemic – vascular malformations) and metabolic (deficiency syndrome B12, Cu, Vit E, N³O,...), are potentially reasons for spinal cord abnormalities. However, the selective dorsolateral spinal cord degeneration is typically for this subacute combined sclerosis, due to the vitamin B12 deficiency, with to pernicious anemia a as result. Other etiologies of vitamin B12 deficiency, includes other intestinal diseases (Crohn’s disease, celiac disease, bacterial overgrowth in intestinal blind loops) and also strict vegetarian diet. Nevertheless, preferential involving of the posterolateral columns of the spinal cord and also the changes of the bone marrow are highly suggestive of vitamin B12 deficiency. The treatment is life-long parenteral vitamin B12 administration and an early diagnosis is important, because the treatment will stop the degenerative myelin sheath degeneration, but in will not restore the destroyed nerve fibers. In our case, the rapid administration of cobalamin, was resulting in a good clinical recuperation and disappearing of the lesions in both spinal cord and bone marrow.

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

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 87.

IMAGES IN CLINICAL RADIOLOGY Duodenal varices L. Yi-Lan, S. Wen-Ko, L. Yu-Peng1

A 76-year-old man had a history of liver cirrhosis secondary to chronic hepatitis B infection. A hepatoma had also been noted 2 years previously. This time, he presented initially at the emergency department because of dysuria and fever for 2 days and tarry stool since the afternoon. The initial upper gastrointestinal endoscopy revealed esophageal varices, gastric ulcer, and duodenitis that was not actively bleeding. Proton pump inhibitors were prescribed. Unfortunately, massive blood stools were noted 3 days later. Emergency esophagogastroscopy and colonoscopy were performed, but no active bleeder was detected. Contrast-enhanced abdominal computed tomography (CT) showed duodenal varices in the second and third portions of the duodenum (Fig. A). The feeding vein of the varices was the pancreaticoduodenal vein originating in the superior mesenteric vein, while the right testicular vein was the draining vein (Fig. B). Owing to the persistent massive bleeding, surgical variceal ligation was performed, following which the patient had no further bleeding episodes. Comment

Hematemesis and melena are common presentations in patients with portal hypertension. However, bleeding from a duodenal varix is extremely rarer than that from esophageal or gastric varices, but is often massive and life-threatening. The etiology of duodenal varices can be classified into intrahepatic (e.g., in cirrhosis) or extrahepatic (e. g., in portal, splenic, or superior mesenteric vein thrombosis). Liver cirrhosis with portal hypertension remains the most common cause of duodenal variceal bleeding. Most of the duodenal varices are located in the duodenal bulb, but varices in the second and third portions of the duodenum are also seen. It may be the bleeder when neither upper nor lower gastrointestinal endoscopy reveals a bleeding site in a patient with portal hypertension and gastrointestinal hemorrhage. The blood flow in duodenal varices is frequently high and therefore, the resulting bleeding is profuse, with a high mortality rate of up to 40%. Endoscopic variceal ligation and endoscopic injection sclerotherapy are widely accepted primary therapies for esophageal variceal bleeding, but recurrence and rebleeding are not uncommon. Interventional radiological procedures such as balloon-occluded retrograde transvenous obliteration (BRTO) and transjugular intrahepatic portosystmeic shunt (TIPSS) seem to be more effective in selected cases. Surgical variceal ligation or shunt placement may be necessary in cases of intractable hemorrhage. The common feeding vein is the pancreaticoduodenal vein originating from the portal vein or superior mesenteric vein. The right gonadal vein and right superior capsular vein function as the draining veins. Multislice helical CT is a powerful diagnostic modality for evaluating the overall status of portosystemic vessels. The axial source and multiplanar reformation images can provide detail anatomy and help in treatment planning.

1. Department of Radiology, Hsinchu Mackay Memorial Hospital, Taiwan, R.O.C.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 88.

IMAGES IN CLINICAL RADIOLOGY Renal fornix rupture following diagnostic coronarography J. Vanrusselt1, K. Vander Eeckt2, R. Oyen1, F. Claus1

A 31-year-old man with an uneventful medical history presented at the emergency department with complaints of exercise-related chest pain for 3 weeks. ECG showed ST-elevations in the inferior leads. A diagnostic coronarography was performed and showed multivessel coronary stenosis. During this procedure 200 ml of a nonionic, low-osmolality monomeric contrast agent (Iomeron 350ÂŽ) and 1250 ml of isotonic saline solution was administered intravenously. After this procedure, the patient suffered from a sudden onset and progressive severe pain in the back and the right lumbar region. A plain CT of the abdomen performed 8 hours post coronarography showed contrast enhanced fluid in the renal sinus and the perinephric/peri-ureteral space (Fig. A (scout view), B (coronal) and C (sagittal) reformatted scans). There was a bladder overdistenstion with a CT-based volumetric estimation of 995 ml. No mechanical cause of upper urinary tract obstruction was present. Subsequent urological work-up included insertion of a bladder catheter (24 hours) and administration of peroral antibiotics. Ultrasound follow-up on the next day revealed no abnormalities and the patient was discharged. Comment

Three major factors are required to explain extravasation of urine (urinoma) from the renal collecting system: a functioning kidney, a tear in the collecting system and urinary outflow obstruction. Rupture of the weakest area of the collecting system, i.e. the calyceal fornix, occurs when the pressure in the pelvicaliceal system exceeds a critical level (variously reported as being between 20-75 mm Hg). The extent and the speed of increase of pressure in the renal fornix are determining factors for rupture. The most common non-traumatic and non-iatrogenic cause of urine extravasation is an acute mechanical ureteral obstruction caused by an impacted urinary stone. Pre-existing urinary disease (i.e. prostate hyperplasia, repeated mechanical stress by vesicoureteral reflux or pyelosinus backflow) or a history of previous acute episodes of mechanical obstruction contribute to an increased risk of future forniceal ruptures. Functional causes of ureteral obstruction are often related to bladder pathology, such as a neurogenic bladder, detrusor muscle deficiency or detrusor sphincter dyssynergia. Hyperdiuresis, either by instrinsic pathologies such as diabetes insipidus, alcohol abuse or iatrogenic conditions including overhydratation or the use of high-osmolality contrast agents, can also increase the pressure in the renal collecting system. In the case presented here, the cause of extravasation is most likely explained by a combination of increased diuresis (due to intravenous overhydratation) and overdistension of the urinary bladder. This unusual presentation is not previously reported in the literature. Complications of urinoma are generally rare as urine is reabsorbed quickly from the retroperitoneal tissues, except with urinary infection or persistent obstruction and/or leakage.

Department of 1. Radiology and 2. Urology, University Hospitals Leuven, Leuven, Belgium.

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JBR–BTR, 2011, 94: 89.

IMAGES IN CLINICAL RADIOLOGY Adrenal gland fusion P. De Visschere, E. Schollaert, G. Villeirs1 A 22-year old female was referred to our hospital for CT-evaluation of the abdomen. Her medical history revealed a congenital lumbosacral spina bifida with meningomyelocele, which was surgically closed at the age of 22 months. She had a neurogenic bladder with hydronephrosis of the right kidney and recurrent upper urinary tract infections. Her left kidney had been resected for renal atrophy. She had a rudimentary uterus with imperforate hymen. A fusion of the adrenal glands, with retroaortic bridging, was incidentally found (A-C). Comment

Congenital fusion of the adrenal glands is a rare congenital anomaly with only about 65 cases reported in literature. The fusion occurs across the midline in the retroperitoneum anterior or posterior to the aorta. The shape of the fused adrenal may vary, with poles oriented cranially or caudally, sometimes referred to as ‘horseshoe adrenal gland’, or with central poles, designated as ‘butterfly shape’. Fused adrenal glands are almost always associated with other congenital anomalies, such as major central nervous system malformations, renal agenesis, asplenia, anomalies of the internal genitalia and complex cardiac anomalies. The exact embryologic pathogenesis of adrenal gland fusion is unclear. The histologic appearance of the fused adrenal gland is similar to that of separate adrenals, and there seem to be no functional impairments.

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

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 90.

