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ISSN 1318-2099 


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ADIOLOGY 
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NCOLOGY 


Radiologi; and Oncologtj December 2004 
Institute of Oncologi; Vol. 38 No. 4 
Zaloška 2 Pages 251-368 
SI-1000 Ljubljana ISSN 1318-2099 
Slovenia UDC 616-006 
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Radiologij and Oncology is a journal devoted to publication of original contributions in diagnostic and interventional radiologi;, computerized tomography, ultrasound, magnetic resonance, nuclear medicine, radiotherapy, clinical and experimental oncology, radiobiologi;, radiophysics and radiation protection. 
Editor-in-Chief Editor-in-Chief Emeritus 
Gregor Serša Tomaž Benulic 
Ljubljana, Slovenia Ljubljana, Slovenia 
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Viljem Kovac Uroš Smrdel 

Ljubljana, Slovenia Ljubljana, Slovenia 
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Marija Auersperg Valentin Fidler Maja Osmak 
Ljubljana, Slovenia Ljubljana, Slovenia Zagreb, Croatia 

Nada Bešenski Be'1aFonzet Branko Palcic 
Zagreb, Croatia Budapest, Hungary Vancouver, Canada 
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Hamburg, Germany Trieste, Italy Zagreb, Croatia 
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Zagreb, Croatia Zagreb, Croatia Portland, USA 
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Ljubljana, Slovenia Pecs, Hungary Ljubljana, Slovenia 
Marjan Budihna Berta Jereb Ervin B. Podgoršak 
Ljubljana, Slovenia Ljubljana, Slovenia Montreal, Canada 

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The 80th Anniversary of Clinical Institute of Radiology Ljubljana 
Guest Editor Prof. Vladimir Jevtic, PhD, MD 



COLOGY 

Ljubljana, Slovenia December 2004 Vol. 38 No. 4 ISSN 1318-2099 UDC 616-006 CODEN: RONCEM 
CONTENTS 
Foreword 251 
Jevtic V 
History of the Clinical Institute of Radiology in Ljubljana on its 80th anniversary (1923-2003). Historia Magistra Vitae 253 
Jevtic V 
Sonographycally guided hydrostatic reduction of childhood intussusception 269 Vidmar D, Višnar Perovic A 
Demonstration of evolution of hemispherical spondysclerosis by contrast enhanced Gd-DTP A magnetic resonance imaging 275 
Jevtic V, Majcen N 
Radiologic imaging of acute pancreatitis 285 Glušic M, Brencic E, Popovic P 

Magnetic resonance angiography of the portal venous system 291 
Berden P 
Interventional radiology in hemodyalysis fistulae and grafts 299 Šurlan M, Popovic P 
Interventional radiological management of the complications of the renal transplantation 309 
Popovic P, Šurlan K 
Annular pancreas causing extrahepatic biliary obstruction 
Ogulin M, Jamar B 
Clinical importance of portal venous gas detected by abdominal sonography: a report of two cases 329 
Gregoric P, Višnar-Perovic A 
Radiographic, computed tomographic and magnetic resonance imaging appearances of primary V-cutting zone of resorption of lumbar vertebral body in Paget' s disease 
Jevtic V 
A calcified cervical intervertebral <lise in a child and a thoracic <lise calcification in an adult with posterior herniation-radiographic, computed tomography and magnetic resonance imaging findings 
Jevtic V 
Unusual radiographic changes of a gout patient 349 
MarkotaJ 
SLOVENIAN ABSTRACTS 353 
NOTICES 363 
AUTHORS INDEX 2004 


SUBJECT INDEX 2004 
Radio/ Oncol 2004; 38(4): 251-2. 

Editorial 
History of the Clinical Institute of Radiology in Ljubljana on its 80 the anniversary (1923 -2003) 
This issue of Radiology & Oncology is dedicated to 80th anniversary of the Clinical Radiology Institute in Ljubljana, the leading radiological institution in Slovenia since its establishment in 1923. Dr. Vladimir Jevtic presents a short history of the Institute. He especially points out that the main problems throughout the whole history were similar and included the lack of profes­sional and economical independence, as well as the shortage of radiologists and radiographers. Despite serious obstacles 80 years of the Clinical Radiology Institute is a history of successful de­velopment of the republic's central radiological institution, a success based on determination, unity and professional integrity of all its members and management. 
Drs. D. Vidmar and A. Perovic state that sonographically guided hydrostatic reduction of in­tussception, which is the most common cause of bowel obstruction in early childhood represents the method of choice because of its high efficiency, lack of complications and radiation expo­sure. 
Drs. V. Jevtic and N. Majcen evaluate the role of magnetic resonance imaging (MRI) in demonstrating evolution of hemispherical spondylosclerosis, a painful syndrome of unclear eti­ology. They were able to demonstrate some typical MRI features which could be of clinical rele­vance. 
Drs. M. Glušic and E. Brencic rewiev the current concepts of imaging of acute pancreatitis and its relationship to pancreatic functional tests and treatment planning. The importance of ra­diological investigations has been increasing in the last decade as the result of introduction of more sophisticated imaging techniques. 
Dr. P. Berden rewievs the clinical indications, the technique of performance as well as limi­tations of magnetic resonance angiography of the portal venous system. 
Drs. M. Šurlan and P. Popovic rewiev the current knowledge concearning radiological evalu­ation and interventional procedures in patients with hemodyalisis vascular access stressing the importance of endovascular prophylactic dilatation of stenosis, the placement of stents and of recanalisation of trombosed fistulas and grafts. In their second contribution they discuss a com­plex topic of interventional radiological management of the complications following renal trans­plantation. Variety of complications may occur after renal transplantation the most frequent be­ing renal and perirenal fluid collections and abnormalities of the vasculature and collecting sys­tem. Different interventional procedures can be used for treatment such as percutaneous drainage of fluid collections, percutaneous transluminal renal angioolasty without or with stents in renal artery stenosis and some other procedures in relatively uncommon urologic complica­tions. 
The rest of the contributions include presentations of several rare but interesting cases. Drs. 
M. Ogulin and B. Jamar present a case of annular pancreas causing extrahepatic biliary obstruc­tion, Drs. P. Gregoric and A. Perovic stress the clinical importance of portal venous gas detec­
ted by abdominal sonography, Dr. V. Jevtic contribute with demonstration of radiographic, com­puted tomographic and magnetic resonance imaging appearances of primary V-cutting zone of resorption of lumbar vertebral body in a case of Paget's disease and with two cases of calcified cervical intervertebral disc in a child and a thoracic disc calcification in an adult with posterior herniation. Finally Dr. J. Markota concludes the issue with an interesting case of unusual radi­ographic changes of a patient with gout. 
The editor thanks to the authors for their contribution to this issue of Radiology & Oncology dedicated to an extraordinary jubilee, 80th anniversary of the Clinical Institute of Radiology in Ljubljana. 
Guest Editor Professor Vladimir Jevtic 
Radiol Oncol 2004; 38(4): 269-73. 


Sonographycally guided hydrostatic reduction of childhood intussusception 
Dubravka Vidmar, Alenka Višnar Perovic 
Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia 
Background. Intussusception is the most common cause of bowel obstruction in children under two years of age. The proximal part of the bowel and its mesentery (the intussusceptum) enter within that part imme­diately beneath it (the intussuscipiens). Being pulled by peristalsis the mesenterial vessels get compressed which result in ishaemia of the bowel wall. Most intussusceptions are ileocolic. The diagnosis can be con­firmed by a contrast enema or ultrasound. Sonography demonstrates a so-called »target-within-a-target« pat­tern (in cross-section) with thickened edematous bowel wall with or without vascularisation and prestenot­ic dilatation with increased peristalsis. Therapeutic reduction can be attempted by a contrast enema (fol­lowing diagnostic procedure) or by air, both under fluoroscopic monitoring, or by normal saline under sono-graphic guidance. Patients and methods. We detected sonographically intussusception in three girls of 15, 16 and 18 months having typical clinical signs. We continued with hydrostatic reduction under the sonographic guidance. The reduction was attempted with a saline enema on body-temperature, introduced by the equipment for con­trast enema. The bottle of normal saline was hung up 1 m over the examination desk. We needed few liters of saline to replace lost liquids due to the incomplete occlusion of rectum. Meanwhile we monitored the mov­ing of the intussusceptum back into the proximal direction. Criteria for a succesful reduction were the dis­appearance of the intussusceptum and the passage of fluid through the ileocecal valve. Results. Success was proven in all three girls. No complications occured and the pain relieved immediate­ly after the procedure. There were no signs of intussusception on sonography after 2 and 12 hours. We saw a slightly edematous wall of ileocecal valve and terminal ileum. Due to their exellent clinical conditions they were discharged from hospital after a second sonography. Conclusions. Sonographically guided hydrostatic reduction of intussusception in children is a method of choice because of its high efficiency and lack of radiation exposure. No complications have been reported to date. 
Key words: intussusception-therapy-ultrasonography; child 
Received 4 November 2004 Accepted 18 November 2004 
Introduction 
Correspondence to: Dubravka Vidmar MSc, MD, 
Intussusception is the most common cause of 
Clinical Radiology Institute, University Medical 
bowel obstruction in early childhood, with 

Centre Ljubljana, Zaloška 7, SI - 1525 Ljubljana, Slovenia. the peak incidence between 6 months and 2 
years of age.1 It is typically presented with an acute onset of colicky abdominal pain. However, the clinical symptoms can be con­fusing, with recurring non-specific abdomi­nal symptoms, especially when the bowel ob­struction is not complete. Intussusception oc­curs when one segment of the bowel (the in-tussusceptum) becomes telescoped into the immediately distal segment of bowel (the in-tussuscipiens). Once trapped, the invaginat-ed segment is propelled by peristalsis farther into the distal segment, pulling its mesentery along it. Intussusception can develop in any free-moving part of the bowel. However, the vast majority of childhood cases are ileoco-lic;2 that is, the ileum becomes telescoped through the ileocecal valve into the cecum. The mesenteric vessels of the intussusceptum become compressed, which leads to ishemia and eventually bowel necrosis, particularly at the apex of the intussusceptum. 
The diagnosis of intussusception is made by a contrast enema or ultrasound. At the time of diagnosis, a radiologist should at­tempt the reduction of intussusception. A therapeutic reduction can be attempted by a contrast enema (following diagnostic proce­dure) or by air insufflation, both performed under the fluoroscopic monitoring. Recently, a new technique - hydrostatic reduction with ultrasound guidance - has been recognized to be equally successful. 
Patients and methods 
Three female patients, 15, 16, and 18 months of age, with a severe colicky abdominal pain and clinically suspected intussusception were evaluated by sonography. The ileocolic intus­susception was detected in all three cases. The examinations were performed with Toshiba PowerVision 6000 SSA-370A ultra­sound scanner. A diagnostic procedure was continued with hydrostatic reduction under the sonographic guidance. The reduction was attempted with a normal saline enema, warmed to body temperature, introduced by the equipment for contrast enema. To achieve the appropriate hydrostatic pressure within the bowel lumen, the bottle of normal saline was hung up 1 m above the examination desk. To form a tight seal and to reduce leak­age of fluid, the catheter was placed in the rectum through the rubber ring, which was taped to gluteal region. However, the occlu­sion was still incomplete and we had to use several litters of saline to replace lost fluid. During the fluid instillation, we monitored how the intussusceptum proceeded in the proximal direction. The criteria for a success­ful reduction were the disappearance of the intussusceptum, followed by the reflux of flu­id from the cecum through the ileocecal valve into the terminal ileum. The mean time of the reduction procedure was 15 minutes. 
Results 
All three attempts at sonographically guided hydrostatic reduction of intussusception were successful. No complications occurred. The pain relieved immediately after the pro­cedure and the patients recovered quickly. The follow-up sonography scan was per­formed 2 and 12 hours after the procedure. In all three cases follow-up scans showed a slightly oedematous wall of ileocecal valve and terminal ileum and a small quantity of free intraperitoneal fluid. Due to the excellent clinical condition of the patients, they were discharged from hospital after the second fol­low-up sonography. 
Disscusion 
Intussusception is the most common cause of bowel obstruction in early childhood, with the peak incidence between 6 months and 2 years of age.1 It is typically presented with an acute onset of colicky abdominal pain; how­ever, when the bowel obstruction is not com­plete, the clinical symptoms can be confusing with the recurring non-specific abdominal symptoms. Intussusception occurs when one segment of the bowel (the intussusceptum) becomes telescoped into the immediately dis­tal segment of the bowel (the intussuscipi-ens). Once trapped, the invaginated segment is propelled by peristalsis farther into the dis­tal segment, pulling its mesentery along it. The mesenteric vessels of the intussusceptum get compressed, the ishemia and eventually bowel necrosis ensue. The apex of the intus­susceptum is the part most prone to the de­velopment of pathologic changes. Most cases of intussusception are idiopathic, with no identifiable lesion acting as the lead point. Rarely, a mechanical lead point, such as in­testinal polyp, Meckel diverticulum, duplica­tion cyst or lymphoma, can be found. Even more rare is the intussusception in correla­tion with cystic fibrosis, Henoch-Schonlein purpura, hemophilia or intussusception after operative abdominal procedures.2 Intussus­ception can begin in any free-moving part of the bowel; however, the ileocolic intussuscep­tion is the most common, with the ileum be­ing telescoped through ileocelcal valve into the cecum. Less frequently, small - intestinal (segment of small intestine enters into the im­mediately distal segment of the small intes­tine), colo-colic (analogous pathology in the colon) or ileocecal (ileocecal valve is the lead point) types can develop. 

The diagnosis of intussusception is made by a contrast enema or ultrasound. Many pathologic conditions of the bowel wall pro­duce the characteristic sonographic appear­ance of a »target« sign on transverse images. In intussusception this appearance is even more characteristic with a »target-within-a-target« sign on transverse images and »hay-fork« sign on longitudinal scans (Figures 1, 2). 
The inner target represents the intussus­ceptum and the outer target is produced by the intussuscipiens. The wall of the intussus­ceptum is oedematous and therefore hypoe­choic on sonography scans. With Doppler im­aging the presence of compromised/absent blood flow in the bowel wall can be demon­strated, which is important in differentiation from the acute inflammation. The bowel loops proximal to the »target-within-a-target« sign are dilated with increased peristalsis. In all three patients that we examined, the ileo-colic intussusception was detected and the described characteristic signs were clearly visible. Ultrasonography is highly accurate in the diagnosis of intussusception with a speci­ficity of 100% and a sensitivity of 88 - 93%.3,4 



After the diagnosis is made, the primary aim should be a non-operative reduction of the intussusception. Up until recently, the non-operative management included a con­trast enema (barium) or air insufflation, both performed under the fluoroscopic monitor­ing. As ultrasound became the imaging modality more and more used also for bowel pathology, the conditions for sonographically guided reduction of the intussusception were formed. Free intraperitoneal fluid and signs of mechanical ileus are not contraindications for this procedure; the procedure is success­ful also in children with fluid in the peri­toneal cavity.1,5 As the saline fills the colon, the apex of the intussusceptum is observed under the continuous ultrasound guidance as it proceeds in the proximal direction. The cri­teria for a successful reduction are the disap­pearance of »target-within-a-target« sign, vi­sualization of ileocecal valve and reflux of flu­id from the cecum into the terminal ileum (Figure 3).5,6 

To achieve the appropriate hydrostatic pressure within the bowel lumen (at least 60 mmHg, not more than 120 mmHg), the canis­ter used to run normal saline into the rectum should be placed 1 m above the examination desk.1 To avoid hypothermia, the fluid should be warmed to body temperature. Even though the catheter was placed in the rectum through the rubber ring, which was taped to gluteal re­gion, the leakage of saline around the catheter was substantial in all three patients. We need­ed several litters of saline to replace lost fluid. All three attempts at a sonographically guided hydrostatic reduction of intussusception were successful, which was confirmed by two fol­low - up sonographic scans performed 2 and 12 hours after the procedure. According to published data, the sonographically guided hydrostatic reduction of childhood intussus­ception is curative in 76 - 93% of cases.6-10 Riebel et al. reported that, in comparison with other conservative methods of reduction, the success rate of sonographically guided hydro­static reduction of intussusception was not substantially worse (versus that of pneumatic reduction) or was even higher (versus that of barium enema reduction).8 
At both follow-up sonographic scans all three patients had slightly edematous wall of ileocecal valve and terminal ileum, which is in accordance with other studies.1 No compli­cations occurred. The pain relieved immedi­ately after the procedure and the patients re­covered quickly. The review of the available literature also did not reveal any complica­tions of this procedure.1,6-10 The mean time of the reduction procedure was 15 minutes, which is similar to previously published re­ports.6 
Conclusion 
From our initial experience and review of the literature we can conclude that the sono-graphically guided hydrostatic reduction of childhood intussusception is a simple, safe and very successful technique that does not expose the child to ionizing radiation and can in many cases replace operative management. 