IMAGES IN CLINICAL RADIOLOGY Pulmonary arteriovenous malformation E. Janssens, P. Leyman, T. De Beule, L. Ardies, P. Dâ&#x20AC;&#x2122;haenens1 A 37-year old patient with Rendu-Osler-Weber syndrome presented to our hospital with hypoxy. Chest radiography shows on the PA view (Fig. A, arrow) a sharply marginated branching lobular mass of uniform density in the right upper/ lower lobe. A multislice spiral contrast-enhanced CT scan of the thorax shows multiple conglomerations of lobulated contrast-filled vessels (Fig. B, arrows) with feeding artery and draining vein. Anterior view of 3D volume-rendered image (Fig. C) displays the largest lesion in the right lower lobe with 2 feeding arteries (arrows) one draining vein (arrowhead). The lesion is 4,6 cm in diameter with 2 feeding arteries of 0,7 and 0,9 mm and one draining vein of 10 mm. Based on the imaging features and the clinical symptoms, the diagnosis of pulmonary arteriovenous malformations (AVMs) was made. Comment Pulmonary AVM, is a condition in which there is an abnormal direct communication between pulmonary arteries and pulmonary veins. The most common cause of pulmonary AVM is congenital. Acquired pulmonary AVM is seen in patients with prior congenital cyanotic heart surgeries, liver disorders (hepatopulmonary syndrome), systemic diseases and venous anomalies. 10% of the cases are identified in infancy or childhood with male predominance in newborns. Pulmonary AVMs are uncommon lesions, but are the cause of considerable morbidity and occasional mortality. Patients become symptomatic at the age of 40-60 years. Epistaxis and hemoptysis are common clinical features. Pulmonary AVMs with high flow or anatomic right-to-left shunt may result in cyanosis, digital clubbing, congestive heart failure and paradoxic embolism with substantial risk for stroke and cerebral abscess. A pulmonary AVM with a diameter less then 2 cm usually does not cause any symptoms. Rendu-Osler-Weber syndrome, is an autosomal dominant disorder and is frequently associated with pulmonary AVM (35%). For this reason, family members with Rendu-Osler-Weber should be screened for pulmonary AVMs. Contrast pulmonary angiography remains the gold standard in the diagnosis of pulmonary AVM, and is usually necessary if resectional or obliterative therapy is being considered. CT is the method for choice for routine detection of pulmonary AVMs, for diagnosis in patients unable to undergo conventional angiography, for follow-up of patients with proven pulmonary AVM and in confirming the presence of residual AVMs at follow-up after embolotherapy. All symptomatic pulmonary AVMs, pulmonary AVMs larger than 2 cm in diameter and pulmonary AVMs with feeding arteries larger than 3 mm should be treated with embolotherapy or surgery. The decision to perform surgical excision or transcatheter embolization planning rests on reaching an accurate estimate of the number, size, and course of vessels.

1. Department of Radiology, Onze-Lieve-Vrouwziekenhuis, Aalst, Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 91.

IMAGES IN CLINICAL RADIOLOGY S

Ileo-colic hernia through the foramen of Winslow

C R. Gutu1, S.H. Sondji2, S. Landen2 , J. Pringot1

A 60-year-old woman was admitted to hospital for acute post prandial epigastric pain and vomiting. Her medical history included hypercholesterolemia, surgery for varicose veins and breast implants. Abdominal palpation elicited pain and guarding in the epigastrium and left hypochondrium. The patient was not febrile. Blood analysis showed a slightly elevated leukocytosis 11,500 (normal value: <10,000), with normal C reactive protein. Liver enzymes including lactico-dehydrogenase were within normal limits. Plain abdominal radiograph showed gaseous dilatation of a hollow abdominal organ (C) situated in the epigastrium contiguous to the stomach (S), with presence of an air-fluid level (Fig. A). Contrast enhanced computerized tomography scan showed a dilated bowel loop (C) in the epigastrium, bordered by the stomach (S) laterally, the left liver lobe (L) and porta hepatis (arrow) medially and the pancreas (P) posteriorly (Fig. B). Computerized tomography scan in a frontal plane just posterior to the hepatic pedicle showed the colon (C) coursing through the foramen of Winslow (arrow) posterior to the portal vein (PV) (Fig. C). These features were suggestive of herniation through Winslowâ&#x20AC;&#x2122;s foramen. Laparoscopy showed a mobile caecum that had rotated upwards counterclockwise and had strangulated through the foramen of Winslow, attracting with it the terminal ileum. The dilated caecum could be seen bulging through the pars flacida of the lesser omentum, but showed no signs of gangrene. Laparotomy was required to reposition the caecum within the peritoneal cavity. Because the ascending colon was long and abnormally mobile it was decided to perform a right colectomy to reduce the risk of recurrence. Comment

The foramen of Winslow is an embryological remnant that constitutes a communication between the peritoneal cavity and lesser sac. This foramen is bordered by the vena cava posteriorly, the hepatic pedicle anteriorly, the caudate lobe of the liver cranially and the first portion of the duodenum caudally. Naturally occurring abdominal internal hernias represent less than 1 percent of all hernias. Herniation through the foramen of Winslow is especially rare, accounting for only 4% internal hernias and less than 200 cases have been reported. Various parts of the bowel may herniate through the foramen of Winslow the most common being the small bowel (63%), the caecum and right colon (30%) and the transverse colon (7%). Risk factors include a large foramen of Winslow, an abnormally mobile caecum and a long small bowel mesentery. Symptoms are nonspecific and include recurring bouts of epigastric pain and bloating. Vomiting may result from compression of the body of the stomach or duodenum by the herniated viscus. If left untreated strangulation leads to bowel obstruction, necrosis and perforation. Surgical management is mandatory to reduce the hernia. To prevent recurrence a mobile caecum can be suture fixated in the right iliac fossa or resected as in the present report. In case of herniation of the small bowel, the foramen of Winslow can be obturated by placing a purse string suture on the peritoneum lining the foramen. Conventional radiography often shows a dilated hollow viscus adjacent to or behind a dilated stomach. Computerized tomography scan shows passage of bowel behind the hepatic pedicle in continuity with a dilated hollow viscus incarcerated in the lesser sac. The herniated organ may occupy the medial part of the lesser sac as in the present report, or be situated more laterally behind the stomach. Non-visualisation of the caecum in the right hemiabdomen is noted when the caecum herniates. Small bowel obstruction presents early when the small bowel herniates. The differential diagnosis includes caecal volvulus and others types of internal hernias located in the left upper quadrant of the abdomen particularly those herniating through the lesser omentum.

1. Departments of 1. Radiology and 2. Surgery, St Elisabeth Hospital, Brussels, Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 92.

IMAGES IN CLINICAL RADIOLOGY Round ligament varicocele J. Heymans1, F.M. Vanhoenacker2,3, F. Vankelecom1

A 24-year-old pregnant woman (at 25 weeks gestation) was referred to our department because of a painless swelling in the left groin which she was feeling for one week. The swelling was more apparent in the upright position and when coughing. The swelling was reducible. Ultrasound demonstrated an anechoic structure with intralesional septa at the left inguinal area (Fig. A, longitudinal ultrasound image). The lesion augmented with the Valsalva manoeuvre and in standing position. Power Doppler confirmed the presence of venous flow (Fig. B). Inverted venous flow was seen after Valsalva (Fig. C, arrow). Based on the imaging findings the presumptive diagnosis of round ligament varicocele was made. The lesion was managed with watchful waiting and resolved completely in the postpartum period. In her second pregnancy the lesion recurred, again with complete resolution after delivery. Comment

Round Ligament Varicocele (RlV) is a rare clinical entity with only sporadic reports in the medical literature. It presents as a progressive groin swelling associated with pregnancy early in the third trimester with spontaneous regression soon after delivery. Progesterone-mediated venous smooth muscle relaxation, a raised cardiac output causing increased venous return from the limbs and leading to engorgement of venous tributaries, and progressive pelvic venous obstruction by the gravid uterus, contribute to RLV formation during the pregnancy. The lesion arises from the veins draining the round ligament and the inguinal canal. The incidence is unknown, but it is probably underdiagnosed. The correct diagnosis can be established by Doppler ultrasound, showing a prominent venous plexus (bag of worms) in the inguinal canal, with dilatation and flow augmentation during Valsalva manoeuvre. The differential diagnosis includes inguinal hernia, lymphadenopathy, lipoma, abscess, haematoma, pseudoaneurysm, AV malformation, cyst of the canal of Nuck and thromboplebitis. The clue to correct diagnosis on ultrasound is the presence of intralesional venous flow. As RLV is usually a painless selflimiting condition, the preferred treatment consists of a wait-and-see policy. Rarely painful complications may occur due to rupture or thrombosis of the varicose round ligament. Prompt surgical exploration is mandatory in the latter clinical scenario. In conclusion the diagnosis of RVL should lie considered when a groin lump is encountered in the second half of pregnancy. Doppler ultrasound allows a quick and reliable diagnosis, avoiding unnecessary surgical exploration.

Department of 1. Gynecology, 2. Radiology, AZ Sint-Maarten, DuffelMechelen, 3. Department of Radiology, Antwerp University Hospital, University of Antwerp, Edegem, Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 93.

IMAGES IN CLINICAL RADIOLOGY Bilateral globus pallidus infarcts in ecstasy use K. De Smet , M. De Maeseneer, Y.A. Talebian, T. Stadnik, J. De Mey

A 41-year-old man was found unconscious at his home by a friend. He was immediately admitted to the hospital through the emergency department. At the emergency department he regained consciousness. He mentionned he had a few alcoholic beverages the night before but otherwise clinical history was negative. On physical examination swelling of the right orbital area was evident. Further clinical history and laboratory tests were unremarkable. CT scan of the brain showed the right periorbital swelling. Also noted was marked hypodensity of the globus pallidus bilaterally. These areas of hypodensity showed no contrast enhancement. Next MRI of the brain was performed. On T2 weighted images symmetric hyperintensity of the globus pallidus was seen bilaterally. On diffusion weighted images strong hyperintensity was evident due to a reduction in apparent diffusion coefficient reflecting cytotoxic edema. Due to the unusual nature of these lesions further clinical history was obtained and the patient admitted to the single use of ecstasy the night before he was admitted. Follow up MRI after 3 weeks showed a decrease of signal intensity on T2 weighted images of the central area of the globi pallidi consistent with the development of liquefaction necrosis. After contrast administration there was marked enhancement of T1 weighted images likely due to passage through the bloodbrain barrier. On diffusion weighted images loss of hyperintensity was evident and an increase in apparent diffusion coefficient was seen. Further clinical evolution was unremarkable. Comment

Acute parenchymal injuries of the basal ganglia have been reported in a number of conditions. These conditions consist of anoxic-ischemic lesions and metabolic conditions including metabolic acidosis, hypoglycemia and exposure to toxic substances. Although these lesions are often symmetrical, they tend to involve the striatum (putamen and caudate nucleus). These structures have a higher rate of oxygen and glucose consumption. Lesions restricted to the globi pallidi are less commonly reported. An important cause corresponds to the acute phase of carbon monoxide poisoning. Other conditions that have been reported include heroin, ecstasy and cocaine. The mechanism of injury with ecstasy is believed to be a local release of serotonin resulting in prolonged vasospasm and downstream ischemia. The globus pallidus is the area of the brain most vulnerable to the effects of ecstasy because it is very rich in serotonin nerve terminals. Imaging findings on CT include a hypointense appearance of the globi pallidi without evidence of contrast enhancement. On T2 weighted MR images symmetrical hyperintensity of the globi pallidi may be evident. T1 weighted images are normal and there is no contrast enhancement. On diffusion weighted images strong hyperintensity may be apparent related to a reduction in apparent diffusion coefficient related to cytotoxic edema. After a few weeks MR findings change. There may be a decrease in hyperintensity on T2 weighted images especially centrally in the lesions due to liquefaction necrosis. On T1 weighted images contrast enhancement may now be seen likely related to a deficiency in the blood-brain barrier. On T2 * sequences a hypointense appearance may be noted because of hemorrhagic transformation. On diffusion weighted images there is a loss of hyperintensity and an increase in apparent diffusion coefficient. In conclusion, acute injuries of the basal ganglia usually involve the striatum. Lesions restricted to the globi pallidi are less common and may be seen with acute carbon monoxide poisoning and drug abuse (heroin, ecstasy, and cocaine).

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

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

IMAGES IN CLINICAL RADIOLOGY Focal eosinophilic hepatitis simulating a solitary metastatic lesion on FDG-PET/CT in a patient with history of head and neck cancer G. Ceulemans, B. Ilsen, D. Verdries, J. de Mey, H. Everaert1

A routine follow-up FDG-PET/CT was performed in a 67-year-old female with a history of head and neck carcinoma. In 2006, a T1 N0 M0 squamous cell carcinoma of the mouth floor had been resected. Subsequent clinical and radiological follow-up on regular base showed no evidence of locoregional recurrence or metastatic disease. There was no actual symptomatic disease. FDG-PET/CT images were obtained from vertex to pelvis and revealed a solitary hypermetabolic focus in the liver, corresponding to a hypodense lesion on non-contrast enhanced CT in segment 4 (Fig. A). A 3-phase contrast-enhanced CT of the liver confirmed the presence of this mass, which appeared to be hypovascular in the portal venous phase (Fig. B). Because metastatic origin was suspected, CT-guided biopsy was performed. Pathology demonstrated a granulomatous eosinophilic hepatitis, suggestive for an infectious etiology. Unfortunately no responsible micro-organism could be identified. Grocottâ&#x20AC;&#x2DC;s methenamine silver stain, used when fungal infection is suspected, was negative. Ziehl-Neelsen stain could not demonstrate acid-fast organisms. Three weeks post-biopsy, MRI of the liver could not demonstrate any residual lesion in the liver. Diagnosis of inflammatory/infectious pseudotumoral lesion was suggested and a wait-and-see attitude was chosen. As expected, FDGPET/CT, performed 3 months after the initial finding, showed resolution of the metabolic active hepatic focus; no other new non-physiological metabolic activities were found (Fig. C). Comment FDG-PET is a useful tool in the evaluation of many tumors, but because FDG-uptake can also occur in benign inflammatory processes, characterization of the lesion should not be done on the basis of the metabolic activity alone. The combination of the FDG-PET data with anatomic and morphologic findings on the CT will reduce the misinterpretation of a potential benign lesion. A 3-phase contrastenhanced CT or MRI of the liver, which are known to be highly specific, will further characterize suspicious lesions. But this case in which a hepatic inflammatory pseudotumor simulates metastatic disease on FDG PET/CT stresses the importance of guided biopsy.

1. Department of Radiology and Nuclear Medicine, UZ Brussel, Brussels, Belgium.

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JBR–BTR, 2011, 94: 95.

IMAGES IN CLINICAL RADIOLOGY Lipedematous scalp: a rare dermatological entity P. Bosschaert, F.C. Deprez1

A 16-year-old Caucasian girl was admitted at the request of her physician who had noticed a soft spongy texture of her scalp. The patient had no significant discomfort or ongoing symptoms and was aware of this abnormality for a long time. There was no previous trauma history. No family members showed any similar conditions. On dermatological examination, her scalp had an increased subcutaneous thickness extending from the occiput to the vertex, compared to that of a normal scalp. The skin appeared normal and hair was abundant. No signs of inflammation were found. Her general health was good. Blood analysis was considered to be within normal limits. Marked thickening of the subcutaneous fat layer on the vertex and occipital areas was noted by magnetic resonance imaging (Fig. A – sagittal T1-weighted image & Fig. B – coronal T2-weighted detail view). On fat-suppressed T1-weighted images, signal intensity of fat tissue was decreased. Brain parenchyma and ventricles appeared normal. Ultrasonographic complementary investigation with a 12-MHz linear transducer showed that the epidermis and dermis were normal but total thickness of the scalp measured 8-9 mm (Fig. C). The thickness of a scalp of a teenager is normally half as thick as our patient’s scalp. Histological study demonstrated the normality of epidermis and dermis, without evidence of inflammation or fibrosis. There was a marked hyperplasia of subcutaneous adipose tissue with mature adipocytes (Fig. D). The findings were consistent with a diagnosis of lipedematous scalp. Comment

Lipedematous scalp or lipoedematous scalp (LS) is a rare disease of unknown etiology characterized by a thick, boggy scalp. Cases associating local hair loss are known as lipedematous alopecia (LA), and are more frequent and easy to recognize. To our knowledge, 8 cases of LS have been reported in the literature. The first of them was described by Cornbleet in 1935. It was a 44-year-old black woman who had soft and thick scalp tissue that felt as if it was underlaid with cotton. Thereafter, authors have reported this pathology, with the support of MRI and/or US for the latest. Although initially it was considered that both entities (LS and LA) occur predominantly in black patients, the increase in the number of reports in Caucasian and Asian patients decreased racial factors in the pathogenesis of the disease. It is worth noting that most of the reported cases occur in women. Only one case has been reported in a child. The mean thickness of the scalp in normal individuals is estimated at 5-6 mm. In the reported cases, scalp thickness was greater, at 10-16 mm. The common histological feature is prominent increase of subcutaneous fat tissue which extends into the deep dermis. The adipose tissue is usually mature and organized. A mild peri-vascular inflammatory infiltrate can be detected in some cases. In this case, there was no loss of hair follicle (seen in LA). This thickening and softening of the scalp may be widespread or limited. In most occurrences, the condition is slowly progressive over a period of a few years and then it stabilizes. In conclusion, LS and LA are scalp disorders that radiologists should have knowledge of because these disorders are not difficult to diagnose when the clinical description of thick and spongy scalp textures are found. Reference 1.