References 
1. 
Limberg B. Invagination. In: Limberg B, editor. Sonographie des gastrointestinaltrakts. Berlin: Springer Verlag; 1998. p. 93-7. 

2. 
Eich FG, Willi UV. Acute abdomen in children. In: Krestin GP, Choyke P, editors. Acute abdomen. Stuttgart: Georg Thieme Verlag; 1996. p. 255- 9. 

3. 
Verschelden P, Filiatrault D, Garel L, Grignon A, Perreault G, Boisvert J, et al. Intussusception in children: reliability of US in diagnosis - a prospec­tive study. Radiology 1992; 184(3): 601-2. 

4. 
Bhisitkul DM, Listernick R, Shkolnik A, Donaldson JS, Henricks BD, Feinstein KA, et al. Clinical application of ultrasonography in the di­agnosis of intussusception. J Pediatr 1992; 121(2): 182-6. 

5. 
Feinstein KA, Myers M, Fernbach SK, Bhisitkul DM. Peritoneal fluid in children with intussuscep­tion: its sonographic detection and relationship to successful reduction. Abdom Imaging 1993; 18(3): 277-9. 

6. 
Peh WC, Khong PL, Chan KL, Lam C, Cheng W, Lam WW, et al. Sonographically guided hydro­static reduction of childhood intussusception us­ing Hartmann’s solution. AJR Am J Roentgenol 1996; 167(5): 1237-41. 

7. 
Rohrschneider WK, Troger J. Hydrostatic reduc­tion of intussusception under US guidance. Pediatr Radiol 1995; 25(7): 530-4. 

8. 
Riebel TW, Nasir R, Weber K. US-guided hydro­static reduction of intussusception in children. Radiology 1993; 188(2): 513-6. 

9. 
Wood SK, Kim JS, Suh SJ, Paik TW, Choi SO. Childhood intussuscetion: US- guided hydrostatic reduction. Radiology 1992; 182(1): 77-80. 

10. 
Crystal P, Farber B, Shabshin N, Barki Y. US ­guided hydrostatic reduction of childhood intus­susception. EJU 1999; 10(Suppl 1): 18S. 


Radiol Oncol 2004; 38(4): 275-84. 



Demonstration of evolution of hemispherical spondysclerosis by contrast enhanced Gd-DTPA magnetic resonance imaging 
Vladimir Jevtic1, Natalija Majcen2 
1Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia; 2Radiologica Department, General Hospital Ptuj, Slovenia 
Background. The purpose of the study was to estimate the value of Gd-DTPA magnetic resonance imaging (MRI) in demonstrating the evolution of hemispherical spondylosclerosis (HSS). Patients and methods. In eighteen patients with chronic low back pain and typical radiographic findings of HSS seen on plain films, Gd-DTPA MRI of the lumbar spine was performed. MRI morphological and sig­nal intensity appearances of HSS were analysed and compared with radiographic changes. Results. On the basis of MRI features, three distinct groups of cases were identifiable. Within the first group the region of dome-shaped osteosclerosis demonstrated low signal intensity on T1-weighted precon­trast spin-echo images, high signal intensity on T2-weighted images and diffuse contrast enhancement on T1-weighted postcontrast images, findings compatible with bone marrow oedema and hyperaemia. The sec­ond group showed high signal intensity vertebral body corners surrounded by low signal intensity area, which indicated the combination of fat accumulation and the sclerotic bone. In the third intermediate group anterior disco-vertebral junctions revealed a mixture of MRI appearances characteristic of the first and the second group. Conclusions. Gd-DTPA MRI is capable of demonstrating a spectrum of features which reflect the evolu­tion of HSS. These typical appearances showed by MRI could be of eventual clinical relevance in following the progression of HSS. 
Key words: spinal diseases; magnetic resonance imaging; gadolinium DTPA; osteosclerosis 
Introduction 
The term HSS was used by Dihlmann1 to de­scribe a peculiar form of localised erosive 
Received 3 November 2004 Accepted 18 November 2004 
Correspondence to: Prof. Vladimir Jevtic, MD, Clinical Radiology Institute, University Clinical Centre, Zaloška 7, SI-1525 Ljubljana, Slovenia; Phone/Fax: +386 1 23 23 556; Email: vladimir.jevtic@mf.uni-lj.si 
spondylopathy with well defined radiograph­ic findings. The most typical features include dome-shaped osteosclerosis which usually af­fects the anteroinferior portion of the verte­bral body with the base at the endplate. Commonly, similar appearances are seen in the neighbouring vertebra. Narrowing of the corresponding disc space indicating disc de­generation is present in the majority of cases. There is a predilection for L4, L5 and L3 ver­tebral bodies and the toracolumbar junction. 

HSS mainly affects middle-aged women and is clinically characterized by chronic low back pain. Since its first description in literature as nonneoplastic scleroses,2 different terms like traumatic lesion of the disco-vertebral junc-tion,3 discogenic vertebral scleroses,4 idio­pathic segmental sclerosis5 have been used to indicate the possible aetiology of the disease entity. However, the exact aetiology and pathogenesis of HSS still remains uncertain. Experience with MRI of this condition, espe­cially with the use of paramagnetic contrast agents is limited.6,7 
The purpose of this study was to investi­gate the morphological and signal intensity MRI appearances of HSS, to compare these features with the conventional radiography and to estimate the value of Gd-DTPA MRI in demonstrating the evolution of HSS. 
Patients and methods 
18 patients (12 women, 6 men, mean age 45 years) with radiographic findings typical of HSS seen on AP and lateral plain films of the lumbar spine were selected for the study. In 5 patients, lateral conventional tomograms were also available. In order to be included in the study, the radiographs were required to demonstrate dome-shaped osteosclerosis with the base at the intervertebral disc affect­ing the anterior part of the vertebral body. Other radiographic findings which were also noted included bone erosions of the endplate at the base of sclerosis, new bone production along the anterior vertebral body contour, the presence of an anterior ostephyte and the disc space narrowing.1 Additional inclusion criteria were chronic low back pain and nor­mal erythrocyte sedimentation rate. In six pa­tients, the exacerbation of low back pain was registered during the last several weeks. MRI of the lumbar spine was performed on a 1.5 T superconducting scanner (Magnetom, Siemens) one to three weeks after plain films. 
A spin-echo sequence with T1W images (TR 500 ms, TE 15 ms, 2 averages) and T2W im­ages (TR 1900 ms, TE 80 ms, 2 averages) was used, followed by the postcontrast examina­tion immediately after Gd-DTPA (0.1 mmol / kg body weight) was injected intravenously as a bolus through a cannula. The field of view was 28 cm with a data acquisition ma­trix of 256 x 256. The region of the lumbar spine was presented in a sagittal plane with 5 mm thick consecutive slices. The axial images of the intervertebral discs and the neighbour­ing parts of the vertebral bodies were ob­tained at the levels of HSS seen on plain films. 
Conventional radiographs and MR images were analysed in a qualitative fashion for morphological and signal intensity differ­ences between normal and pathological dis-co-vertebral junctions. On the basis of MRI features, an attempt has been made to recon­struct the eventual evolution of HSS. 
Results 
Three distinct MRI patterns of disco-vertebral junction abnormalities were found at the lev­els of HSS seen on the plain film radiography. Within the first group of three patients the re­gion of dome-shaped osteosclerosis demon­strated low signal intensity on T1-weighted precontrast images, high signal intensity on T2-weighted images and a diffuse intense contrast enhancement on T1-weighted post-contrast images. There was also focal Gd-DT­PA accumulation within the endplate ero­sions at the base of sclerosis. In one of the pa­tients, these typical MRI appearances were seen at the anterosuperior part of the verte­bral body L5 while the neighbouring an-teroinferior part of the vertebral body of L4 showed MRI findings characteristic of the second group (Figures 1a, 1b, 1c). 
The second group comprised five patients with MRI features of high signal intensity an-terior portions of the vertebral bodies on T1­weighted precontrast and T2- weighted im­ages surrounded by a band-like low signal in­tensity area. No contrast enhancement could be registered within the region HSS of (Figures 2a, 2b, 2c). The accumulation of paramagnetic contrast agent within the end-plate erosions was seen in four of these pa­tients. In one of the cases, typical MRI changes developed during the six months fol­lowing a disc surgery. 


In the remainder of the twelve patients, disco-vertebral junctions demonstrated het-erogenous MRI appearances which represent­ed a mixture of signal intensity changes and morphological findings from the first and the second group (Figure 3). A focal contrast en­hancement was seen within the erosions of 

Figure 1b. T1 - weighted sagittal (TR 500 ms, TE 15 ms) precontrast image reveals high signal intensity an-teroinferior part of the vertebral body L4, findings consistent with fat accumulation (big arrow head) and low signal intensity anterosuperior part of the verte­bral body L5 indicating bone marrow oedema (small arrow heads). Note also that the erosion of the verte­bral body L4 is sharply corticated while the erosion at the level of L5 shows indistinct contour. 
the vertebral body endplates. In two of the patients from this intermediate group, MRI showed the posterior disc herniation and in one the presence of ischemic spondylolysis localised at the same level as HSS. 
The erosions of the vertebral body end-plates typically localised at the anterior junc­tions of the peripheral bone rim and the car­tilaginous endplate (Figures 3a, 3b, 3c, 3d, 3e) were identified by MRI in all of the patients. In three cases the erosions were not seen on the plain films. With the exception of six pa­tients belonging to the first and the third group, in whom indistinct cortical bone was revealed (Figure 1); in the rest of the vertebral bodies the erosions were clearly corticated. Additional erosions localised more dorsally were demonstrated in two patients from the second and six from the third group (Figures 4a, 4b, 4c). 



Varying amounts of new bone production along the anterior vertebral body contour contiguous with the anterior ostephytes (Figure 4) were revealed on the plain films in patients from all three groups. However, the signal intensity MRI appearances of the pe­riosteal apposition differed between the groups. Within the first and the second group new bone production was of low signal inten­sity on T1-weighted precontrast images and of high signal intensity on T2-weighted and T1­weighted postcontrast images (Figures 3, 4). 
Similar findings were revealed in one case from the third group, while the rest demon­strated the linear high signal intensity area along the anterior surface of the vertebral bodies on all MRI sequences (Figure 2). 
The anterior ostephytes were more pro­nounced in patients from the second and the third group. Their signal intensity character­istics were similar to MRI features of the neighbouring vertebral body bone marrow. 
At the level of HSS an absence of normal high signal intensity on T2-weighted images affecting the anterior part or the whole disc space indicating disc degeneration was re­vealed in all of our patients with the excep­tion of focally increased signal intensity with­in the bone erosions. 



Discussion 
The exact aetiology and evolution of HSS is not completely clear. Therefore, different terms indicating possible aetiology or radi­ographic features have been applied to this entity.1-5 In comparison to other radiological techniques, MRI proved to have a unique ability not only to present an excellent anatomical image but also to reflect closely pathophysiological and pathoanatomical changes in different osteoarticular diseases. The experience with MRI of HSS is limited6,7 especially with the use of paramagnetic con­trast agent GD-DTPA and no detailed de­scription of the eventual evolution of MRI changes has been made. 
MRI findings of low signal intensity on T1­weighted spin-echo images and of high signal intensity on T2-weighted images within the area of bone sclerosis seen in the patients from the first group (Figure 1) have already been reported.6,7 In addition we were able to demonstrate a marked contrast enhancement affecting the same region. These MRI features were compatible with the presence of bone marrow oedema and hyperaemia. With the exception of different distribution, which has been focal in HSS and widespread in early de­generative disc disease, there was an obvious resemblance in MRI appearances between de­scribed changes in HSS and Modic I lesions8 in which the existence of fibrovascular tissue below the vertebral body endplates was proved histologically. Furthermore, we showed similar focal MRI findings at the an­terior disco-vertebral junctions in patients with ankylosing spondylitis, having early Romanus lesions.9 Some histological studies proved that the bone erosions of the vertebral bodies at the attachment of the annulus fi­brosus in spondylitis anterior were occupied by the vascularised granulation tissue.10,11 Within the so-called Type a localised disco-vertebral destructive lesions, which radi­ographically resemble HSS, Cawley et al12 re­vealed a peripheral focal infiltration by carti­laginous and fibrous tissue, new bone deposi­tion with thickened trabeculae and oedema­tous bone marrow, histological evidence of trauma with persistent pressure. These simi­lar histological and MRI appearances seen in various disco-vertebral lesions are evidently nonspecific phenomena and reflect the limit­ed reactive abilities of the osteoarticular sys­tem to etiologically different joint diseases. 