Yasar S., Mansur A.T., Goktay F., et al.: Lipedematous scalp and lipedematous alopecia: report of three cases in white adults. Journal of Dermatology, 2007, 34: 124-130.

1. Department of Radiology, Clinique St-Pierre, Ottignies-LLN, Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 96.

IMAGES IN CLINICAL RADIOLOGY Schwannoma of the seminal vesicle K. Boeren1, Y. De Bruecker1, Y. Vankan1, D. Perdieus1

A 61-year -old male presented with a five month history of atypical left lower quadrant abdominal discomfort. There was no relevant past medical history and routine laboratory tests and physical examination were unremarkable. Work up included an abdominal CT of the lower abdomen. It revealed a well-delineated left intrapelvic soft tissue mass with some low attenuation areas, indistinguishable of the left seminal vesicle (Fig. A). He subsequently underwent a MRI of the pelvis. Axial T2-weighted MRI (Fig. B) demonstrated a well encapsulated mass, indistinguishable of the left seminal vesicle and a normal appearance of the right seminal vesicle. Coronal T1-weighted MRI (Fig. C) with fat saturation after the injection of intravenous gadolinium revealed the avid contrast uptake of the lesion with a small non-enhancing cystic component. It also depicted the extrinsic compression of the mass on the sigmoid colon and rectum. CT and MRI findings were strongly suggestive of a tumor with cystic degeneration, infiltrating in or originating from the left seminal vesicle. Surgical laparoscopic exploration with conversion to laparatomy demonstrated the mass, located on the course of the left vas deferens and originating from the left seminal vesicle. Total resection of the left seminal vesicle was needed. Macroscopic examination of the specimen demonstrated a yellowish heterogeneous and encapsulated mass originating from the left seminal vesicle. Microscopic examination with immunohistochemical staining for S-100 protein revealed a strong and diffuse expression of the Schwann cell compatible with an ancient schwannoma. The patient could be discharged 5 days after surgery. The patient was free of recurrence 5 months after surgery. Comment

A schwannoma is a benign peripheral nerve sheath tumour composed of Schwann cells. They are generally encountered in young and middleaged adults and commonly located in the retroperitoneum, mediastinum, head and neck. Schwannomas are usually asymptomatic until they become large and compress the surrounding tissues or they are found incidentally. Schwannomas are exceedingly rare in the male genital system. Most primary tumours of the seminal vesicle are benign including papillary adenoma, cystadenoma, fibroma and leiomyoma. Primary malignant tumours include adenocarcinoma, leiomyosarcoma and haemangiosarcoma. Only few cases of seminal vesicle schwannoma have been reported in the literature. Schwannomas are characterized by CT as well-circumscribed masses with variable heterogeneous densities due to areas of different cellularity and areas of cystic degeneration. The advantage of MRI is that it provides better tissue contrast than CT. However, preoperative diagnosis is difficult based on imaging studies alone due to the nonspecific presentation and imaging findings. Most striking diagnostic feature in the presented case is the presence of cystic components in an otherwise predominantly solid tumour, well demonstrated on MRI. These imaging findings are suggestive for an ancient schwannoma. Reference 1.

Latchamsetty K.C., Elterman L., Coogan C.L.: Schwannoma of a seminal vesicle. Urology, 2002, 60: 515.

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

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 97.

IMAGES IN CLINICAL RADIOLOGY Agenesis of the pubic symphysis detected with SPECT-CT G. Ceulemans1, M. Keyaerts1, M. De Maeseneer2, D. Verdries2, H. Everaert1

The pelvis is composed of 3 paired bones (ischiac, pubic and iliac bones) and the sacrum. Any part of the pelvis can be congenitally absent, but the sacrum is the most commonly affected. The absence can be partial or complete; unilateral or bilateral and can occur in an isolated fashion or be part of a malformation syndrome. A 99m Tc Methylene Diphosphonate (MDP) bone scan was performed in a 25-year old male because of chronic low back and pelvic pain. The patientâ&#x20AC;&#x2122;s history revealed bladder extrophy at birth for which he underwent an ureterosigmoidostomy. Total body and additional SPECT/CT images were acquired 3 hours after the injection of 740 MBq of 99m Tc-MDP. No pathological foci, which could explain the experienced pains, were detected. The reconstructed bladder had an irregular shape and urinary activity was seen in the left colon. No anterior pelvic bone activity was present (Fig. A). SPECT CT of the pelvis demonstrated the absence of the anterior branches of the pubic bones and pubic symphysis (Fig. B). Because of the lack of anterior pelvic stabilization, the posterior part of the pelvic floor is surcharged, which can explain the pain syndrome. Fusion images also showed the urinary flow to the reconstructed bladder and the intestinal excretion (Fig. C). A urinary escape route explains the activity in the left colon (Fig. D). Hypoplasia of the ischiopubic region is a rare congenital anomaly; few cases are reported in literature (1). This condition is often associated with genitourinary and anal malformations. A plain radiograph of the pelvis can detect most of these abnormalities and lead to the recognition of an unsuspected disorder. Reference 1.

Ischiopubic hypoplasia: a rare constituent of congenital syndromes. Acta Orthop Belg, 2003, 69: 29-34.

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

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 98.

IMAGES IN CLINICAL RADIOLOGY Primary breast tuberculosis S. Termos1, E. Sbeity2, M. Oweidat1, Z.R. Korban2, G.S. Abi Saad2

A 67-year-old Mediterranean single lady presented with a right breast lump that had been gradually increasing in size for four months. On palpation, the mass measured 3 x 5 cm in size and felt solid and irregular in nature. No redness or change in skin color was noted. A draining sinus from the medial aspect of the ipsilateral axilla was noted. This was associated with purulent discharge and a palpable 2 cm axillary lymph node. The patient reported no fever, cough or sputum production. Her chest Xray was normal. Ultrasound of the breasts showed a large hypoechoic solid nodule with slightly irregular contour in the right breast (A) raising the suspicion of a phylloides tumor or fibroadenoma. Multiple axillary lymph nodes were also noted, one of which was associated with a sinus tract. Mammography revealed a suspicious irregular mass in the right breast (B). Magnetic resonance imaging (MRI) of the breasts showed a macro-lobulated cyst with a necrotic component and a thick peripheral rim (C). There was extension to the pectoralis major muscle with linear extension to the lymph nodes, some of which were necrotic. Core needle biopsy of the cystic mass ruled out malignancy but showed abundance of inflammatory cells. The patient was taken to the operating room for excision of the right breast mass. An incision over the mass was extended to the axilla whereby the mass was totally excised down to the pectoral muscles together with the axillary sinus which was communicating with both lymph nodes. The frozen section was negative for malignancy. Pathological evaluation revealed an abscess lesion showing necrotizing granulomatous changes with cavernous formation surrounded by purulent inflammatory infiltrate and a granulomatous reaction composed of histiocytes, multinucleated giant cells, lymphocytes, and plasma cells. Caseous acellular necrosis was also noted. The tuberculosis skin test (PPD) was strongly positive. The patient was treated with antituberculous regimens as per WHO recommendations and showed complete remission. Primary breast tuberculosis is a rare entity (0.25-3.20% of all breast lesions). Unlike the unique case reported herein, primary breast tuberculosis is mainly associated with direct abrasion like rib infection or breast feeding and is mostly reported the reproductive age, when the breast duct and sinuses are most prone to changes and dilation (1). The spread to the lymph nodes follows a certain pattern, with the ipsilateral axillary and cervical lymph nodes affected in the majority of the cases (1). Our patient presented with a four month history of a right breast lump, with no redness or change in skin color, but associated with palpable axillary lymph nodes and a sinus tract. Breast tuberculosis presents a diagnostic challenge as it may be mistaken for a pyogenic abscess or breast carcinoma on imaging modalities. Pathological evaluation is necessary to confirm the diagnosis. Despite performing all the necessary diagnostic imaging studies for our patient, an accurate diagnosis was only confirmed with pathological studies. Treatment consists of incision and drainage, partial mastectomy, or simple mastectomy with or without axillary dissection, depending on the case. This is usually followed by standard antituberculous therapy for cure. Reference 1.