Within the second group of patients, high signal intensity anterior portions of the verte­bral bodies on T1-weighted precontrast and T2-weighted images, surrounded by a band-like low signal intensity area without contrast enhancement on T1-weighted postcontrast images indicated a bone marrow fat conver­sion combined with a sclerotic bone (Figure 2) nonspecific reaction which has also been de­scribed in longstanding disc degeneration8 or advanced nonactive sacroiliitis.13 
The most numerous was the third interme­diate group of cases in which a combination of signal intensity changes and varying de­grees of contrast enhancement represented a mixture of MRI appearances characteristic of the first and the second group. MRI features within the anterior parts of the vertebral bod­ies were compatible with a combination of bone marrow oedema and hyperaemia, fat ac­cumulation and sclerotic bone (Figure 3). The distribution of these changes within the indi­vidual vertebral bodies suggested the possi­bility that the initial bone marrow oedema at the vertebral body margins has been progres­sively replaced by fatty and sclerotic bone marrow, findings similar to those seen in pro­gressive disc degeneration.8 



The reported incidence of the endplate erosions in HSS varies.1,4 In three of our pa­tients the erosions were not identified on the plain films. However, with the use of MRI as a tomographic method, they were demon­strated in all the cases. This finding supports the opinion of some authors that the anterior defect of the vertebral body endplate repre­sents the initial lesion1,14 and that the com­mon feature in HSS is the herniation of disc material into the vertebral body4 which might be provoked by the subclinical endplate trau­ma.3 The fact that the erosions were not clear­ly corticated in several of the patients from the first and the third group while the major­ity of cases from the third and all from the second group showed corticated erosions, suggests the possibility of advancing process of cortical healing. Gd-DTPA contrast accu­mulation within the erosion was consistent with the histological findings of the focal re­placement of the disc and the disc-bone bor­der by vascularised fibrous tissue in periph­eral disco-vertebral destructive lesions report­ed by Cawley et al.12 
The frequent location of HSS at the lum­bosacral and the toracolumbar junctions has been attributed to the increased stress at these levels produced by the transition of a mobile to a fixed part of the axial skeleton. It has been postulated that the increase in the segmental mobility due to tears affecting the periphery of the intervertebral disc causes the overstretching of the anterior longitudinal lig­ament and provoke the osteoblastic produc­tion of the marginal osteophytes.1 Indeed high signal intensity of the new bone produc­tion and of the contiguous ostephytes on T2­weighted and T1-weighted postcontrast im­ages (Figures 3, 4) consistent with the pres­ence of oedema and hyperaemia may indicate the instability of the corresponding vertebral dynamic segment. On the other hand, the or­ganized periosteal apposition and marginal ostephytes of high signal intensity on all MRI sequences (Figure 2), due to a fat transforma­tion, presumably represent the end stage of 



Figure 4a. Disc degeneration at the level of L4-L5 with HSS affecting the anteroinferior part of the vertebral body L4. Lateral radiograph shows dome-shaped os­teosclerosis (small arrow heads), an anterior erosion of the endplate (big arrow head) and periosteal appo­sition along the anterior surface of the vertebral body (arrow). 
stabilization of abnormally mobile vertebral segments at the level of HSS. 
The clinical relevance of different MRI fea­tures in HSS is not clear. Modic et al8 sug­gested the possibility that early disc degener­ative changes with the presence of subchon­dral bone marrow oedema might be sympto­matic. Stäbler et al15 showed that the Schmorl’s nodes with adjacent bone marrow oedema were seen more frequently in symp­tomatic than in asymptomatic patients. It would seem therefore that the cases of HSS surrounded by widespread bone marrow oedema could eventually represent sympto­matic or »active« lesions. It is of interest to note that all six patients with recent exacer-



Figure 4c. T1-weighted Gd-DTPA postcontrast sagittal image reveals linear contrast enhancement at the an­terior contour of vertebral body L4, the anterior part of the annulus fibrosus L4-L5 (small arrow heads) and within the endplate erosions (big arrow heads). There is no contrast accumulation in the region of osteoscle­rosis. 
bation of low back pain belonged to the first and the second groups in which varying amounts of bone marrow oedema and hyper-aemia were demonstrated by MRI. Analogously, it can be assumed that the cases of HSS similar to Modic II lesions8 seen with­in the second group of our patients are pre­sumably less symptomatic or »nonactive«. 
Although the lack of histology in our study precludes definite conclusions on the basis of the histological results of others3,4,7,8,10-12 and according to MRI appearances in our patients the eventual evolution of HSS could be pos­tulated. The findings are in favour of the the­ory that the initial lesion could be anterior erosion at the junction between the epiphy-seal ring and the cartilage endplate1,3,4,14 fol­lowed by the instability of the corresponding vertebral dynamic segment. Due to a compro­mised vertebral body integrity and resulting instability, the bone underlying erosion is ex­posed to a persistent pressure, which similar­ly to the initial disc degeneration provokes bone marrow oedema and hyperemia.8 The process of repair resembling healing of the fracture12 ensues, characterized by the in­growth of vascular fibrous tissue into the ero­sion and the vertebral body and consecutive new bone production within the bone and along its anterior surface. A favourable out­come may eventually result in which the cor­tication of the endplate erosion, the rein­forcement of the vertebral body in the form of bone sclerosis and the anterior disco-verte­bral junction shown as the organized pe­riosteal apposition and marginal osteophytes lead ultimately to the spontaneous stabiliza­tion of the corresponding vertebral dynamic segment. In cases with an unfavourable out­come the instability persists and may eventu­ally be followed by new bone erosions and the progressive disc degeneration. In our study, MRI proved to be a sensitive indicator of these complex dynamic changes. 
It is concluded that GD-DTPA MRI is ca­pable of demonstrating the evolution of HSS. It seems to enable the differentiation of a spectrum, including the initial phase charac­terized by a compromised integrity of the an­terior endplate, followed by the intermediate phase of reactive changes, leading finally to the stabilization of the abnormally mobile vertebral dynamic segment. MRI appearances could be of eventual clinical relevance in fol­lowing the progression of HSS. 

References 
1. 
Dihlmann W. Hemispherical spondylosclerosis-a polyetiologic syndrome. Skeletal Radiol 1981; 7: 99­106. 

2. 
Ackerman W, Schwarz GS. Nonneoplastic sclero­sis in vertebral bodies. Cancer 1958; 11: 703-8. 

3. 
Martel W, Seeger JF, Wicks JD, Washburn RL. Traumatic lesions of the discovertebral junction in the lumbar spine. Am J Roentgenol 1976; 127: 457­64. 

4. 
Sauser DD, Godman AB, Kaye JJ. Discogenic ver­tebral sclerosis. J Can Assoc Radiol 1978; 29: 44-50. 

5. 
McCarthy EF, Dorfman HD. Idiopathic segmental sclerosis of vertebral bodies. Skeletal Radiol 1982; 9: 88-91. 

6. 
Sobel DF, Zyroff J, Thorne RP. Discogenic verte­bral sclerosis: MR imaging. J Comput Assist Tomogr 1987; 11(5): 855-8. 

7. 
Jensen ME, Hayes CW, DeBlois GG, Laine FJ. Hemispherical spondylosclerosis: MR appear­ance. J Comput Assist Tomogr 1989; 13(3): 540-2. 

8. 
Modic MT, Masaryk TJ, Ross JS, Carter RJ. Imaging of degenerative disc disease. Radiology 1988; 168: 177-86. 

9. 
Jevtic V, Rozman B, Kos-Golja M, Watt I. MR-Bildgebung bei Seronegativen Spondyloarthriti-den. Radiologe 1996; 36: 624-31. 

10. 
Baggenstoss AH, Bickel WH, Ward LE. Rheumatoid granulomatous nodules as destruc­tive lesions of vertebrae. J Bone Joint Surg 1952; 34A: 601-9. 

11. 
Ball J. Entheshopathy of rheumatoid and ankylos­ing spondylitis. Ann Rheum Disease 1971; 30: 213­23. 

12. 
Cawley MID, Chalmers TM, Kellgren JH, Ball J. Destructive lesions of vertebral bodies in ankylos­ing spondylitis. Ann Rheum Disease 1972; 31: 345­58. 

13. 
Ahlström H, Feltelius N, Nyman R, Hšllgreen R. Magnetic resonance imaging of sacroiliac joint in­flammation. Arthritis and Rheumatism 1990; 33: 1763-9. 

14. 
Resnick D, Niwayama G. Segmental sclerosis of vertebral bodies. In: Resnick D,editor. Diagnosis of bone and joint disorders. Philadelphia: W. B. Saundres; 1995. p. 1434-6. 


15. 
Stäbler A, Bellan M, Weiss M, Gartner C, Brossmann J, Reiser MF. MR imaging of enhacing intraosseous disk herniations (Shmorl’s nodes). AJR 1997; 168: 933-8. 

16. 
Herbsthofer B, Eysel P, Eckardt A, Humke T. Diagnostik und therapie der erosiven osteochon­drosis intervertebralis. Zeitschrift fur Orthopadie und Ihre Grenzgebiete 1996; 134(5): 465-71. 


Radiol Oncol 2004; 38(4): 285-90. 



Radiologic imaging of acute pancreatitis 
Mojca Glušic, Erika Brencic, Peter Popovic 
Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia 
Background. Acute pancreatitis comprises a broad spectrum of inflammatory changes in the gland and has a variety of causes. The most common are alcoholism and biliary tract disease. This paper discusses the current concepts of diagnosis and the relationship between morphology as depict­ed by imaging, pancreatic function tests and treatment planning. Conclusions. Our understanding of the morphologic changes produced by the inflammatory process has ex­panded in the last decade as more sophisticated imaging techniques have been used for evaluation. 
Key words: pancreatitis - radiography; acute disease 
Introduction 
Pancreatitis is defined and classified accord­ing to clinical, morphologic and histological criteria. Acute pancreatitis is defined as an acute inflammatory process of the pancreas, caused by activation of the proteolytic en­zymes within the gland.1 
The most common etiologic factors of acute pancreatitis are cholelithiasis and alco­hol abuse, the others are rarer (trauma, sur­gery, ERCP, viral and bacterial infections, pancreatic tumours, drugs, hyperlipopro­teinemia, primary hyperparathyroidism, idio­pathic). 
Received 3 November 2004 Accepted 17 November 2004 
Correspondence to: Mojca Glušic, MD, Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia, SI-1525 Ljubljana, Slovenia; Phone: +386 1 522 85 30. 
The clinical spectrum of acute pancreatitis varies from mild to severe disease. 
Mild acute pancreatitis is the most com­mon form of the disease, and is characterized macroscopically by interstitial - oedematous inflammation of the gland. Microscopic find­ings include infiltration of the interstitial space with leukocytes, occasional small scat­tered foci of acinar cell necrosis, and both in­tra- and peripancreatic fat necrosis. Patients with mild pancreatitis typically present with sudden abdominal pain and tenderness. Fever and leukocytosis may be present. 
Patients with severe acute pancreatitis may initially experience symptoms similar to those in mild disease, but often the pain is worse and they often show additional clinical and laboratory evidence of systemic dysfunc­tion and multisystem failure. The length of hospitalization is longer and may be compli­cated by hypotension, pulmonary insufficien­cy, renal failure, gastrointestinal bleeding, metabolic acidosis, hypocalcaemia, dissemi­nated intravascular coagulation, and sep­sis.1,2 

Clinical diagnosis 
The clinical diagnosis of acute pancreatitis is straightforward when patients present with appropriate symptoms and when laboratory findings are confirmatory. Diagnostic diffi­culties arise when patients present with non­specific symptoms that mimic other acute ab­dominal conditions or when laboratory tests are non-diagnostic. Serum amylase and lipase levels represent the most commonly used lab­oratory tests to diagnose pancreatitis. These test values are imperfect disease indicators, however, because they may be normal in up to 10% of patients. Serum amylase increase is not specific for acute pancreatitis, the height of serum amylase and/or lipase does not cor­relate with the severity of pancreatitis.2,3 
Objective assessment of the severity of an acute attack of pancreatitis is critical to pa­tient management, because the clinician must be able to differentiate mild acute (intersti­tial) pancreatitis from severe acute (necrotiz­ing) pancreatitis. Approximately 50% of pa­tients present with mild acute pancreatitis and require only minimal supportive therapy and limited hospitalization. Mortality is rare in this group unless a serious complication occurs or the disease evolves into a more se­vere form. Patients with severe acute pancre­atitis have mortality rates of 10-20%, with death often due to shock associated with ear­ly respiratory and renal failure or sepsis. 
High-risk patients who may benefit from aggressive clinical and surgical management must therefore be identified. Disease severity can be evaluated objectively using the Ranson criteria: 
- At admission: Age over 55 years White cells over 16000/ mm3 Blood glucose over 11 mmol/l 
LDH over 5.83ukat/l (350UI/l) 
AST over 2.0 ukat/l (250UI/l) 
- During initial 48h: Hematocrit decrease over 10% Blood urea increase over 5 mg/100 ml Calcium less than 8 mg/100 ml (2 mmol/l) PO2 less than 8 kPa (60 mm Hg) Base deficit over 4 mmol/l (mEq/l) Fluid deficit over 6000 ml 
Three or more Ranson criteria depicted during first 48 hours indicate severe acute pancreatitis. Patient with six or more Ranson criteria is very likely to die. 
Radiologic diagnosis 
The primary roles of radiologic imaging in pa­tients with suspected pancreatitis are: 
- 
to confirm or exclude the clinical diagnosis of acute pancreatitis, 

- 
to determine, if possible, the cause of the disease, 

- 
to stage disease severity, 

- 
to detect complications, 

- 
to provide imaging guidance for percuta­neous therapy. 


Contrast-enhanced CT is the imaging modality of choice for evaluating patients with acute pancreatitis.2-5 It can accurately di­agnose and stage the disease as well as pro­vide the necessary information for percuta­neous management. Sonography, endoscopic retrograde cholangiopancreatography, and angiography play secondary roles. Ultra­sound is primarily used to detect biliary stones and to follow the size of pancreatic flu­id collections and pseudocysts. Diagnostic endoscopic retrograde cholangiopancreatog­raphy is seldom performed during acute at­tacks of pancreatitis, because it may exacer­bate the disease or introduce infection. Endoscopic retrograde cholangiopancreatog-raphy with sphincterotomy may be per­formed to alter the course of disease in pa­tients with suspected biliary pancreatitis. Angiography is reserved for diagnosis and treatment of vascular complications.4 

The value of MRI in acute pancreatitis re­mains to be established. Thus far, it has not been widely applied in the care of patients with acute pancreatitis, though it can be used in patients unable to receive iodinated con­trast media.6,8 
On conventional SE and GRE T1-weighted images, the normal pancreas is approximate­ly isointense with the liver. On T2-weighted images the normal pancreas is moderately hy­perintense compared with the liver. T1­weighted breath hold images after bolus in­jection of extracellular contrast agent (gadolinium) show intense parenchymal en­hancement which peaks before the arrival of contrast in the superior mesenteric vein, and fades fairly quickly. The liver-specific con­trast medium manganese-DPDP is also taken up by the pancreatic exocrine tissue, where it produces an increase in signal intensity on T1-weighted images. 
Oedema of the pancreas causes diffuse sig­nal reduction on T1-weighted images and re­duced enhancement after intravenous con­trast agent. In more severe cases unenhanced gradient echo T1-weighted images may show peripancreatic oedema as areas of low signal extending into the fat surrounding the gland. Dynamic post-contrast acquisition is a sensi­tive method for demonstrating the presence and extent of pancreatic necrosis, shown as areas of diminished or absent parenchymal enhancement. Exudate and fluid collections within or around the pancreas can be seen on T1, but are also well shown on T2-weighted images, where they appear as areas of high signal intensity. T2-weighted images also give a clear distinction between the fluid and sol­id components of localized exudates and pseudocysts. This is important in patients who are candidates for percutaneous drainage of pancreatic collections, which of­ten appear as areas of homogeneous low at­tenuation on computed tomography even when the collection is mostly solid. Because of the high sensitivity of gradient echo images to susceptibility effects produced by fresh bleeding, the presence of a hemorrhagic com­ponent in acute pancreatitis is probably de­tectable more readily and over a longer time course by MR than by CT, although the clini­cal value of this finding is still uncertain. 
MRCP - MR cholangiopancreatography 
MRCP provides a non-invasive alternative to diagnostic ERCP, particularly useful in pa­tients in whom ERCP is technically difficult or unsuccessful (e.g. following gastric or pan­creatic surgery, or in patients with tight stric­tures of the main duct). 
MRCP relies on extreme T2 weighting which effectively eliminates signal from all tissues except stationary free water protons, so that the images display only those struc­tures containing localized fluid collections. With careful selection of the imaging volume, a demonstration of the pancreatic duct and the main bile ducts can be obtained. 
MRCP has the advantage of being com­pletely non-invasive, however it does not of­fer the opportunity to carry out therapeutic procedures, it is also contraindicated in pa­tients with metallic clips or stents, with ex­ception of titanium, relatively lower resolu­tion also limits the demonstration of branch ducts, except when they are evidently dilated. 
CT should be performed at the peak of pancreatic arterial perfusion using thin-sec­tion (5 mm or less) scanning. 
CT finding of mild acute pancreatitis is a slight to moderate increase in the size of the pancreas. Although pancreatic enlargement is typically diffuse with associated contour ir­regularity, it can be segmental, most com­monly involving the head. As disease severity increases, evidence of peripancreatic inflam-matory stranding is seen, manifesting as in­creased density to the surrounding fatty tis­sue, thickening of the peripancreatic fascial planes, and heterogeneity of the pancreatic parenchyma. Rupture of the secondary pan­creatic ductules leads to both intra- and ex-travasation of pancreatic secretions. In such cases, CT reveals both intrapancreatic and peripancreatic fluid collections. They are composed of blood, pancreatic enzymes, flu­id, and debris. Acute collections have fluid density, lack an inflammatory capsule or wall, and are confined by the anatomic space in which they form. They are most commonly seen adjacent to the pancreas in the anterior pararenal space and the lesser sac. Extensive collections may spread throughout the peri­toneal cavity, and may dissect as far as the neck, pericardium, pleura, mediastinum, and groin. Solid organ involvement within the hi-lar regions of the spleen, kidneys, and liver can also occur. 