Tewari M., Shukla H.S.: Breast tuberculosis: diagnosis, clinical features & management. Indian J Med Res, 2005, 122: 103-110.

1. Department of Surgery, Division of General Surgery, Makased General Hospital, Beirut, Lebanon, 2. Department of Surgery, Division of General Surgery, American University of Beirut Medical Center, Beirut, Lebanon.

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JBR–BTR, 2011, 94: 99.

IMAGES IN CLINICAL RADIOLOGY Grynfelt hernia B. Coulier1

0 A 74-year- old patient was addressed to the department of gastroenterology with complaints of epigastric pain. Hepatic tests where moderately altered with signs of cholestasis. Contrast enhanced abdominal CT demonstrated carcinoma of the lower back of the gallbladder with numerous distant epigastric tumoral lymphadenopathies (not illustrated). The abdominal CT fortuitously demonstrated two very rare types of hernia for which the patient presented no symptom: an Amyand hernia (indirect inguinal hernia containing the appendix) and a very rare lumbar hernia through the infracostal superior lumbar triangle of Grynfelt (Fig. A, B, C). Extraperitoneal perirenal fat was protruding (white arrow) through the fascia transversalis and the aponeurosis of the transverse abdominis muscle through an orifice limited externally by the oblique muscles (O), internally by the erector spinae (S) and quadratrus lumborum (Q) and superiorly by the 12th rib (black star). Partially interstitial disruptions of transverse abdominis and internal oblique muscles are also visible more laterally (star). The protrusion is covered by the elongated latissimus dorsi muscle (black arrow).

✶ Q

Comment

✩

0 Q

Lumbar hernias are very rare representing no more than 2% of all abdominal hernias. They are classified on the basis of their anatomic position, such as superior (superior triangle or square of Grynfelt), inferior (inferior triangle of Petit) or diffuse and on the basis of their etiology (congenital, acquired or incisional). Congenital hernias (20% of lumbar hernias) perforate preferentially through the inferior lumbar triangle while acquired hernias (80% of lumbar hernias) are predominantly associated with the superior lumbar triangle. These acquired hernias are further subdivided into primary forms – 55% of lumbar hernias occurring nontraumatically – and secondary forms – accounting for approximately 25% of lumbar hernias –. Older patients with excessive weight loss, increased abdominal pressure or increased physical labor are predisposed to primary forms of acquired hernias – which affect the left side more often –. Secondary forms arise from surgical procedures – flank incisions, renal surgery or iliac bone graft harvesting – or non surgically causes – traffic accidents, falls, lumbar abscesses, penetrating wounds –. The very narrow lumbar space is bordered by the 12th rib superiorly, the iliac crest inferiorly and the mass of the erector spinae muscles medially. Two orifices can be described: an inferior and superficial, triangle shaped – Petit’s triangle – and a superior, deep, triangle or squared shaped – Grynfelt square –. The superior lumbar hernia through the lumbar inverted triangle or square of Grynfelt is larger and deeper. This triangle or square is defined medially by the erector spinae muscle group, laterally by the internal oblique muscle and superiorly by the 12th rib. The fascia transversalis and the aponeurosis of the transverse abdominis muscle form the floor and the roof is formed by the latissimus dorsi muscle. This area can be naturally weakened by the exit of vessels or nerves. Grynfelt hernia produces in 2/3 of cases in males with or without peritoneal sac. In the first case colon may protrude into a peritoneal sac and in the second posterior retroperitoneal fat or kidney may protrude. CT and MRI are the best modalities to diagnose the abdominal defect. If indicated a surgical procedure is the best treatment performed by direct or laparoscopic approach, with or without a mesh according to the cause and size of the defect. Result are usually good with no pain or recurrence. Reference 1. Cesar D., Valadao M., Murrahe R.J.: Grynfelt hernia: case report and literature review. Hernia, 2010, 5 (Epub ahead of print).

1. Department of Diagnostic Radiology, Clinique St Luc, Bouge Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 100-102.

CELEBRATE THE POWER OF IMAGING: THE EUROPEAN DAY OF RADIOLOGY

Summaries of the two topics chosen for the press conference organized by the Royal Belgian Radiological Society (RBRS) Computed tomography (CT) is the main source of radiation from diagnostic procedures D. Tack1

Approximately 1.800.000 CT examinations are performed every year in Belgium. With a mean dose 0,5 mSv, the annual collective dose from CT could induce up to 450 cancer. This number has to be compared to the 45 000 observed new cancers yearly. The deleterious effect of scanner radiation is thus undetectable among cancers induced by smoking, alcohol, and western diet. Risk from radiation is based on cancer mortality rates observed among atomic bomb survivors who underwent high level radiation. Overestimation of collective radiation risks in the filed of low level radiation (below 0,2 Sv) as used for CT is suspected first because a majority of patients undergoing CT are aged 60 years or more, and second because the numerous defense mechanisms that prevent cancer induction at lowdoses in human bodies are not taken into account by the linear no threshold model of carcinogenesis used as legal rule for risk calculations. On the other hand, CTis a rapid and efficient technique that providesaccurate diagnosis of various disorders such as acute appendicitis complete staging of severely injured patients, reliable monitoring of tumors and therapy guidance or planning. CT yields very high confidence in diagnosis that is required for treatment. The balance between radiation risk from CT and clinical benefit is thus almost always very high. However, because of its success and performance, overuse of CT is suspected. This overuse has been addressed by RIZIV / INAMI

B in collaboration with the Consilium Radiologicum. Objective is to promote guidelines for an appropriate use of medical imaging tests and to reduce the rate of unjustified examinations. The expected effect should be a collective dose reduction but also financial.

1. Service de Radiologie, RHMS, Clinique Louis Caty, Baudour.

When a CT is performed, according to guidelines, radiologists are in duty of limiting the delivered radiation dose by optimizing the CT technique. This is the practical application of the ALARA principle (As Low As Reasonably Achievable). The process of optimization is under the control of the Federal Agency for Nuclear Control (FANC/AFCN). The method for dose limitation is based on surveys. With the collaboration

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and approval of radiologists, the FANC will conduct surveys on CT on annual basis instead of every three to five years. In patients with long life expectancy, typically in children and young adults suspected of benign disorders, the radiation dose of CT can be lowered down to the dose of radiographic examinations as illustrated in Figure 1. Figure 1 A (axial view) and B (coronal view) illustrate low-dose abdominal CT in a 11-year old boy who had previous inconclusive ultrasound examination and suffered from right iliac fossa pain. Dose

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report from CT examinations shows DLP value at 51 mGy.cm, equivalent to one plain abdominal film. Arrow: normal aerated appendix. Technical parameters: Unenhanced abdominal 64 (2 x 32) MDCT scanner (Se,sation 64 Siemens Medical Healthcare; 100 KV and 37 effective mAs. Tube current modulation activated. Index of image quality = 70 mAs Eff. Mean CTDIvol at 1,68 mGy.

McCollough C.H., Mettler F.A., Pearce M.S., Suleiman O.H., Thrall J.H., Wagner L.K.: Managing Radiation Use in Medical Imaging: A Multifaceted Challenge. Radiology, 2011, 258: 889-905. 2. The 2007 Recommendations of the International Commission on Radiological Protection. ICRP publication 103. Ann ICRP, 2007, 37: 1-332. 3. McCollough C.H., Primak A.N., Braun N., Kofler J.,Yu L., Christner J.: Strategies for reducing radiation dose in CT. RadiolClin North Am, 2009, 47: 27-40.

References 1.