Pancreatic necrosis is defined as focal or diffuse areas of unenhancing, nonviable pan­creatic parenchyma. Regions of necrosis show no or diminished enhancement. In a large series of patients who underwent both CT and surgery, Berger et al. showed CT to have an overall accuracy of 87% in diagnosing necrosis. CT specificity was 100% when necrosis involved more than 30% of the gland. A 21% false-negative rate was seen in patients with minor (less than one third) necrosis, which fell to 11% in those patients with major (greater than 50%) necrosis.4 
Local complications of acute pancreatitis 
Acute fluid collections may be seen in 40 ­50% of patients with acute pancreatitis. Approximately 50% are small and resolve spontaneously. Collections which persist may evolve into pancreatic pseudocysts, a process requiring at least 4 weeks. 
Pseudocysts are encapsulated collections which appear marginated on CT because of a nonepithelialized inflammatory fibrous wall or capsule. Approximately half of all pseudo-cysts resolve spontaneously, especially unin­fected pseudocysts less than 5 cm in diame­ter. Those which do not may either stabilize or decrease slightly in size, remaining clini­cally asymptomatic, or they may enlarge and cause complications. Major pseudocyst com­plications shown by CT include arterial pseudoaneurysm formation, with or without cyst hemorrhage, superinfection (suggested by air within the cyst), venous occlusion (sug­gested by perigastric and mesenteric varices), biliary and gastrointestinal tract obstruction, and solid organ invasion. 
Local septic complications 
Sterile necrosis, defined as pancreatic necro­sis without infection, must be differentiated from both infected necrosis and pancreatic abscess. The mortality of infected necrosis (39-67%) is significantly greater than that as­sociated with sterile necrosis (13-14%) These entities may be distinguished if evidence of bacterial infection is obtained by CT-guided fine-needle aspiration.9 Accurate differentia­tion of infected pancreatic necrosis from pan­creatic abscess is also essential. Infected necrosis carries a much higher morbidity and mortality than does pancreatic abscess.9 
Pancreatic abscess is a localized collection of pus located near the pancreas. In contrast to infected necrosis, which can develop at any time during the course of acute pancre­atitis, pancreatic abscesses typically present 4 weeks or more after the onset of symptoms. A pancreatic abscess may be diagnosed by CT if a fluid collection containing liquid pus is identified adjacent to a normally enhancing pancreas. 
Pancreatic ascites presents as free in-traperitoneal fluid containing high amylase levels. It is usually seen in more severe forms of pancreatitis, only rarely in association with a normal-appearing pancreas. 

Pancreatic haemorrhage may be seen in cases of traumatic pancreatitis, as well as in cases of severe acute pancreatitis where sig­nificant hemorrhagic had necrotizing compo­nents coexist. 
Besides local complications severe forms of acute pancreatitis are often accompanied by systemic complications - hypotension, pul­monary insufficiency, renal failure, gastroin­testinal bleeding, metabolic acidosis, hypocalcaemia, disseminated intravascular coagulation, sepsis. 
Staging of acute pancreatitis2-5,9 
CT scan provides important information in accordance with the Balthazar-Ranson crite­ria of severity, where inflammatory process 
and gland necrosis are separately graded.  
Inflammatory process (a): Grade A Normal pancreas Grade B Focal or diffuse enlargement of pancreas Grade C Pancreatic and peripancreatic inflammatory changes Grade D Single fluid collection Grade E Two or more fluid collections and/or the presence of gas in/or adjacent to pancreas  0 1 2 3 4  
Gland necrosis (b): No necrosis Less than 30% 30-50% Greater than 50%  0 2 4 6  
CT severity index (CTSI): a+b.  

Patients with a CTSI of 0-3 show a 3% mor­tality rate and an 8% morbidity rate, whereas in patients with a CTSI of 7-10, mortality and morbidity rates are 17 and 92% (Figure 1). 
CT retains a disadvantage of exposure to x rays, which is of importance in younger pa­tients and in patients in whom CT examina­tion is repeated. 
Value of CT examination is limited in pa­tients, in whom intravenous contrast agent is contraindicated, due to severe renal insuffi­ciency or allergy. 
In patients with suspected severe acute pancreatitis, early CT study is suggested by many authors for confirmation of the diagno­sis and detection of severity of disease. It should be done within 24-48 hours from the beginning of the disease. CT should be re­peated in 7-8 days, or earlier in case of clini­cal deterioration. 
Conclusions 
Pancreatic necrosis, depicted by CT scan, and peripancreatic inflammatory collections are the two prognostic indicators of severity of acute pancreatitis. The most serious compli­cations develop in patients with peripancreat­ic collections and some of these patients die. Such complications occur mostly in individu­als with associated early or late pancreatic necrosis. In most individuals fluid collections tend to resolve spontaneously if the pancreas maintains its integrity. 
The limitations of the early CT examina­tion are related to potential development of complications in patients with a normal pan­creas, as well as to the development of late pancreatic necrosis in these individuals. For these reasons, patients with peripancreatic 

Figure 1. Mortality, morbidity according to CT index. 

fluid collections, pancreatic necrosis, or both should undergo follow-up CT examination in 7-8 days or earlier if their clinical condition deteriorates. 
To improve the prognostic accuracy of the initial CT examination, a CT severity index, based on combined assessments of peripan­creatic inflammatory collections and degree of pancreatic necrosis, was developed. 
Patients with a high CT severity index (7 to 10 points) showed a 92% morbidity and a 17% mortality, whereas those with a low severity index (0 to 3 points) had 3% morbidity and no mortality. 
Detection of pancreatic necrosis, either at the first examination or at follow-up study, or a high CT severity index at the initial CT ex­amination are ominous predictive indicators of severe pancreatitis, which enable the radi­ologist to identify a group of patients in whom most life-threatening complications will occur. 
References 
1. 
Kocijancic A, Mrevlje F. Interna medicina. Ljubljana: DZS; 1993. p. 408-10. 

2. 
Banks PA. Practice guidelines in acute pancreati-tis. Am J Gastroenterol 1997; 92: 377-83. 

3. 
Balthazar EJ, Robinson DL, Megibow AJ, et al. Acute pancreatitis: Value of CT in establishing prognosis. Radiology 1990; 174: 331-6. 

4. 
Balthazar EJ, Freeny PC, van Sonneneberg E. Imaging and intervention in acute pancreatitis. Radiology 1994; 193: 297-306. 

5. 
Elmas N. The role of diagnostic radiology in pan-creatitis. Eur J Radiol 2001; 38: 120-32. 

6. 
Semelka RC, Ascher SM. MR imaging of the pan­creas. Radiology 1993; 188: 593-602. 

7. 
Kumbasar B, Acunas B. Interventional radiology in inflammatory pancreatic disease. Eur J Radiol 2001; 38: 133-6. 

8. 
Ito K, Koike S, Matsunaga N. MR imaging of pan­creatic diseases. Eur J Radiol 2001; 38: 78-93. 


9. Birnbaum BA. Imaging in acute pancreatitis. Radiology of the liver, biliary tract, and pancreas, cate­gorical course syllabus American Roentgen Ray Society. San Diego: 1996. p. 151-6. 
Radiol Oncol 2004; 38(4): 291-7. 


review 


Magnetic resonance angiography of the portal venous system 
Pavel Berden 
Clinical Institute of Radiology, Clinical Medical Centre, Ljubljana, Slovenia 
Background. Imaging of the portal venous system is necessary in different clinical conditions. Three-di­mensional (3D) contrast-enhanced magnetic resonance angiography (MRA) is useful in obtaining high qual­ity portal vein images. A fast gradient-echo MR imaging sequence with minimum repetition time and echo time is used. Up to 40 ml of paramagnetic contrast is injected into peripheral vein as a bolus. The Arrival of contrast medium in the aorta is preferably detected with an automated system, when breath-hold sequence is started, and repeated two times, to depict arterial and venous phase. Maximum-intensity-projection (MIP) imaging is the usual postprocessing method. Conclusions. In patients with portal hypertension, MRA can present collateral pathway and patency of the portal vein or portosystemic shunt. In portal vein thrombosis MRA provides information about the location and length of portal vein obstruction and helps in therapeutic strategy decision. MRA is a proper technique in Budd-Chiari syndrome, where it is important to determine the location and length of hepatic outflow ob­struction. MRA is a very good modality before liver transplantation to depict vascular anatomy and portal vein patency, and after liver transplantation to image possible liver complications. Its limitations include in­appropriate positioning of the 3D acquisition slab, respiratory motion artefacts, and metal implants (e.g. pacemaker). 
Key words: portal vein; magnetic resonance angiography; vascular patency 
Introduction 
The portal venous system must be evaluated before planning the treatment of patients with portal hypertension, portal vein throm­bosis, hepatic veins occlusion or a tumour of the liver, pancreas, or bile duct. 
Received 3 November 2004 Accepted 18 November 2004 
Correspondence to: Pavel Berden, MD, MSc, Clinical Institute of Radiology, Clinical Medical Centre, Zaloška 7, SI-1000 Ljubljana, Slovenia. Phone: +386 1 522 3415. E-mail: pavel.berden@kclj.si 
Colour Doppler ultrasonography (US), catheter angiography, computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) can be used for portal ve­nous system imaging. Colour Doppler US is non-invasive, relatively inexpensive and can provide information on portal blood flow, but it is operator and patient dependent (acoustic window, uncooperative patient).1 Catheter angiography (indirect portography, percuta­neous transhepatic portography, and direct splenoportography) are invasive and limited by flow dynamics.2 CTA can demonstrate the portal venous system in a short time, but this technique uses ionizing radiation and re­quires a large amount of iodinated contrast material.3 

Three-dimensional (3D) contrast-enhanced magnetic resonance angiography (MRA) was initially used manly in arteriography of the aorta and renal arteries.4,5 Respiratory motion had previously been a major source of arte-fact in abdominal imaging. With faster se­quences it has become evident that this tech­nique has greater capability in abdominal and liver imaging. MRA has the ability to cover large regions of interest within a single breath hold. Superb images of the portal, mesenteric and systemic veins can be obtained routinely. Source images can be obtained to help evalu­ate parenchymal lesions. The combination of parenchymal and vascular information allows accurate staging of liver neoplasm. In addi­tion, vascular complications of hepatic trans­plantation can be clearly demonstrated with MRA.6 Its advantages over digital subtraction angiography (DSA) include its large field of view, its short imaging time, and its non-in­vasive nature and low risk of complications, which permit repeated studies. 
In this article, we briefly discuss some technical aspects of 3D contrast enhanced MRA, reformatting methods and limitations. We present the advantages of MRA in differ­ent clinical conditions - portal hypertension, portal vein thrombosis, Budd-Chiari syn­drome and liver transplantation. 
Technique 
A fast 3D spoiled gradient-echo MR imaging sequence with minimum repetition time and echo time is used, with low flip angles rang­ing from 20° to 30°. Tissue contrast is low; vascular contrast is achieved with high in-travascular concentrations of gadolinium, which is injected intravenously as a bolus. By the time extra cellular contrast agent reaches the portal vein, it is rather diluted. That is why a dose of 0.2 to 0.3 mmol/kg body weight and flow rates from 2.5 to 4 ml/sec are recommended.7 
The best images are obtained when the ac­quisition of the central portion of k-space cor­responds with the maximum concentration of contrast material in the vessels of interest.6 The range of contrast travel times is broad and depends on patient age, cardiovascular status and hydration state; it is advisable to perform timing with a test bolus,8 or prefer­ably, with an automated triggering, in which the vessel of interest is continuously scanned until the signal intensity reaches a specified level - at that time the 3D sequence is star­ted.9 Centric phase encoding is used in con­junction with these techniques; central k space, which is responsible for image con­trast, is acquired at the beginning of the scan, when vascular contrast is maximal.10 
These timing strategies are generally used to optimize the arterial-phase imaging. Acquiring two additional 3D volumes after the optimized arterial-phase imaging almost always yields good visualization of the portal and systemic veins with one or both of the later sequences.6 
Our typical portal MRA examination con­sists of axial fast spin-echo MR imaging through the region of interest. This is useful for the evaluation of liver and spleen and helps determine landmarks for the 3D vol­ume. A contrast bolus - 40 ml of Magnevist with flow-rate 2.5 ml/s is then injected. Smartprep (GE Medical Systems) is used to automatically detect arrival of contrast medi­um in the aorta. The arterial-phase breath-hold sequence in coronal plane is acquired 5 seconds after the arrival of contrast medi­um in the abdominal aorta. The first-phase sequence is followed immediately by two ad­ditional acquisitions with 10 seconds interse­quence delay. One sequence takes 14 to 20 seconds, depending on volume of interest. Before the examination, patients were in­structed in breath-holding in the same posi-tion. A final post-MR angiography axial fat-saturated spoiled gradient-echo sequence is performed to help visualize parenchymal le­sions. 

Data processing 
Data processing is an important aspect of 3D contrast-enhanced MRA. A variety of refor­matting techniques are now available to the radiologist, and each technique has its own strengths and weaknesses, which can lead to pitfalls and artefacts in inexperienced hands. It is important to be well versed in different reformatting techniques. 
Maximum-intensity-projection (MIP) im­aging is the most common method. It is well suited to contrast-enhanced MRA, particular­ly arterial-phase imaging, in which back­ground signal is low and arterial contrast is high. MIP images obtained from the entire data set are almost always contaminated by artefacts, which can limit the visibility of ves­sels. Image quality can be improved by ob­taining sub volume MIP images or by manu­ally editing the entire data set.6 Subtraction of a precontrast data set from the arterial- phase data to eliminate background noise is prob­lematic in the abdomen, where any discrep­ancy in breath holding between acquisitions can result in misregistration artefact. Arterial-phase images of the abdomen are almost al­ways diagnostic without subtraction (Figure 1a) as long as good bolus timing has been achieved. Subtraction is much more useful in the venous phase.11 Even in imperfect sub­traction conditions due to different breath-hold positions between each acquisition, ex­cellent suppression of arterial signal and en­hancement of adjacent organs can be ob­tained after post-processing by using a partial volume MIP technique (Figure 1b).12 We rou­tinely use subvolume MIP in three orthogonal and oblique projections if necessary (depend­ing on patient anatomy). We improve portal venous images by subtracting the arterial phase from the portal venous phase image us­ing available software. 
However, source images should be exam­ined too, because nonocclusive thrombus can easily be missed on MIP images and subtrac­tion is an artificial technique. Volume render­ing, surface rendering, and virtual endoscopy may be useful in certain applications.13 
Clinical applications 
Contrast-enhanced 3D MRA can demonstrate the intrahepatic and extrahepatic portal ve­nous system as well as hepatic veins. Clinical applications of this method include portal hy­pertension (portosystemic shunt, portal vein obstruction, and hepatic vein obstruction), hepatic encephalopathy, hepatocellular carci­noma and pancreatobiliary tumours and liver transplantation (pre-and posttransplantation evaluation).14 In patients with portal hyper­tension, MRA can be used to evaluate por­tosystemic shunt, hepatopetal collateral path­ways, and obstruction of the portal or hepat­ic veins. In planning treatment for hepatic en­cephalopathy, it is important to identify the causative portosystemic shunt. In patients with hepatocellular carcinoma or pancreato-biliary tumours, one must determine the presence or absence of portal vein invasion when planning treatment. 