Hricak H., Brenner D.J., Adelstein S.J., Frush D.P., Hall E.J., Howell R.W.,

NEURORADIOLOGY PLAYS A CRUCIAL ROLE IN THE MANAGEMENT OF STROKE PATIENTS P.M. Parizel1, B. Lubicz2

Stroke is a clinical syndrome defined as a focal neurologic deficit of sudden onset. The event can be triggered by a sudden reduction of the blood supply to the brain (“ischaemic stroke”), or by a cerebral haemorrhage (“haemorrhagic stroke”). Table 1 provides a classification of different stroke types. In Europe, stroke is the third most common cause of death and the leading cause of permanent disability. Each year, an estimated 1.1 million people suffer strokes in the European Union, while 15 million people suffer a stroke worldwide, resulting in 5 million deaths and 5 million people permanently disabled, according to the World Health Organization. With the arrival of promising new therapies aimed at re-establishing blood flow, reducing the size of the infarction and protecting the surrounding brain at risk, the traditional role of neuroimaging has changed dramatically in recent years. Neuroradiology contributes significantly, not only to the early diagnosis of stroke, but also to the initiation of appropriate treatment, thereby improving patients’ chances of survival and full recovery. New

Table 1. — Classification of stroke. 1. Haemorrhagic stroke 1. Intracerebral haemorrhage (e.g. due to hypertension or amyloid angiopathy) 2. Subarachnoid haemorrhage 2.1. Aneurysm rupture 2.2. Rupture of an arterio-venous malformation (AVM) 2. Ischaemic stroke 1. Thrombotic stroke 1.1. Internal carotid artery distribution (“anterior circulation”) 1.2. Vertebrobasilar distribution (“posterior circulation”) 1.3. Lacunar infarcts (due to occlusion of penetrating branches) 2. Embolic stroke 2.1. Middle cerebral artery distribution 2.2. Anterior cerebral artery distribution 2.3. Posterior cerebral artery distribution 2.4. Vertebrobasilar distribution 3. Increased coagulability (including veno-occlusive disease) 3.1. Primary (e.g. protein S- or protein C-deficiency, antitrombine IIIdeficiency, …) 3.2. Secundary (e.g.. anti-phospholipid syndrome, paraneoplastic, …)

developments in neuroimaging have considerably improved our understanding of the pathophysiology of acute stroke. Multimodal and multiparametric imaging techniques now

From: 1. President, European Society of Neuroradiology, Professor & Chair, Dept. of Radiology, Antwerp University Hospital & University of Antwerp, 2. Professor & Head, Neuroradiology section, Dept. of Radiology, Hôpital Erasme, Free University of Brussels.

play a crucial role in the diagnosis, clinical management, therapy and outcome prediction of patients with an acute stroke. Magnetic resonance imaging (MRI), a modality that uses magnetic fields to reveal contrast between the different soft tissues of the body, is of great value in the early diagnosis of ischaemic brain tissue when combined with diffusion-weighted imaging, a method that produces in

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vivo images of biological tissues by measuring water diffusion. Within the 3 to 4.5 hour therapeutic time window after onset of symptoms, many patients with an ischaemic stroke can be treated with thrombolysis, i.e. the dissolution of a blood clot with intravenously administered drugs. So far, it is the only specific treatment option for acute ischaemic stroke that has proven effective. Ischaemic stroke accounts for about 80 to 85% of cases while the remainder are related to intracerebral hemorrhage, mainly caused by arterial hypertension or blood vessel malformation – aneurysm, arteriovenous malformation, etc. Clots can also be removed through endovascular procedures such as endovascular fibrinolysis or thrombolysis and/or thrombectomy, which are performed by interventional neuroradiologists. In ischaemic stroke, most experts agree that MRI is the most sensitive imaging modality, since it allows early visualisation of ischaemic brain tissue. However, in most European hospitals, for practical and logistical reasons, computed tomography (CT) remains the first-stop imaging technique to exclude a haemorrhagic stroke. CT, which uses x-rays combined with computer software to provide 3-dimensional and transaxial images of the brain, has been shown to be fast, reliable, and effective in excluding intracranial haemorrhage in an emergency setting. Unfortunately, CT is not sensitive enough to show the ischaemic brain tissue in the first hours after onset of symptoms. Thanks to recent developments in CT technology, and improved data processing software, several methods exist to overcome the sensitivity limitations of CT, such as perfusion imaging. Perfusion CT is a technique which enables visualisation of the passage of blood – and contrast material – through the brain over

JBR–BTR, 2011, 94 (2)

time. Perfusion CT is of great value for identifying patients who are good candidates for thrombolytic treatment, even beyond the standard treatment time window of three hours, thereby increasing the numbers of patients that can be treated. Imaging enables the gathering of necessary information to differentiate diagnoses and to apply the required therapy. The fundamental goals of neuroimaging in acute stroke remain to rule out intracranial haemorrhage, demonstrate ischaemic brain tissue (cytotoxic edema), reveal tissue blood flow and identify areas of potentially salvageable brain tissue (penumbra), and assess the patency of the intra and extracranial vessels. Most university hospitals and large community hospitals in Belgium have all the necessary radiological equipment. However, there is a shortage of neuroradiologists and radiologists in general within these hospitals. A successful stroke service is very labour-intensive, since a 24/7 on-call system must be organised, and emergency examinations must be performed and interpreted quickly and accurately. There is a shortage of academically trained radiologists and neuroradiologists who are able and willing to participate in a 24/7 on-call service for stroke patients. Concerning interventional neuroradiologists, there would be an absolute shortage of manpower if all ischaemic strokes would be considered for endovascular treatment in the future. Haemorrhagic stroke is widely considered as a medical emergency, and prompts primary care physicians and emergency room doctors towards undertaking swift action. Unfortunately, a patient with an acute neurologic deficit without intracranial haemorrhage – an ischaemic stroke – is often not considered as an emergency. Ischaemic stroke does not hurt, unlike, for example, a

myocardial infarction. And yet, a brain infarct, commonly called stroke, must be considered like a heart attack and requires immediate and aggressive treatment, to prevent permanent neurologic deficit. Stroke is now, thanks to new therapeutic options, a potentially reversible and curable disease, provided that treatment is started soon enough. There should be a large-scale information campaign to educate both the general public and radiologists. Everybody knows that a sudden and severe constrictive pain in the chest, jaw and left arm can be an indicator of an acute heart attack. Similarly, when a patient experiences an acute neurologic deficit, this should be interpreted as the sign of an acute brain attack, and the patient should be treated within 3 to 4.5 hours of symptom onset. That is one of the major issues if we want to improve the treatment of ischaemic strokes. Another issue concerns the organisation of local hospitals. Emergency room physicians and paramedics must be familiar with the signs and symptoms of acute stroke, and should react quickly when they are identified. Last but not least, it is important to emphasize that endovascular treatment of ischaemic stroke is still not reimbursed in Belgium. We have the tools to offer this type of treatment but we can’t use them in daily practice. We strongly believe that our politicians need to be informed about this problem, and we are convinced that the general public, as well as our colleagues, need to informed about the new treatment options for acute ischaemic stroke. Stroke remains the only neurologic disorder for which physicians are potentially able to completely reverse disabling deficits, provided that patients are treated within the so-called therapeutic time window (3 to 4.5 after symptom onset).

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JBR–BTR, 2011, 94: 103-104.

ABSTRACTS OF PAPERS PRESENTED AT THE ANNUAL SESSION OF THE RESEARCH GROUP ON ABDOMNAL AND DIGESTIVE IMAGING ORGANIZED IN LIEGE ON FEBRUARY 18, 2011 BY SECTION ABDOMINAL IMAGING Scirrhous variant of hepatocellular carcinoma: a case-report D. Wendum, O. Scatton, B. Bessoud, O. Rosmorduc, J.F. Fléjou1 We report a case of a rare variant of hepatocellular carcinoma (HCC) developed in a non-cirrhotic liver in a 64 yearold patient. A 64-year-old patient was admitted because of abdominal pain associated to a liver mass. CT-scan showed large hypovascular nodules in the right liver lobe. Alpha-fetoptotein levels were very high (58000 ng/ml). There was no sign suggesting chronic liver disease. No primary carcinoma was found (in particular no gastric or ovarian carcinoma). After transarterial chemoembolization and portal embolization, a right hepatectomy was performed. Histopathological analysis of the liver specimen showed a moderately differentiated HCC with fibrous stroma with no diagnostic criteria for fibrolammelar HCC (Scirrhous HCC). The tumour cells expressed Heppar-1, glypican-3, AFP and also cytokeratin 19. The nontumoral liver showed no fibrosis, no steatosis or iron deposition. The diagnosis of primary liver carcinomas with fibrous stroma, the diagnostic criterias of fibrolamellar HCC and the significance of cytokeratin 19 expression in HCC will be discussed. 1. Service de Radiologie, Antoine, Paris, France.

Hôpital Saint

Mesenteric lesions: anatomo-radiological correlations E. Danse, C. Sempoux, R. Detry, A. Mourin1 Two cases of mesenteric lesions are reported. The first one concerns a 60 old woman for whom a calcified mesenteric mass was detected on abdominal CT required for a non specific pelvic pain. Small bowel enema was performed before surgery. The mass was totally removed. Pathology concluded to a calcifying fibrous tumor of the mesentery. The second case concerns a 83 old man complaining of abdominal pain and weight loss. A ill-defined solid mesenteric mass was found together with ascites and enlarged lymph nodes. Surgical exploration was performed and macrobiopsies were taken. The final diagnosis was sclerosing mesenteritis. Imaging findings are presented with close correlation with macroscopic and microscopic illustrations of the lesions. This presentation is the opportunity to review the imaging findings suggestive of mesenteric diseases and to correlate these findings with pathological data.

1. Service d’Imagerie Médicale, UCL Saint-Luc, Brussels, Belgium. Accumulation of large amounts of intraperitoneal soft tissue material, mimicking pseudomyxoma peritonei K. Buccauw, R. Vanslembrouck, K. Op De beeck, S. Haegeman, M. Thijs, D. Vanbeckevoort1 A 37-year-old man, with no relevant issues in his medical history, presented with low abdominal discomfort, weight loss and red blood loss per anum. The patient underwent both an ultrasound and a CT scan which showed an accumulation of large amounts of intraperitoneal soft tissue material with small amount of ascites. Subsequently, an exploratory laparotomy was performed with resection of this extensive peritoneal soft tissue mass, omentectomy, segmental enterectomy and appendectomy. Rather surprisingly, this lesion was histologically consistent with a high-risk gastrointestinal stromal tumor (GIST). The patient is further treated with systemic chemotherapy. 1. Department of Radiology, UZLeuven, Leuven, Belgium. An uncommon cause of proximal intestinal subobstruction : wilkie syndrome E. Halet, H. Peeters, D. Van De putte, L. Delrue, M. De Vos1 A 23-year-old Caucasian man with a history of a hernia operation presented at the emergency room because of longstanding complaints of weight loss, vomiting and abdominal pain worsening over time. At time of presentation he was complaining of diffuse abdominal pain and vomiting. On physical examination there was abdominal distention with percussion pain. Routine laboratory tests were normal. A Ct-scan was performed showing duodenal dilation and retraction of the ileum, suggestive for a subobstruction due to adhesions. A laparascopy was performed but could not show any adhesions nor internal herniations. Because the complaints persisted a transit of the small bowel (Rx SMD) was performed showing a severely slowed down gastrointestinal transit with pendular movements at the proximal duodenum. Decompression of the duodenum was associated with a temporary higher motility. These findings are highly suggestive for a Wilkie syndrome also known as Superior mesenteric artery syndrome. It is most commonly caused by loss of the mesenteric fat pad resulting in a compression of the third portion of the

duodenum by the abdominal aorta and the overlying superior mesenteric artery. A conservative treatment with high caloric drinks, small meals and prokinetics was started in order to gain weight and reverse the precipitating factor. Over the following months the patient gained weight and the symptoms resolved. In conclusion: a rare case of subobstruction due to compression of the duodenum by the superior mesenteric artery also called Wilkie syndrome. 1. Department of Radiology, UZGent, Ghent, Belgium. Imaging features of caroli disease and syndrome: a restropective analysis in 8 patients H. Lefere, F. Claus, M. Thijs, G. De Hertogh, C. Verslype, W. Laleman, D. Vanbeckevoort, W. Van Steenbergen1 Segmental, nonobstructive dilatation of intrahepatic bile ducts is referred to as Caroli disease (CD). When associated with congenital hepatic fibrosis, the term Caroli syndrome (CS) is used. These disease entities share a common pathogenetic mechanism called ductal plate malformation. The clinical and radiological records of 8 patients admitted between 1992 and 2009 with pathologically proven CD or CS were reviewed. Available imaging studies were retrospectively scored for the presence of central dot signs*, the degree of intra- and extrahepatic bile duct dilatation, intrahepatic calculi and secondary signs of portal hypertension such as splenomegaly and oesophageal varices. (*The ‘central dot sign’ is defined in Caroli patients in the literature as a bundle or dot of strong contrast enhancement within a dilated intrahepatic bile duct.) Two patients had the ‘pure form’ Caroli disease, whereas in the other six cases the diagnosis of Caroli syndrome was made. Age at diagnosis ranged from 3 to 74 years. Presenting signs and symptoms: (hepato)splenomegaly (n = 4), hematemesis and/or melena (n = 3), cholangitis (n = 3). There was no evidence for malignancy in any of these patients. 7 out of 8 patients showed central dot signs on various imaging modalities. In the remaining case, where no contrastenhanced studies were available, hepatic lesions very closely resembling central dots (‘dot-like’ sign) were seen. Right hepatic lobe predominant disease was present in 6 cases. Intrahepatic bile calculi were found in three patients. Secondary signs of portal hypertension were observed in all but one patient. The central dot(-like) sign can be considered a hallmark sign of Caroli disease

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104 and Caroli syndrome. It was reliably detected by current imaging techniques in all patients. 1. Department of Radiology, University Hospital Gasthuisberg, Leuven, Belgium.

JBR–BTR, 2011, 94 (2) Atypical focal hepatic mass in a young woman E. Vanhoutte, J. Soens, E. Willems, C. Verslype, D. Vanbeckevoort, D. Bielen1

Retroperitoneal fat-containing tumours F. De Munck, E. Vanderlinden, F. Vandenbroucke, A. Hoorens1

Diffusion Weighted Imaging DWI is a new powerful technique for detecting metastases showing higher sensitivity values than the classical MR sequences for subcentimetric liver metastases. Little is known about false positive findings. We like to present the selective imaging findings correlated with pathology of two patients with an oncological history and false positive DWI findings. The first patient had a history of a Ewing sarcoma treated with chemo-radiation and surgery who also had an associated hemochromatosis. The second patient had a cholangiocarcinoma which was preoperatively treated with radiotherapy. In the first patient, multiple hypervascular nodules without iron overload mimicking metastases were found in the liver. The false positive DWI was created by the iron overload in the surrounding ‘normal’ liver parenchyma. The hypothesis for these lesions are sideronecrotic nodules with nodular regenerative hyperplasia. The second patient showed acute radiation induced hepatitis in the radiation field with inside two DWI false positive hypovascular pseudolesions, probably due to vascular changes creating hypoperfusion with hypoxia and nutritional ischemia. DWI is a very powerful technique for detecting liver metastases but treatmentinduced microvascular changes may induce false positive findings.

We report the case of a young woman of 22 years who presented with vague abdominal complaints and a palpable epigastric mass. Her medical history revealed a deep venous thrombosis in the leg, treated with a vena cava filter and marcoumar. The initial CT scan in portovenous phase demonstrated a large mass in the left liver lobe with a central scar, thrombosis of the left portal vein and mediastinal adenopathy. Additional triple-phase CT study of the liver showed a large heterogeneous mass predominantly hyperdense and with a central hypodense stellate scar with inlying calcifcations. The central scar did not show any significant enhancement. An explorative laparoscopy was performed and biopsies were taken. Histopathologic examination confirmed the diagnosis of fibrolamellar hepatocellular carcinoma (FLC). These distinct imaging features can help to distinguish FLC from other benign and malignant lesions such as FNH, giant hemangioma, conventional HCC and malignant degeneration of hepatocellular adenoma. Diagnosing FLC is important, because in contrast to the benign lesions, FLC preferentially is treated by surgical resection. Even an advanced disease of FLC with lymphadenopathy, invasion of adjacent organs or limited metastasis does not preclude curative resection. In this particular case, medical treatment was chosen because of the presence of the mediastinal adenopathy. Diagnosing FLC is important because of the different prognosis and therapy. Therefore, it should be included in the differential diagnoses of a large hepatic mass with central scar and inlying calcifications in a young patient with no underlying liver disease.

A 30-year-old and 51-year-old woman presented at the emergency department with respectively impression of a left flank mass and unrelenting abdominal pain. In both patients ultrasonography showed a large heterogeneous mass involving almost the entire left flank. We want to give an overview of the diagnostic possibilities for such a tumours. On abdominal computed tomography (CT), the masses appeared well-circumscribed and contained fat. There was a heterogeneous contrast captation. The first patient underwent resection of the mass. In the second patient a CT-guided biopsy was performed. Pathologic examination of both lesions revealed fat-containing tumours. The first patient had an angiomyolipoma of the kidney and the second patient had a retroperitoneal dedifferentiated liposarcoma. Angiomyolipoma is a tumour composed of varying admixtures of blood vessels, smooth muscle cells and adipose tissue; any one or two of these elements may predominate. Liposarcoma is one of the most common soft tissue sarcomas of adult life. Together with an adrenal myelolipoma, they represent the three most common fat-containing masses in the retroperitoneal region. The latter is a benign tumour composed of mature fat and interspersed hematopoietic elements that resemble normal bone marrow. Final diagnosis of these retroperitoneal fat-containing tumours is usually not possible based on imaging characteristics alone as these lesions have overlapping features. Demographic and clinical data, however, will allow refining the diagnostic options and will help to determine treatment.