Portal hypertension 
Different pathologic conditions like liver cir­rhosis, chronic hepatitis, and Budd-Chiari syndrome can lead to portal hypertension and hepatic encephalopathy. It is important to evaluate portosystemic collateral pathways because such patients are at high risk of he­patic coma and massive haemorrhage from oesophagogastric varix. Portosystemic shunts can be formed anywhere in the abdomen and include oesophagogastric varix, paraumbili-cal vein, mesenteric-gonadal, mesenteric­retroperitoneal, intrahepatic portosystemic, and splenorenal shunts. Therefore, it is nec­essary to examine the whole abdomen.14 
Hepatic encephalopathy is caused by a massive portosystemic shunt, which can be easily detected with MRA, as well as oesoph­agogastric varices, especially when MRA is performed with arterial-phase subtraction (Figures 2a, 2b). 
Artificial portosystemic shuts (surgical or percutaneous transhepatic-TIPS) are used to reduce flow and pressure in varix and dimin­ish the risk of variceal bleeding. 3D contrast MRA can be a useful guide for shunt plan­ning and it can present shunt patency. MRA assesses patency of any kind of shunt, as long as metallic clips do not obscure portal venous anatomy. TIPS shunts are more difficult to assess due to metallic stents. If the stainless steel stent is used to bridge the portal and systemic venous systems, the lumen cannot be evaluated by MRA.7 In conjunction with phase contrast techniques, shunt flow vol­ume can be determined non-invasively.15 



Portal vein thrombosis 
Different pathologic conditions can cause portal vein thrombosis, like pancreatitis, por­tal hypertension, trauma, malignancy and co­agulopathy.16 The acutely thrombosed portal vein is expanded with thrombus and contains no flow. Over time portal venous collateral pathways develop in both hepatopetal and hepatofugal directions. Hepatopetal collateral pathways include the cavernous transforma­tion of the portal vein that develops in main portal vein obstruction, the dilated pancreati­coduodenal venous arcades that develop in superior mesenteric vein obstruction and the dilated gastroepiploic, short gastric, and coro­nary veins that develop in splenic vein ob­struction. Cavernous transformation of the portal vein represents a network of small col­lateral vessels (Figure 1b). It is identified by characteristic enhancement pattern in the he­patic hilum during portal venous phase of MRA.17 
It is important to assess portal venous pa-tency in these diseases. MRA provides infor­mation about the location and length of por­tal vein obstruction and also about portal col­lateral pathways.18 In potential candidates for liver transplantation, it is necessary to evalu­ate portal venous patency.19 
Budd Chiari 
Budd-Chiari syndrome is a rare disorder characterized by hepatic outflow occlusion and is difficult to diagnose by any method.7 It is caused by various conditions including congenital or idiopathic obstruction, hepatic vein thrombosis, hepatic veno-occlusive dis­ease after liver transplantation, and hepatic tumours. The major symptoms are ascites, hepatomegaly, and abdominal pain. It is clas­sified into three types according to the loca­tion of the occlusion. Type 1 is defined as oc­clusion of the inferior vena cava, type 2 as oc­clusion of major hepatic veins and type 3 as obstruction of the small centrilobular venules. Imaging methods should help in de­cision, whether it can be treated with antico­agulants, surgery, or interventional proce­dures. In planning treatment, it is important to determine the location and length of he­patic outflow obstruction.14 MRA is an ap­propriate technique to diagnose hepatic vein occlusion. Budd-Chiari can be confirmed by observing absence of hepatic veins and more heterogeneous enhancement of peripheral liver.7 
Liver transplantation 
Patent portal vein is required for liver trans­plantation. When ultrasound fails to ade­quately visualize the portal vein, MRA offers a safe and accurate imaging of portal venous anatomy and anatomy of others important veins - inferior vena cava, superior and inferi­or mesenteric vein, splenic vein and varices.7 

Following liver transplantation, MRA is a very good modality to image possible liver complications. In suspicion of allograft is-chemia, portal vein is the first to evaluate, since blood supply to the liver is primarily via this vessel. The most common site of stenosis is at the anastomosis. Hepatic artery is much smaller in calibre and eventual stenosis of this vessel is difficult to assess.20 Throm­bosed artery results in ischemia of the com­mon bile duct which can lead to biliary stric­tures and leaks. Inferior vena cava (IVC) anastomoses may also become flow limiting ­IVC is generally well depicted on portal phase of MRA. 
Before MRA, T1- and T2-weighted images should be performed to look for possible oth­er postoperative complications - abscesses, fluid collections, hepatic masses. With fast breath-hold sequences even biliary obstruc­tion may be evaluated. 
Limitations 
General contraindications to MR imaging (pacemakers, aneurysm clips, or claustro­phobia) also apply to contrast-enhanced 3D MRA, which has several other limitations. 
This technique is unable to demonstrate the flow direction of the portal venous sys­tem, unlike phase-contrast or time-of-flight MRA.15 Metallic clips, stents, and emboliza­tion coils can cause considerable artefact and obscure important structures. Artefacts from respiratory motion and peristaltic bowel movement degrade image quality, especially in debilitated patients who are unable to hold their breath. When subtraction techniques are used, respiratory misregistration also de­grades image quality.14 Even when the study is optimal, the resolution of gadolinium-en­hanced MR angiography is relatively low compared with that of conventional angiogra­phy, and visualization of small peripheral ar­teries is very limited.6 There is a risk of aller­gic reactions to contrast media, although the incidence is low. Gadolinium-enhanced MR angiography, although less expensive than conventional angiography, is still an expen­sive examination. 
Conclusion 
A precise assessment of the portal vein and collateral pathways is potentially helpful for treatment and planning purposes. Three-di­mensional gadolinium-enhanced MRA is helpful in evaluating the anatomy of the por­tal venous system and its pathologic condi­tions, such as portosystemic shunt, portal vein thrombosis, portal vein invasion by he­patic and pancreatobiliary tumours, and he­patic vein obstruction.21 It is frequently use­ful in both pre- and postoperative imaging of artificial portosystemic shunts and liver transplant recipients. 
A variety of methods to increase the speed of 3D acquisition are under investigation.22,23 Time-resolved MR angiographic techniques allow repeated acquisition of a volume of in­terest during the passage of the contrast ma­terial bolus. Novel imaging and reformatting techniques may allow faster acquisition or improved resolution. Echoplanar imaging may become a viable alternative to the stan­dard gradient-echo acquisition.6 
Several intravascular contrast agents are currently undergoing clinical trials. These agents have much longer vascular half-lives and may allow high-resolution imaging of the arterial and venous system with appropriate respiratory gating.24,25 
MRA combines speed, excellent contrast, and relative simplicity and has been applied to virtually all regions of the body from the brain to the extremities. 

References 
1. 
Johansen K, Paun M. Duplex ultrasonography of the portal vein. Surg Clin North Am 1990; 70: 181­90. 

2. 
Gaylord GM, Davis LP. Hepoatobiliary and pan­creatic imaging. In: Gaylord GM, Davis LP, Baker SR, editors. Diagnostic and interventional radiology ­a clinical manual. Philadelphia: W.B. Saunders Company; 1989. p. 157-75. 

3. 
Brink JA. Spiral CT angiography of the abdomen and pelvis: interventional applications. Abdom Imaging 1997; 22: 365-72. 

4. 
Leung DA, McKinnon GC, Davis CP, Pfammatter T, Krestin GP, Debatin JF. Breath-hold contrast-en­hanced three-dimensional MR angiography. Radiology 1996; 200: 569-71. 

5. 
Prince MR. Gadolinium-enhanced MR aortogra­phy. Radiology 1994; 191: 155-64. 

6. 
Glokner JF. Three-dimensional gadolinium-en­hanced MRA angiography: applications for ab­dominal imaging. Radiographics 2001; 21: 357-70. 

7. 
Portal venous system. In: Prince MR, Grist TM, Debatin JF, editors. 3D contrast MR angiography. 3rd edition. New York: Springer-Verlag; 2003. p. 171-84. 

8. 
Hany TF, McKinnon GC, Leung DA, Pfammatter T, Debatin JF. Optimization of contrast timing for breath-hold three-dimensional MR angiography. J Magn Reson Imaging 1997; 7: 551-6. 

9. 
Prince MR, Chenevert TL, Foo TK, Londy FJ, Ward JS, Maki JH. Contrast-enhanced abdominal MR angiography: optimization of imaging delay time by automating the detection of contrast material arrival in the aorta. Radiology 1997; 203: 109-14. 

10. 
Shetty AN, Bis KG, Vrachliotis TG, Kirsch M, Shirkhoda A, Ellwood R. Contrast-enhanced 3D MRA with centric ordering in k space: a prelimi­nary clinical experience in imaging the abdominal aorta and renal and peripheral arterial vascula­ture. J Magn Reson Imaging 1998; 8: 603-15. 

11. 
Lebowitz JA, Rofsky NM, Krinsky GA, Weinreb JC. Gadolinium-enhanced body MR venography with subtraction technique. AJR Am J Roentgenol 1997; 169: 755-8. 

12. 
Nishida N, Sakai G, Morimoto A, Isota M, Kaminou T, Matsuoka T, et al. Gadolinium en­hanced three-dimensional magnetic resonance portography with subtraction. Brit J Radiol 2001; 74: 147-52. 


13. 
Calhoun PS, Kuszyk BS, Heath DG, Carley JC, Fishman EK. Three-dimensional volume rendering of spiral CT data: theory and method. Radiographics 1999; 19: 745-64. 

14. 
Okumura A, Watanabe Y, Dohke M, Ishimori T, Amoh Y, Oda K. Contrast-enhanced three-dimen­sional MR portography. Radiographics 1999; 19: 973-87. 

15. 
Applegate GR, Thaete FL, Meyers SP, Davis PL, Talagala SL, Recht M, et al. Blood flow in the por­tal vein: velocity quantitation with phase-contrast MR angiography. Radiology 1993; 187: 253-6 

16. 
Abbitt PL. Portal vein thrombosis: imaging fea­tures and associated etiologies. Curr Probl Diagn Radiol 1992; 21: 115-47. 

17. 
Glassman MS, Klein SA, Spivak W. Evaluation of cavernous transformation of the portal vein by magnetic resonance imaging. Clin Pediatr 1993; 32: 77-80. 

18. 
Leyendecker JR, Rivera E, Washburn WK, Johnson SP, Diffin DC, Eason JD. MR angiography of the portal venous system: techniques, interpre­tation, and clinical applications. Radiographics 1997; 17: 1425-43. 

19. 
Shaked A, Busuttil RW. Liver transplantation in patients with portal vein thrombosis and central portocaval shunts. Ann Surg 1991; 214: 696-702. 

20. 
Stafford-Johnson DB, Hamilton BH, Dong Q, Cho KJ, Turcotte JG, Fontana RJ, et al. Vascular com­plications of liver transplantation: evaluation with gadolinium-enhanced MR angiography. Radiology 1998; 207: 153-60. 

21. 
Saddik D, Frazer C, Robins P, Reed W, Davis S. Gadolinium-enhanced three-dimensional MR por­tal venography. AJR Am J Roentgenol 1999; 172: 413-7. 

22. 
Sodickson DK, Manning WJ. Simultaneous acqui­sition of spatial harmonics (SMASH): fast imaging with radiofrequency coil arrays. Magn Reson Med 1997; 38: 591-603. 

23. 
Peters DC, Korosec FR, Grist TM, et al. Undersampled projection reconstruction applied to MR angiography. Magn Reson Med 2000; 43: 91­101. 

24. 
Kroft LJ, de Roos A. Blood pool contrast agents for cardiovascular MR imaging. J Magn Reson Imaging 1999; 10: 395-403. 

25. 
Knopp MV, von Tengg-Kobligk H, Floemer F, Schoenberg SO. Contrast agents for MRA: future directions. J Magn Reson Imaging 1999; 10: 314-6. 


Radiol Oncol 2004; 38(4): 299-308. 


review 


Interventional radiology in haemodialysis fistulae and grafts 
Miloš Šurlan, Peter Popovic 
Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia 
Background. The aim of the paper is to review the role of interventional radiology in the management of haemodialysis vascular access. The evaluation of patients with haemodialysis vascular access is complex. It includes the radiology/ultrasound evaluation of the peripheral veins of the upper extremities with venous mapping and the evaluation of the central vein prior to the access placement and radiological detection and treatment of the stenosis and thrombosis in misfunctional dialysis fistulas. Preoperative screening enables the identification of a suitable vessel to create a haemodynamically-sound dialysis fistula. Clinical and ra­diological detection of the haemodynamically significant stenosis or occlusion demands fistulography and endovascular treatment. Endovascular prophylactic dilatation of stenosis greater than 50% with associated clinical abnormalities such as flow-rate reduction is warranted to prolong access patency. The technical suc­cess rates are over 90% for dilatation. One-year primary patency rate in forearm fistula is 51%, versus graft 40%. Stents are placed only in selected cases; routinely in central vein after dilatation, in ruptured vein and elastic recoil. Conclusions. Thrombosed fistula and grafts can be declotted by purely mechanical methods or in combi­nation with a lytic drug. The success rate of the technique is 89-90%. Primary patency rate is 8% to 26% per year and secondary 75% per year. 
Key words: kidney failure, chronic; hemodialysis; catheters, indwelling; radiology, interventional 
Introduction 
Renal failure is treated by dialysis or renal transplantation. About 63% of patients are treated with haemodialysis, 9% with peri­toneal dialysis and 28% with renal transplan-
Received 3 November 2004 Accepted 20 November 2004 
Correspondence to: Prof. Miloš Šurlan, MD, PhD, Clinical Radiology Institute, University Clinical Centre, Zaloška 7, SI-1525 Ljubljana, Slovenia; Phone/Fax: +386 1 23 23 556; E-mail: milos.surlan@kclj.si 
tation.1 Haemodialysis can be performed through central venous catheters (internal jugular, subclavian and femoral vein) or through a permanent arteriovenous access. Long-term patency of central catheters is low, because they are prone to infection and thrombosis.2 Chronic haemodialysis is per­formed by the autogenous arteriovenous fis­tula and the synthetic bridge graft. Native fis­tulas are the most durable type of vascular ac­cess and least prone to complications.3 A re­cent American article reported 54% primary patency for grafts at one year, compared with 75-91% for native fistulas.4 Peritoneal dialysis is performed after placement of an abdominal catheter and uses the peritoneum as the ex­change membrane. Renal transplantation has become the treatment of choice for end-stage renal disease (ESRD) because of long-term survival and improved life quality in cases when transplantation is performed instead of haemodialysis. Because of the limited long­term patency of haemodialysis grafts or fistu­las, repeated surgical or percutaneous radio­logical repair is necessary to preserve the long-term patency of the dialysis access, and preservation or improvement of the renal function. Percutaneous radiological treat­ment provides the least invasive procedure, intended to prolong life of the dialysis grafts or fistulas. 

Radiological management and endovascular treatment haemodialysis fistulas and grafts 
The first indications for interventional radiol­ogy were stenoses, which were difficult to treat surgically because of their location (cen­tral veins) or because of their propensity to early recurrence. The first radiological reports in 1980s were disappointing due to inade­quate armamentarium and the inexperience of radiologists.5 In the last decade, a decisive turning point came with the availability of high-pressure balloons, hydrophilic guid­ewires, stents, declotting techniques such as the pulse-spray and thromboaspiration, which helped radiologist to improve success rates.3,6 The advantages of the endovascular approach-minimal invasiveness, better imag­ing and better venous preservation - rapidly became very clear. The publication of the American DOQI guidelines in 1997 gave the first official recognition to the value of inter-ventional radiology for the treatment of both stenoses and thrombosis.7 
Radiological patient evaluation prior to access placement 
The role of preoperative screening is twofold: first, to identify usable vessel to create auto-genous fistulas or a synthetic bridge graft, and second to detect occult central venous stenosis. Radiological screening is performed by ultrasound, venography, and in future it will also be done by MRI.8-10 This helps sur­geons to create native or good synthetic grafts fistulas. Native fistulas, which are never used and early graft failures, are associated with the common problem of inadequate vessel (artery or vein) selection. Patients with ESRD often have multiple venepunctures and nu­merous intravenous accesses inserted and thus increased likelihood of venous stenosis or occlusion. Robbin found that 77% [40 of 
52] of patients had a history of previous cen­tral catheter placement or major surgery in which a central catheter may have been placed.10 Thirteen patients [25%] had a histo­ry of catheter placement on the same side as the planned haemodialysis access. 
A patient who has had prior central ve­nous catheterisation (jugular or subclavian) should be screened with venography and ul­trasound to exclude occult central venous stenosis. Surratt et al. found a 40% prevalence of subclavian vein stenosis in patients who had previously had dialysis catheterisation in this venographic study.11 Occult central ve­nous stenosis is nearly always asymptomatic, and becomes unmasked only when high ve­nous flow occurs due to the ipsilateral fistula or graft. Patients may develop marked arm swelling, which can impair wound healing as well as impede the use of the vascular access. Therefore, if central venous stenosis is de­tected, serious consideration should be given to placing access in the opposite extremity. 
With ultrasound, vessels can be assessed for size, stenosis, and occlusion.9-13 Although ultrasound can be used to evaluate the veno-graphic anatomy of the arm, venography can provide the access surgeon with a »road map« of the entire arm. It also excludes central ve­nous stenosis.8,9 Venography is performed by puncturing the dorsal vein of the hand. Opacification of the forearm veins is obtained after placement of a tourniquet in the upper arm in order to create congestion. The venous status (presence, absence, mean diameter, stenosis, and occlusion) of the cephalic and basilic vein in the forearm, at the elbow and in the upper arm can be evaluated as well as the patency of the central veins. Care should be taken to image the axillary vein with the arm in abducted position to avoid pseu­dostenosis. In cases of contraindications to iodine injection (for example allergy or previ­ously non-dialysed patients), carbon dioxide gas or gadolinium can be used as contrast agents.13 

Radiological stenosis detection and indication for treatment 
The underlying stenosis is predominantly present at the venous anastomosis of the graft, in the revealed area of the forearm na­tive fistulas and in the venous outflow far from the anastomosis of upper arm fistulas.14 The underlying stenosis is unmasked in more then 85% of cases thrombosis the grafts and in almost all cases for native fistulas.14,15 Thrombosis occurs roughly 10 times more frequently on prosthetic grafts then in native fistulas.15 
Among the numerous methods described for stenosis screening, radiologists can use ul­trasound and MRI examinations.7,16 Ultrasound provides both anatomic and physiologic information that can be useful in screening and problem-solving.17 The typical ultrasound findings in access stenosis in­clude areas of locally increased velocity (greater than 400 cm/sec) and/or turbulence and the detection of hypoechogenic material consisting of intimal hyperplasia forming an anatomically visible stenosis. Duplex ultra­sound is able to diagnose efferent vein stenoses with an accuracy of 96%, synthetic graft stenoses with an accuracy of 86%, and anastomotic stenoses in native fistulas with an accuracy of 81%.16,18 Doppler measure­ment of velocity is then multiplied by the cross-sectional area of the graft to give vol­ume flows in millilitres per minute. Normal graft usually has volume flows well in excess of 1300 ml/minute, and it has been shown that volume flow less than 300 ml/minute or 450 ml/min is correlated with impending graft failure.19 Ultrasound evaluation can be performed on abnormalities on puncture sites including pseudoaneurysms, aneurysm dilatations of cephalic vein (which usually are not clinically significant) and aneurismal di­latation in PTFE grafts, which can be very sig­nificant. Patients with non-invasively estab­lished haemodynamic significant stenosis or occlusion require fistulography and endovas­cular treatment (Figures 1, 2, 3).4,20,21 
Dialysis fistulography is the least invasive method. Fistulography can be performed with the dialysis needles in place. The only, if any, risks involved in the procedure are the risk of contrast allergy and further reduction in residual renal function,21 The latter consid­eration can be obviated with carbon dioxide or gadoliniums fistulography in selected cas­es.13 A well-performed fistulogram is the foundation of all percutaneous interventions in haemodialysis access (Figures 1a, 2a, 4a). The technique of fistulography has been well­described.5 A complete fistulogram must show the entire ingraft or fistulas from the ar­terial side all the way through to the venous circulation, with evaluation of the venous outflow, and the central veins (Figure 1a). 
DOQI guidelines 10 and 17 recommend treating stenoses greater than 50% only when there are concomitant clinical abnormalities and flow-rate reduction or pressure changes.7 Dilatation of asymptomatic stenosis detected by systematic colour flow duplex ultrasonog­raphy was beneficial only for »virgin« grafts (those that had never been previously dilated 


Figure 1. Fistulography. a. Stenosis in the anastomosis fistulae between brahial artery and cephalic vein, due to neointimal hyperplasia. b. PTA with 8 mm balloon; c. the result is a good anastomosis patency 
or revised). The treatment of haemodynami­cally significant stenosis reduces the rate of thrombosis and prolongs the average use-life of the access.8, 22-26 
Nevertheless, clinical examination should remain the key detection method. Clinical ab­normalities include direct palpation of the stenosis under the skin and localised loss or reinforcement of the thrill. Stenosis of the ar­terial inflow or stenoses located in the anas­tomotic area can be responsible for a fistula, which is too flat, or for vacuum phenomena during dialysis. Stenosis in the cannulation areas can make routine needling difficult. Venous stenosis located far from the anasto­mosis causes congested fistula with loss of thrill, increased compression times after dial­ysis with formation of aneurysms and the de­velopment of collaterals. Finally, limb oede-ma indicates central venous obstruction (Figures2a, 4a). However, once haemodynam­ically significant stenosis is detected, the op­timal timing of treatment for the prevention of thrombosis remains to be determined for both fistula and graft. 
Dialysis-access thrombosis is usually de­tected clinically. A graft that no longer has a palpable pulse or thrill is clearly thrombosed and does not need any further evaluation for the diagnosis of access failure. Native fistu­las, on the other hand, characteristically de­velop only thrombosis of segments of their venous outflow, and ultrasound and/or fistu­lography can be extremely helpful in delin­eating the length of thrombosis, as well as the character of venous reconstruction above the thrombosis site. Fistulography is usually done in anticipation of the percutaneous treatment of thrombosis and is extremely useful in planning revascularisation. 
Endovascular treatment, haemodialysis access, native fistulas and grafts 
Treatment of venous stenosis is important clinically because it preserves the access sites for future use. 
Percutaneous angioplasty 
Percutaneous transluminal angioplasty, which is an outpatient procedure, successful­ly treats over 80% of stenosis in both native and synthetic fistulas and in both venous and 
tracts.4,6,14,20,21 
arterial outflow Angioplasty can be performed on both anastomotic and more proximal lesions including central stenoses (Figures 1a, 1c, 2b, 2c). Prospective angioplasty of all venous stenoses that nar­row the lumen by more than 50% improves fistula function and prolongs access survival. Angioplasty therapy is safe, effective, and easily performed, and has become a standard therapy for the management of venous steno-sis affecting dialysis-access fistulas and 

graft.6,20,21 
Direct fluoroscopy observation is neces­sary to perform angioplasty, with digital ca­pability being very advantageous. Hepa­rinisation is unnecessary. During dilatation, flow is occluded for only short intermittent periods, and clotting of the access therefore rarely occurs. Because the procedure is po­tentially very painful, the patient requires ad­equate sedation.21 Patients must be moni­tored very closely during this process. Since the requirements for adequate sedation varies considerably, the dosage must be care­fully titrated. 
Before angioplasty fistulography was per­formed to evaluate the anatomy and patholo­gy of the fistulas or graft and its draining veins up through the superior vena cava (Figures 1a, 2a, 4a). The needle is inserted an-terograde into the shunt-leading vein or graft. A hydrophilic-coated, steerable, 0.035-inch Terumo guidewire is passed up through the stenoses to the level of central veins. In cases where the vein is tortuous or occluded in a short segment, guidewire manipulation is al­so required with diagnostic catheter support, which can be a considerable challenge. A bal­loon catheter is passed over the guidewire and advanced to the most central lesion. It is important for the balloon to be slightly larger than the affected vein and that a high-pres­sure balloon is used.4,21 The basic technique of angioplasty as applied to the access graft and associated venous range is dependent upon the use of a large diameter, high-pres­sure balloon catheter. Unless the veins are unusually small, a 6-8 mm balloon is used in both graft and peripheral veins and a 12 mm balloon is used centrally. A pressure of 10 at­mospheres is routinely utilized. If this is not effective in breaking the lesion, pressures of 15 and 20 atmospheres are sequentially ap­plied. The balloon is allowed to remain ex­panded for one to two minutes, with each in-


Figure 2. A patient with malfunctional forearm dialysis fistulas and oedema of the arm. Fistulography. a. High grade stenosis of the right brachiocephalic vein (arrow); b. PTA with the high pressure balloon; c. the result is a good patency. 
flation. Multiple dilatations are used for re­sistant lesions. Post-procedural fistulography is performed to assess and document the re­sults of the therapy (Figures 1c, 2c, 4d). The ability to measure intra-access blood flow im­mediately after the procedure may also prove beneficial.18 Haemostasis is obtained follow­ing the removal of the vascular sheath by manual compression. Using a bandage is rel­atively inexpensive and very effective in most cases. 
Patency rates with angioplasty vary ac­cording to the follow-up period and the types of access and vessel treated. Unfortunately stenoses do recur relatively rapidly. The largest series of angioplasty grafts have high success rates ranging from 94 to 98% in unas­sisted (or primary) patency rates, ranging from 17 to 40% at one year.4-6,21 Over the pe­riod of a year, secondary patency rates of 82% and 85% were obtained in the forearm and in the upper arm respectively, but with more frequent reintervention in the upper arm (11 vs. 18 months). The initial success rate gener­ally ranges from 80-94%.14,21 The unassisted patency rate for angioplasty generally ranges from 31-45% per year. The only two large se­ries for forearm native fistulas reported a suc-cess rate ranging from 91-95% and one-year primary patency rates from 44-51%.4,5,21 This article also presents the positive influence of the age of the vascular access on the outcome dilatation of fistulas. Manninen reports a sig­nificantly poorer outcome when stenoses were located near the anastomosis and when the feeding artery was »small«.22 When the outcomes of each of the lesions were com­pared to that of the anastomosis group, long venous, midgraft and subclavian groups had statistically inferior unassisted patency rates.4,21 The poorest results e to be found in the literature are those associated with simple dilatation of the central vein (23 to 29% pri­mary patency rate at 6 months).26 Angio­plasty treatment of venous stenosis based on prospective monitoring for increasing steno-sis is effective. It results in a decreased inci­dence of thrombosis and extended usability of the dialysis vascular accesses.4-6,21 

Complications associated with venous an­gioplasty include severe allergy to iodine, in­fection, thrombosis and vein ruptures. Loss of vascular access following vessel rupture or thrombosis has become extremely rare, since stents and catheter thrombectomy are avail­able. After a seemingly effective dilatation, some lesions recoil, which may occur imme­diately or over a period of days after the pro­cedure.4,20,21 Deaths related to procedures are extremely rare.4 
Use of stents for venous stenosis associated with dialysis vascular access 
The role of the endoluminal stent in the man­agement of venous stenosis of dialysis access is unclear. Although stents can help manage some access difficulties, they are not perma­nent solutions. There is a consensus concern­ing the value of stent placement for the rup­ture of an outflow vein after balloon angio­plasty, when prolonged balloon inflation fails23 and for treatment of stenosis recoil. Elastic lesion may first completely dilate with the angioplasty balloon; significant residual stenosis occasionally remains, suggesting an elastic lesion. The use of stent is suggested in cases of the rapid recurrence of stenotic le­sion following angioplasty (Figure 4). Are stents significant for delaying restenosis? Same authors report intervals between inter­ventions that double in length after stent placement, others disagree.4,24-26 The pres­ence of residual stenosis or developed throm­bosis after stent placement might indicate in­sufficient pre-dilatation, and placement of stent during incomplete declotting proce­dures. In general, a 50% post-angioplasty stenosis may be used as a threshold for fur­ther intervention with stent. However, all au­thors of recent literature agree that only self-expandable stents should be placed in dialy­sis access and that indication must be select­ed. The diameter of the stent must be at least 1 or 2 mm larger than the diameter of the largest balloon used to dilate the stenosis. Its length should be as short as possible, to cov­er the lesion only. The stent must not be placed in stenotic lesions that cannot be di­lated or a stenotic lesion at a venous anasto­mosis. At the venous anastomosis, a forearm fistula or graft stent can overlap the basilic vein and prevent the future creation of trans­posed brachiobasilic fistulas, or protruded stents into the subclavian vein from the final arch of the cephalic vein in which it could in­duce stenosis, which would preclude the fu­ture use of the basilic and axillary veins for direct fistula drainage of an upper arm graft. A stent placed in the subclavian vein must not overlap the ostium of a patent internal jugular vein. This vein is essential for placing the central catheter or for bypassing a subcla­vian stenosis. In order to avoid inducting stenosis on the contra-lateral trunk, a stent placed in the right or left brachiocephalic vein must not protrude into the superior vena ca-va. The stent must be placed in the brachio-cephalic trunk only, without overlapping ei­ther the subclavian or internal jugular os­tium. This means, however, that future access 


Figure 4. A patient with malfunctional dialysis fistulas and oedema of the arm. Fistulography. a. High grade steno-sis of the subclavian vein with collateral flow (arrow). b. PTA with high pressure balloon of 12 mm diameter. c. Relatively good result after the PTA; d. better result after the placement of the stent. 
sites must be anticipated before placing the stents. Authors recommend primary stent placement due to poor results after simple central vein dilatation (Figures 4b, 4c, 4d).24,25 
Primary patency rate following the venous use of stents is relative poor, being approxi­mately 20% per year. However, with aggres­sive re-intervention, the cumulative patency rate is roughly around 70% per year. Modalities that have been used for stent maintenance include thrombolysis, stent an­gioplasty, new stent, and the use of the Simpson or Redha atherectomy device. As previously mentioned, the principal difficulty underlying the inability to maintain patency is the development of neointimal hyperpla­sia. 
The six-month and one-year stent primary patency rate in central veins was only 42% and 20%. Haage (84% and 54% respectively) and Mickely (90% and 70% respectively) ob­tained better results.24,25 
The most typical complication is inaccu­rate placement or migration of stents.24,25 Only two casualties have been reported linked to stent placement, by infection and presumed right atrium perforation.4 
Endovascular treatment of dialysis fistula thrombosis 
The most common complication of perma­nent vascular access are thromboses which, when not mended, account for 80 to 85% of access loss. The major predisposing factor is stenosis on vein side anastomosis of the vas­cular access, responsible for 85% of thrombo-sis.2,4,6,14,20,21 Other causes of fistula throm­bosis include arterial stenosis, post-dialysis fistula compression, hypotension, increased haematocrit levels, hypovolemia, or hyperco­agulable states.4,6,27 The therapeutic options of fistula thrombosis include surgical thrombectomy, thrombolysis with throm­bolytic agents, thromboaspiration and me­chanical dissolution. If these modalities are successful, a fistulogram can then be per­formed and detected stenoses treated with angioplasty or surgical revision.4-6,14,20 
Surgical thrombectomy is a quick, outpa­tient procedure, has a very low complication rate, and is initially successful in 90% of cas­es.4,21 However, failure to correct the under­lying outflow stenosis leads to rapid rethrom­bosis. 
The endovascular declotting techniques published to date can be divided into phar­maco-mechanical and purely mechanical methods. The earliest attempts to treat fistula thrombosis with thrombolytic agents, such as urokinase and streptokinase, originally yield­ed disappointing results.27 However, recent dosing adjustments and technical advances have improved the success rate and reduced the incidence of bleeding in patients for whom there is no contraindication to throm­bolytic therapy.28 For example, the use of the pulse-spray technique, which combines thrombolytic therapy with hydromechanical clot disruption, rapidly established access pa-tency in over 90% of cases with minimal com­plications. The pulse-spray method consists of placing two multi-sideholed catheters with tip-occluding wires in a criss-cross fashion in the thrombosed graft. The forceful and rapid injection of 0.2-0.3 ml aliquots of a 10 ml mix­ture combining 250,000 units of urokinase and 5000 units of heparin are than applied every 30 sec. to each catheter with a tuber­culin syringe. The successful administration of tissue plasminogen activator has also been reported. 
Pharmaco-mechanical methods include thrombolytics at low or high dose, infused lo­cally through regular needles or specific catheters for some minutes or hours before detachment or the crushing of residual thrombus with a balloon, more rarely with an aspiration catheter. These were previously described as the Bookstein »pulse-spray« method, the Cynamon »lyse and wait« method, the Goodwin and Craggbrush infu­sion technique.28-30 The commonly occurring venous stenosis should be corrected. 