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

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

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

False positive diffusion weighted imaging findings in an oncological setting B. Op de Beeck, A. Snoeckx, M.J. Spinhoven, V. Van Marck, T. Moreels, D. Ysebaert, M. Peeters1

JBR–BTR, 2011, 94: 104.

ABSTRACTS OF PAPERS FOR FULL MEMBERSHIP CHEST Lung cancer: how to measure the tumor and its influence on T staging in the new TNM classification C. Mai, F. De Keyzer, J. Verschakelen, J. Coolen, W. De Wever1 Purpose: In the new TNM classification, lung tumor measurement becomes important for T-stage assessment. However, no guidelines are proposed how to measure tumor. Purpose of this study was to evaluate if tumor measurement on different window settings, with different imaging techniques, can influence T- and group-staging in the new TNM classification. We also compared T stage assessed with the old classification versus T stage according to the new TNM

classification, and again we evaluated the impact on final TNM stage. Methods and materials: 49 consecutive lung cancer patients who underwent PETCT were retrospectively evaluated. Tumor size on mediastinal and lung window settings was compared. A possible influence on T- and group-stage was evaluated. In a subgroup of 23 patients, the same evaluation was done on a dedicated chest-CT and compared with the results on PET-CT. Statistical analysis was done using BlandAltman-plot-method, together with a paired t-test, and the McNemar test. Results: Tumor measurements on lung window were larger than on mediastinal window, which was statistically significant (p < 0.05). This led to different T-stage in 6 patients (12.2%) and different group-stage in one patient (2%). When we compared T- and group-stages based

on the old classification with the new Tand group-stages, we found a different Tstage in 12 patients (24.5%) and a different group-stage in 15 patients (31%). There was no statistical difference for tumor measurement done on dedicated CT and on PET-CT. T-stage was different in 2 patients (8.7%). Conclusions: Tumor measurement is statistically different between lung and mediastinal window on PET-CT and dedicated CT. However, this difference has no significant influence on T staging and on group staging in the new TNM classification. PET-CT can be used for T-staging in lung cancer. Stage migration in the new TNM classification is comparable with other studies. 1. Department of Radiology, KULeuven, Leuven, Belgium.

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JBR–BTR, 2011, 94: 105-106.

FORTHCOMING COURSES AND MEETINGS NATIONAL MEETINGS 19.11.11 Annual RBRS symposium 2011 Imaging of the spine and the spinal cord: state-of-the-art Organization: Dr B. Desprechins 12.05.11 RBRS – Abdominal and Digestive Imaging Antwerp, UZ Information: bart.op.de.beeck@uza.be 21.05.11 RBRS – Bone and Joints Imaging Information: Pieter.Van.Dyck@uza.be 26.05.11 RBRS – Breast Imaging Leuven, UZ Gasthuisberg Information: monika.philips@uzleuven.be 03-05.06.11 1st ESUR TEACHING COURSE ON PROSTATE MRI Ghent Information: www.prostatemricourse.com 10.06.11 RBRS – Head and Neck Radiology Rotterdam, Erasmus MC Information: robert.hermans@uzleuven.be 14.06.11 RBRS – Chest Radiology Brussels, UCL St Luc Information: benoit.ghaye@uclouvain.be

Annual Symposium 2011: 19.11.11 RBRS- Cardiovascular and Interventional Radiology 24.06.11, 30.09.11, 16.12.11 RBRS – Bone and Joints Imaging 21.05.11 RBRS – Breast Imaging 26.05.11

20.06.11 RBRS – Neuroradiology Gent, AZ St Lucas Information: nsadeghi@ulb.ac.be

03.10.11 RBRS – Neuroradiology Liège, CHU Information: nsadeghi@ulb.ac.be

21.06.11 RBRS – Pediatric Radiology Liège, CH Information: brigitte.dep@hotmail.be

11.10.11 RBRS – Pediatric Radiology Brussels, UZ Information: brigitte.dep@hotmail.be

24.06.11 RBRS – Cardiovascular and Interventional Radiology Mont-Godinne, UCL Information: Dr J.F. De Wispelaere, jean-francois.dewispelaere@uclouvain.be 08-10.09.11 24TH ANNUAL MEETING AND REFRESHER COURSE OF THE ESHNR Brugge Information: casselmanjw@telenet.be 30.09.11 RBRS – Cardiovascular and Interventional Radiology Leuven, KUL Information: Dr G. Maleux, geert.maleux@uzleuven.be

18.10.11 RBRS – Chest Radiology Brussels, UCL St Luc Information: benoit.ghaye@uclouvain.be 16.12.11 RBRS – Cardiovascular and Interventional Radiology Information: Dr M. Laureys, marc.laureys@chu-brugmann.be 06-08.09.12 RBRS – Abdominal and Digestive Imaging Update in Abdominal and Urogenital Imaging Bruges, Congress Center Oud Sint Jan Information: http://www.update-medical-imaging.be

01.10.11 RBRS – Cardiac Imaging How to perform cardiac CT in clinical practice Antwerp, KBC Tower Information: antwerpsymposium@gmail.com

RBRS – Pediatric Radiology 21.06.11, 11.10.11

RBRS – Neuroradiology 20.06.11, 08-10.09.11, 03.10.11

RBRS – Chest Radiology 14.06.11, 18.10.11

RBRS – Head and Neck Radiology 10.06.11

RBRS – Cardiac Imaging 01.10.11

Miscellaneous: 24-25.03.11, 03-05.06.11

RBRS – Abdominal and Digestive Imaging 12.05.11, 06-08.09.12

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

INTERNATIONAL MEETINGS 04-07.05.11 Advanced MRI 2011-02-01 Graz, Austria Information: www.diagnostikzentrum.com 15-05-2011 International Conference of Non-Invasive Cardiovascular Imaging 2011 Amsterdam, The Netherlands Information: http://www.escardio.org/ congresses/ICNC10/Pages/welcome.aspx

21-05-2011 ESGAR 2011 European Society of Gastrointestinal and Abdominal Radiology Venice, Italy Information: www.esgar.org 08-06-2011 Congrès 2011 Meeting CIRA-SFICV 10e réunion annuelle de CIRA conjointement avec la SFICV Montreal, Canada

Information & Registration For Canadian and International participants: Registration (starting January 2011): www.ciraweb.org E-mail: info@ciraweb.org Tel.: 514-282-2744 For participants from France: Registration (starting January 2011): agence@coralys.fr E-mail: agence@coralys.fr Tel.: 04 67 79 24 95

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106 09-11.06.11 Crete, Greece 18th European Society of Musculoskeletal Radiology Meeting (ESSR) Main theme refresher course: Bone marrow. Additional refresher courses on different MSK topics. Scientific papers on all aspects of MSK Radiology Information: http://www.essr.org/cms/website.php?id= /en/essr_home.htm 10.06.11 RBRS – Head and Neck Radiology Rotterdam, Erasmus MC Information: robert.hermans@uzleuven.be 18.06.11 Paris, France 8EME JOURNEE DE RADIOLOGIE HEPATOBILIAIRE DU GROUPE HOSPITALIER BICETRE-PAUL BROUSSE Theme: Les nouveautés technologiques –

JBR–BTR, 2011, 94 (2) Le carcinome hépato-cellulaire revisité en 2011 – L’exploration moderne des voies biliaires Information: Secrétariat du Pr M.F. Bellin, veronique.rey@bct.aphp.fr 22-06-2011 Computer Assisted Radiology and Surgery – 25th International Congress and Exhibition 2011 Berlin, Germany Information: http://www.cars-int.org/ 21-24.09.11 USA, San Diego ISS MUSCULOSKELETAL IMAGING COURSE FUNDAMENTALS TO ADVANCED CONCEPT Information: www.internationalskeletalsociety.com 21-25.10.10 JOURNEES FRANCAISES DE RADIOLOGIE Paris, France Information: www.sfrnet.org

08.11.11 11TH WORLD FEDERATION OF INTERVENTIONAL AND THERAPEUTIC NEURORADIOLOGY CONGRESS South Africa, Cape Town Information: www.wfitn2011.org 27.11-02.12.11 RSNA ANNUAL MEETING Chicago, USA Information: www.rsna.org