Purely mechanical methods include clot extraction or disruption methods with the Trerotola and Sharaffuddin balloon-based methods, the Beathard spray-spray with saline method, the manual catheter-directed thromboaspiration, the Schmitz-rode rotating pigtail and all kinds of declotting devices. The major concern regarding these techniques is the possibility of clinically significant pul­monary emboli developing. To reduce the possibility of large pulmonary emboli, a de­vice has been developed which consists of a high speed rotating camp tip which pulver­izes the clot into tiny particles such as: Arrow-Trerotola PTD, Hydrolyser, Amplatz Thrombectomy device and many others that are likely to appear. 
The technical success rates for pharmaco-mechanical and mechanical methods are 89­95%. Long-term primary patency rates are rel­atively poor in all reports, ranging from 8 to 26% per year.4,21 However, secondary patency rates of 75% have been reported.4 Treatment results of native fistula are better.4,21,31 
The rates of significant complications range from 0-9%.4,21 Complications include thrombus migration and vessel rupture, re­garded as a significant complication, as well as infection, ischemic hand, remote or local bleeding, requiring transfusion or surgery, pseudoaneurysms and fluid overload.4,5,31-33 
The mortality rate is low. Literature re­ports data on just six casualties linked to the declotting procedure. The causes of death were pulmonary or septic embolism and hemiplegia due to paradoxical embolism in patients with a patent foramen ovale and a right-to-left shunt.4 
References 
1. Windus D. A Nephrologist’s approach to the dial­ysis patient. J Vasc Intervent Radiol 2001; 12(Suppl 1, Part 2): P39-42. 
2. 
Hodges TC, Fillinger MF, Zwolak RM, Walsh DB, Bech F, Cronenwett JL. Longitudinal comparison of dialysis access methods: Risk factors for failure. J Vasc Surg; 1997; 26: 1009-19. 

3. 
Ascher E, Hingorani A, Mazzariol F, Gunduz Y, Fodera M, Yorkovich W. Changes in the practice of angioaccess surgery: Impact of dialysis outocme and quality initiative recommendations. J Vasc Surg 2000; 31: 84-92. 

4. 
Turmel-Rodrigues L, Pengloan J, Bourquelot P. Interventional radiology in hemodialysis fistulae and grafts: Multidisciplinary approach. Cardiovasc Intervent Radiol 2002; 25: 3-16. 

5. 
Gaux JC, Bourquet P, Raynaud A, Seurot M, Cattan S. Percutaneous transluminal angioplasty of stenotic lesions in dialysis vascular accesses. Eur J Radiol 1983; 3: 189-93. 

6. 
Turmel-Rodrigues L, Pengloan J, Baudin S, Testou D, Abaza M, Dahdah G, et al. Treatment of steno-sis and thrombosis in haemodialysis fistulas and grafts by interventional radiology. Nephrol Dial Transplant 2000; 15: 2029-36. 

7. 
Schwab SJ, Besarab A, Beathard G, Brouwer D, Etheredge E, Hartigan M, et al. NKG-DOQI clinica practice guidelines for vascular access. Am J Kidney Dis 1997; 30(Suppl 1): 56-62. 

8. 
Geoffroy O, Tassart M, La Blanche AF, Khalil A, Duedal V, Rossert J, et al. Upper extremity digital subtraction venography with gadoterate meglu-mine before fistula creation for hemodialysis. Kidney Int 2001; 59: 1491-7. 

9. 
Menegazzo D, Laissy JP, Dürbach A, Debray MP, Messin B, Delmas V, et al. Hemodialysis access fis­tula creation: Preoperative assessment with MR venograhy and comparison with conventional venography. Radiology 1998; 209: 723-8. 

10. 
Robbin ML, Gallichio MH, Deierhoi MH, Young CJ, Weber TM, Allon M. US vascular mapping be­fore hemodialysis access placement. Radiology 2000; 217: 83-8. 

11. 
Surratt RS, Picus D, Hicks ME, Darcy MD, Kleinhoffer M, Jendrisak M.. The importance of preoperative evaluation of the subclavian vein in dialysis access planning. AJR Am J Roentgenol 1991; 156: 623-5. 

12. 
Malovrh M. Native arteriovenous fistula: preoper­ative evaluation. Am J Kindey Dis 2000; 39(6): 1218­25. 

13. 
Spinosa D, Angle F, Hagspiel K, Schenk W, Matsumoto A. CO2 and gadopentetate dimeglu-mine as alternative contrast agents for malfunc-



tioning dialysis grafts and fistulas. Kidney Int 1998; 54: 945-50. 
14. 
Kanterman R, Vesely T, Pilgram T, Guy B, Windus D, Picus D. Dialysis access grafts: Anatomic loca­tion of venous stenosis and results of angioplasty. Radiology 1995; 195: 135-9. 

15. 
Silva M, Hobson R, Pappas P, Jamiz Z, Araki C, Goldberg M, et al. A strategy for incerasing use of autogenous hemodialysis procedures: Impact of preoperative noninvasive evaluation. J Vasc Surg 1998; 27: 302-8. 

16. 
Robbin ML, Oser RF, Allon M, Clements MW, Dockery J, Weber TM, et al. Hemodialysis access graft stenosis: US detection. Radiology 1998; 208: 655-61. 

17. 
Oudenhoven L, Pattynama P, de Roos A, Seeverens H, Rebergen S, Chang P. Magnetic res­onance, a new method for measuring blood flow in hemodialysis fistulae. Kindey Int 1994; 45: 884­9. 

18. 
Nonnast-Daniel B, Martin RP, Lindert O, Mugge A, Schaeffer J, vd Lieth H, et al. Colour Doppler ul­trasound assessment of arteriovenous haemodial­ysis fistulas. Lancet 1992; 339: 143-5. 

19. 
Sands J, Young S, Miranda C. The effect of doppler flow screening studies and elective revisions in dialysis access failures. ASAIO J 1992; 38: M524-7. 

20. 
Shwab S, Oliver M, Suhocki P, McCann R. Hemodialysis arteriovenous access: Detection of stenosis and response to treatment by vascular ac­cess blood flow. Kidney Int 2001; 5: 358-62. 

21. 
Beathard G. Angioplasty for arterovenous grafts and fistulae. Semin Nephrol 2002; 22(3): 202-10. 

22. 
Manninen HI, Kaukanen ET, Ikaheimo R, Karhapaa P, Lahtinen T, Matsi P, et al. Brachial ar­terial access: endovascular treatment of failing Brescia-Cimino hemodialysis fistulas—initial suc­cess and long-term results. Radiology 2001; 218: 711-8. 

23. 
Raynaud A, Angel C, Sapoval M, Beyssen B, Pagny J, Auguste M. Treatment of hemodialysis access rupture during PTA with Wallstent implantation. J Vasc Interv Radiol 1998; 9: 437-42. 

24. 
Mickley V, Görich J, Rilinger N, Storck M, Abendroth D. Stenting of central venous stenoses in hemodialysis patients: Long-term results. Kidney Int 1997; 51: 277-80. 

25. 
Haage P, Vorwerk D, Piroth W, Schuermann K, Guenther R. Treatment of hemodialysis-related central venous stenosis or occlusion: Results of 


primary Wallstent placement and follow-up in 50 patients. Radiology 1999; 212: 175-80. 
26. 
Hoffer E, Sultan S, Herskowitz M, Daniels I, Sclafani S. Prospective randomized trial of a met-alic intravascular stent in hemodialysis graft main­tenance. J Vasc Interv Radiol 1997; 8: 965-73. 

27. 
Young AT, Hunter DW, Castaneda-Zuniga WR, So SK, Mercado S, Cardella JF, et al. Thromobsed syn­thetic hemodialysis access fustulas: Failure of fib-rinolytic therapy. Radiology 1985; 154: 639-42. 

28. 
Valji K, Bookstein J, Roberts A, Oglevie S, Pittman C, O’neil M. Pulse-spray pharmacomechanical thrombolysis of thrombosed hemodialysis access grafts: Long-term experience and comparison of the original and current techniques. AJR Am J Radiol 1995; 164: 1495-500. 

29. 
Cynamon J, Lakritz P, Wahl S, Bakal C, Sprayregen S. Hemodialysis graft declotting: Description of the »Lyse and Wait« technique. J Vasc Interv Radiol 1997; 8: 825-9. 

30. 
Goodwin S, Arora L, Razavi M, Sayre J, Mc Namara T, Yoon C. Dialysis access graft thrombol­ysis: Randomized study of pulse-spray versus con-tinous urokinase infusion. Cardiovasc Intervent Radiol 1998; 21: 135-7. 

31. 
Turmel-Rodrigues L, Pengloan J, Rodrigue H, Brillet G, Lataste A, Pierre D, et al. Treatment of failed native arterio-venous fistulae for hemodialy-sis by interventional radiology. Kidney Int 2000; 57: 1124-40. 

32. 
Haage P, Vorwerk D, Wildberger J, Piroth W, Schurmann K, Guenther R. Percutaneous treat­ment of thromobosed primary arteriovenous he-modialysis access fistulae. Kidney Int 2000; 57: 1169-75. 

33. 
Kinney T, Valji K, Rose S, Yeung D, Oglevie S, Roberts A, et al. Pulmonary embolism from pulse-spray pharmacomechanical thrombolysis of clot­ted hemdialysis grafts: urokinase versus he-parinized saline. J Vasc Interv Radiol 2000; 11: 1143-52. 


Radiol Oncol 2004; 38(4): 309-21. 


review 


Interventional radiological management of complications in renal transplantation 
Peter Popovic, Katarina Šurlan 
Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia 
Background. The most frequent radiologically evaluated and treated complications in renal transplantation are perirenal and renal fluid collection and abnormalities of the vasculature and collecting system. Renal and perirenal fluid collection is usually treated successfully with percutaneous drainage. Doppler US, MRA and digital subtraction angiography (DSA) are most important in the evaluation of vascular complications of re­nal transplantation and management of the endovascular therapy. Conclusions. Stenosis, the most common vascular complication, occurs in 1% to 12% of transplanted renal arteries and represents a potentially curable cause of hypertension following transplantation and/or renal dysfunction. Treatment with percutaneous transluminal renal angioplasty (PTRA) or PTRA with stent has been technically successful in 82 to 92% of the cases, and graft salvage rate has ranged from 80-100%. Complications such as arterial and vein thrombosis are uncommon. Intrarenal A/V fistulas and pseudoa­neurysms are occasionally seen after biopsy, the treatment requires superselective embolisation. Urologic complications are relatively uncommon; they consist predominantly of the urinary leaks and urethral ob­struction. Interventional treatment consists of percutaneous nephrostomy, balloon dilation, insertion of the double J stents, metallic stent placement and external drainage of the extrarenal collections. The aim of the paper is to review the role of interventional radiology in the management of complications in renal trans­plantation. 
Key words: kidney transplantation; renal artery obstruction; radiology interventional; angioplasty, balloon 
Introduction 
Renal failure is treated by dialysis or renal transplantation. Renal transplantation has become the treatment of choice for end-stage 
Received 3 November 2004 Accepted 20 November 2004 
Correspondence to: Peter Popovic, Clinical Radiology Institute, University Clinical Centre Ljubljana, Zaloška 7, E-mail: peter.popovic@kclj.si 
renal disease (ESRD) because of long-term survival and improved life quality in cases when transplantation is performed instead of hemodialysis.1-3 The most frequent renal transplantation complications are the follow­ing: renal and perirenal fluid collections, de­creased renal function, and abnormalities of the vascular, tubular system, and renal parenchyma. Postoperative fluid collections are common, after transplantation, and they include haematomas, seromas, urinomas, lymphoceles and abscesses. Vascular compli­cations of transplantation include occlusion or stenosis of the arterial or venous supply, arteriovenous fistulas, and pseudoaneury­sms. Urological complications consist pre­dominantly of urinary leaks and urethral ob­struction. Percutaneous and endovascular management of these complications has be­come an important component in the man­agement of transplant patients and has led to further improvement in graft salvage rates. 

Perirenal fluid collections 
Perinephric fluid collections are the most common complications in renal transplanta­tion, occurring in approximately 50% of trans­plant patients.4 The majority of these are asymptomatic, but approximately 15 to 20% may cause symptoms secondary to local mass effect that can produce pain, hydronephrosis, lower extremity oedema and compromise transplant function.4,5 These fluid collections can also become secondarily infected. The majority of these collections can be detected by ultrasound (US). US-guided aspiration and drainage is essential for the correct diagnosis and management of symptomatic post trans­plant fluid collections. However, computer tomography (CT) often delineates fluid collec­tions and their anatomic relationship to adja­cent structures better than US, particularly in obese patients. In addition, puncture and drainage can be performed with CT guidance in cases when US fails to demonstrate access to the collection. 
Lymphoceles 
Lymphocele formation is a late complication of renal transplantation caused by lymphatic obstruction or leak. It can occur in up to 15% of renal transplantations.6,7 Simple needle as­piration of the fluid using sterile technique will make the diagnosis. At biochemical analysis, a lymphocele has the same levels of protein, urea nitrogen, creatinine, elec­trolytes, and occasionally, lipids as serum, so differentiation from urinoma, haematoma, seroma, or abscess is possible.8-10 Most lym­phoceles are discovered incidentally, are small or sterile and asymptomatic, and do not require therapy. If symptomatic, they are usu­ally secondary to local mass effect, with com­pression of the urethra resulting in hy­dronephrosis, compression of the iliac vein with resultant lower extremity oedema, or deep venous thrombosis, or a combination of both. Only rarely cases do secondary com­pression of renal artery lead to postoperative hypertension. Symptomatic lymphoceles can be treated with either percutaneous or surgi­cal techniques. Despite the relatively high success rates of surgical treatment (90% suc­cess rate), open surgery carries more risks, greater morbidity and longer hospitalisa­tion.10-13 The operation of choice is laparo­scopic peritoneal marsupialisation (fenestra­tion) of the cyst into the peritoneal cavity. The major advantage of the laparoscopic ap­proach is the absence of postoperative ileus, with the opportunity to continue the enteral immunosuppressive regimen and a lower re­currence rate (4%).5,13 Percutaneous therapy varies from simple aspiration to placement of a drain (Figures 1a, 1b), with or without scle­rotherapy. Percutaneous needle aspiration is the usual technique for diagnosis, but simple percutaneous aspiration of the lymphocele re­sults in 80%-90% recurrence rate and an in­fection of 25%-50%.5,14-16 Indwelling catheter drainage alone has been reported in most se­ries as reaching cure rates of 50%-80%.8,12,17,18 The introduction of a sclerosing agent in con­junction with catheter drainage has improved success rates to 79%-94%, with recurrence rate up to 31%.9,10,12,19-22 A number of agents, including povidone iodine, bleomycin, alco­hol, doxycycline and talc have been used for sclerosis, but none of these agents universal­ly. The major advantage of percutaneous drainage and sclerotherapy is the very low in­cidence of major complications. The most fre­quently reported complication is secondary infection of the lymphocele, with reported rates of 7%-17%.14,23-25 The major disadvan­tages of percutaneous drainage and scle­rotherapy are the need for multiple treat­ments and the requirement of the catheter to be left in place for a significant period of time. 

Urinomas 
Urinomas due to extravasations of urine from the renal pelvis, urethra, or ureteroneocys­tostomy usually occur in the first 1-3 weeks following transplantation and may result from of disruption of the ureterovesical anas­tomosis, incomplete bladder closure, is-chemia of the collecting system, post biopsy injury, or severe obstruction. The diagnosis is usually made by US or CT. Characterisation of the fluid can be achieved by obtaining a sample via US-guided aspiration and deter­mining the creatinine concentration of the sample. After confirmation of the diagnosis, percutaneous catheter placement is indicat­ed. Anterograde pyelography is the best test for confirming the source of leak. It is dis­cussed in the section on urinary complica­tions. 
Haematomas 
Postoperative perirenal haematomas occur frequently but are usually small and asymp­tomatic and should be considered a normal sequel to surgery.6,26 In US, the acute haematoma appears as a fluid collection with echogenic debris. Later the clot lysis-de­creased echogenicity appears. The CT ap­pears as fluid collection with hyper attenuat­ing areas prior to intravenous contrast mate­rial administration, a finding which is consis­tent with fresh blood. Size, location, and growth determine the significance of these collections. An increase in size may indicate the need for interventional management or surgery. Large haematomas can cause symp­toms secondary to mass effect but usually on­ly present a problem when they become sec­ondarily infected. If the patient is asympto­matic and there are no signs of infection, these collections can be treated conservative­ly if the haematoma does not increase in size. Aggressive interventional percutaneous drainage can successfully resolve an infected haematoma but larger calibre drains (12 or 


Figure 1. Lymphocele. a. US image demonstrates a large hypoechoic fluid collection with single septation in the left side of the pelvic cavity. b. Percutaneous catheter drainage (X-rays) 
14 Fr) are usually required. Immediate post­operative haematoma can be secondary to graft rupture or injury to the vascular pedicle. Emergency surgery is mandatory in these cases. 
Perirenal abscess 
Perirenal abscess is an uncommon early com­plication of renal transplant. When a patient has fever and US or CT demonstrates perire­nal collection with air, the diagnosis of perire­nal abscess is clear. The treatment of abscess is based on antibiotics together with a percu­taneous or surgical drainage procedure de­pending on the size of the abscess and the clinical course. Bouali et al and Lang report success rates of 67% and 96% in a series of 31 and 33 cases of abscesses treated percuta­neously together with low rate in complica­tions.27,28 Percutaneous drainage under US or CT guidance avoids the risk inherent in sur­gery and anaesthesia, saves considerable time and meets greater patient acceptance. We recommend insertion of a percutaneous catheter into abscess to obtain a specimen for culture, and to drain the pus-filled cavity in order to hasten recovery and shorten the du­ration of anti-microbial therapy. 
Vascular complications 
Vascular complications are found in less than 10% of renal transplant recipients, but they are an important cause of graft dysfunc­tion.6,29-35 The most frequent vascular compli­cations of renal transplantation include stenosis, thrombosis, arteriovenous fistulas, aneurysms, and pseudoaneurysms in the graft artery and in the recipient iliac arterial system. In contrast to other causes of trans­plant dysfunction, vascular complications are associated with high morbidity and mortality. The diagnostic screening methods are ultra­sound with duplex and colour Doppler modes and three-dimensional (3D) gadolini­um (Gd)-enhanced magnetic resonance an­giography (MRA).36,37 Digital subtraction an­giography (DSA) remains the standard proce­dure for final diagnosis and checking en-dovascular treatment of vascular complica­tions. Endovascular management is the initial treatment of choice for vascular complica­tions in renal transplantation. 
Renal artery stenosis 
Stenosis, the most common vascular compli­cation of renal transplantation, occurs in 1%­12% of transplanted renal arteries and repre­sents a potentially curable cause of hyperten­sion following transplantation and/or renal dysfunction.30-34,39-42 The cause of transplant renal artery stenosis (TRAS) is multifactorial and includes surgical technique (clamp injury to the vascular endothelium, perfusion pump cannulation injury of the donor vessel, faulty suture technique), angulations due to dispro­portionate length between graft and iliac ar­tery, kinking of the renal artery, type of allo-graft, immunological factors, and cy­tomegalovirus arteritis.40,41 In long-standing transplants, progression of underlying arte­riosclerosis in the recipient iliac artery can al­so be a source of arterial stenosis. The inci­dence of renal artery stenosis is more com­mon in cadaver transplant (most renal allo-grafts originate in cadavers), and it can occur as early as two days or as late as several years after the procedure.38,43 In cadaver trans­plant, allograft revascularisation is usually performed as an end-to-side anastomosis with the external iliac artery. When a living, related donor is used, an end-to-side anasto­mosis with the external iliac artery (AIE) may still be used, but an end-to-end anastomosis with the internal iliac artery (AII) is often pre­ferred.44 The clinical presentation often mim­ics that of rejection, but a diagnosis of renal allograft arterial stenosis may be strongly suggested on the basis of sonography and biopsy. A renal allograft biopsy is generally performed prior to angiography in order to rule out chronic rejection of other forms of renal parenchyma disease. Doppler US has become the preferred screening modality for stenosis of the transplanted renal artery.45 Doppler ultrasound has been reported to have a sensitivity of 85% to 100% and speci­ficity of 86% to 100% in the diagnosis of TRAS.5,44-48 Data suggest that this technique is highly accurate, but is highly dependent upon the experience of the ultrasonographer. In obese patients, colour Doppler evaluation can be difficult and MRA or CT angiography can be helpful as an adjunctive non-invasive diagnostic test for TRAS. The gold standard for diagnosis of transplant renal artery steno-sis remains DSA, being diagnostic in 93% of cases.49 It should be performed in patients with clinical and Doppler US findings of TRAS or in patients with clinical findings of stenosis despite normal US results. However, it is invasive and in patients with marginal re­nal function it can induce acute tubular necrosis secondary to contrast toxicity. A use­ful alternative to nephrotoxic iodinated con­trast agents is provided by CO2 or Gadolinium DSA. 

The options available to correct stenosis of the renal artery include conservative treat­ment, transluminal angioplasty (PTRA) with or without stenting and surgery. If the steno-sis is relatively minor and the blood pressure controllable with medication, it is reasonable to continue with conservative treatment. The conservative option becomes particularly at­tractive if the lesion is unsuitable for PTRA or when PTRA is used but it fails. Surgery should only be undertaken for graft arterial stenosis if the other alternatives of PTRA or conservative treatment are not appropriate. PTRA has become accepted as the initial pro­cedure of choice in the treatment of renal al­lograft arterial stenosis, both in allograft renal and native iliac artery stenoses (Figures 2a, 2b, 2c). The best approach to end-to-end anastomoses (AII) is from the contralateral-femoral artery, whereas end-to-side anasto­moses (AIE) are usually more accessible from an ipsilateral approach. Non-selective pelvic arteriography was performed to exclude in­flow lesions by means of a femoral approach as previously described. A narrowing of greater than 50% of the luminal diameter was considered haemodynamically significant. All patients who underwent interventional radiological treatments received intra-arterial boluses of heparin (5000 IU) during the pro­cedure. The technical success of PTRA was defined as a residual stenosis of less than 30% 


Figure 2. Transplant renal artery stenosis. a. Cadaver renal transplantation, with a single renal artery and end-to-side anastomosis to the right external iliac artery. Arteriogram shows a stenosis of the transplant renal artery (ar­row). b. Balloon dilatation. c. Repeat arteriogram after PTRA with 5-mm diameter angioplasty balloon. 
after angioplasty and no flow-limiting intimal flap. Clinical success was defined as more than 15% reduction in serum creatinine level, more than 15% reduction in mean diastolic blood pressure with the number of anti-hy­pertensive medications equal to that before PTRA, or more than 10% reduction in mean diastolic blood pressure with a reduction in the number of anti-hypertensive medica­tions.40 Technical success has ranged from 82% to 93%, and graft salvage rates have ranged from 80%-100%.30-34,41-50 Although up to 20% of cases will develop recurrent steno-sis, but are usually amenable to repeat PTRA,30-34,39,43,50 periprocedural morbidity is generally low, and significant complications have been reported in 0% to 12% of cases.44,51 Complications are usually related to puncture site complications and rarely to distal extrem­ity embolisation, extensive arterial dissection, renal artery thrombosis and renal artery rup­
ture.30-34,39,43,50 
The success of stent place­ment used in combination with PTRA for a wide variety of vascular lesions suggests that deployment of metallic stents may be useful in those with recurrent stenosis of the trans­plant renal artery, failure to satisfactorily eliminate the stenosis after repeat balloon di­latation, intimal dissection with luminal com­promise, and stenosis involving the renal ar­terial ostium (Figures 3a, 3b, 3c, 3d). Stent de­ployment in six patients with recurrent steno-sis was evaluated in retrospective study.52 At almost three years post procedure, all arteries were patent without significant stenosis, and no additional interventions were required. The role of stent placement for the treatment of TRAS and its effect on long-term patency has yet to be investigated. 
Renal artery thrombosis 
Renal artery thrombosis is an uncommon complication of transplantation and usually occurs in the early postoperative period, al­most invariably leading to graft loss. The most common causes are faulty surgical anas­tomoses, persistent hypotension, dehydra­tion, and procoagulant conditions such as lu­pus anticoagulant, severe acute rejection, and progression of a stenosis to thrombosis. Spontaneous late thrombosis of the renal ar­tery is a rare event, and renal artery stenosis is an obvious risk factor. Thrombosis of long­term grafts after intervention such as angiog­raphy or attempted angioplasty is more com­mon than spontaneous renal artery thrombo­sis. Renal artery thrombosis after PTRA may be minimized by keeping the patient well an-ti-coagulated during the procedure and by the intra-arterial administration of nitro-glycerine in order to prevent vascular spasm. The diag­nosis is relatively simple when duplex and colour Doppler techniques fail to demon­strate intra renal venous and arterial flow, with angiography providing confirmation pri­or to intervention.53 In selected cases, the ear­ly diagnosis of vascular thrombosis may en-


Figure 3. Transplant renal artery stenosis. a. Cadaver renal transplantation, with end-to-side anastomosis to the right external iliac artery. Arteriogram shows a stenosis of the transplant renal artery. b. Balloon dilatation. c. Metallic stent after incomplete PTRA (arrow). d. Repeat arteriogram after procedure shows a widely patent trans­plant renal artery with no residual stenosis. 
able graft salvage thrombolytic treatment or clot aspiration. The use of thrombolytic ther­apy in treating renal artery thrombosis has been reported as successful.44,54,55 
Intrarenal arteriovenous fistulas and pseudoaneurysms 
Intrarenal arteriovenous fistulas and pseudoaneurysms are occasionally seen after biopsies. They occur in 1%-18% of renal biop­sy.5,56,57 Intrarenal arteriovenous fistulas may appear when an artery and vein are lacerated; pseudoaneurysms result when only the ar­tery is lacerated. Arteriovenous fistulas with­in the kidney are usually asymptomatic, and normally resolve spontaneously. When le­sions are sizable, marked arteriovenous shunting may result in renal ischemia, hyper­tension or hematuria.6,57 They are easily iden­tified at colour and Doppler US. Helical CT is a good alternative when US cannot define the nature of the lesion. However, a negative US and CT evaluations does not exclude the di­agnosis, and, if clinical suspicion remains, these patients should be evaluated with an­giography. When symptomatic or large, in-trarenal arteriovenous fistulas and pseudoa­neurysms may be effectively treated with se­lective arterial catheterisation and embolisa­tion. Transcatheter embolisation is a safe and effective alternative to surgery; however, it may result in a segmental infarction and im­paired renal function if the feeding vessel is embolised. Treatment requires superselective embolisation in order to preserve the maxi­mum amount of renal parenchyma (Figures 4a, 4b). A potential complication is occlusion of the main renal artery due to migration of the embolising agent. Coils are typically cho­sen as the embolic agent for arteriovenous fistulas because of the greater control in de­ployment when compared to Gelfoam em­bolisation.3 Perini et al58 performed em-bolotherapy in 21 patients with renal allo-grafts and vascular complications. Technical success was achieved in 20 of 21 patients (95%) without serious complications, and no long-term graft dysfunction was noted in 58% of those treated. 


Figure 4. Intrarenal arteriovenous fistula following biopsy. a. Angiogram obtained with selective injection of the main renal artery shows early filing of the transplant renal vein. b. On an angiogram obtained after subselective embolization with coils, early draining veins are not visualized. 
Renal vein thrombosis 
Renal vein thrombosis is an uncommon com­plication that usually occurs in the first post­operative week. When occurring in the early post transplant period it is usually associated with surgical complications and often results in the loss of the graft. At a later stage, when graft function has stabilised, its development may be associated with underlying disorders such as glomerulonephritis, immunosuppres­sive therapy, acute rejection, or extension of lower extremity venous thromboses.9,58,59 The clinical features, with the effect on urine output, vary from primary non-functioning, similar to that seen with arterial thrombosis, to sudden loss of urine output and rising cre­atinine in a graft which is different than in one functioning perfectly. The clinical signs are striking, often with severe pain resulting from rapid local graft swelling. The usual out­come of renal vein thrombosis is infarction, and transplant nephrectomy is usually per­formed to prevent infection.53 Whenever such a diagnosis is made, surgery is always urgent, because, apart from the necessity to relieve the pain, delay is associated with an increasing risk of graft rupture, which may result in catastrophic graft haemorrhage. The sonographic diagnosis dependents mainly on the Doppler portion of the examination. On grey-scale US images, the allograft may ap­pear swollen and hypoechoic. At Doppler US examination, venous flow is absent, and the arterial waveform shows reversed, plateauing 
flow.6,60,61 
diastolic The diagnosis is con­firmed by venography with selective venous catheterization and therapeutic thrombolysis. There are several case reports in the literature on the attempts to treat transplant renal vein thrombosis with arterial, venous, or a combi­nation of arterial and venous thrombolysis and percutaneous mechanical thrombecto-my, but results vary.55,59,62 It is uncommon to achieve complete thrombolysis, but partial ly-sis of the vein may result in a marked clinical improvement. 
Urological complications 
Urological complications after renal trans­plantation are relatively uncommon. They predominantly consist of urinary leaks and urethral obstruction. The quoted incidence of urological complications ranges from 5% to 14%.6,63-66 Urologic complications can be di­vided into early and late categories. Early complications are defined as those that occur within three months of the transplant, and late complications are those that occur after this period of time.64 Leaks tend to occur ear­ly, although obstruction may occur at any post transplant stage. These complications must be diagnosed early, because delays in diagnosis can result in the loss of transplant­ed kidney as well as increased patient mor­bidity and mortality. The most commonly performed interventional procedure in the re­nal transplant patient is percutaneous ante-grade nephrostomy for urinary obstruction or 
leak.44,67 
Urethral obstructions 
Urinary tract obstruction can occur early or late after renal transplantation and are ob­served in less than 5% of patients.6,53,65,66,68 Patients with obstruction are typically asymp­tomatic, and the diagnosis is made during evaluation because of a rising serum creati-nine level and is confirmed by ultrasound ex­amination of the transplanted kidney. The common causes of obstruction are urethral stricture or kinking (accounting for more than 50% of obstruction), urethral blood clot, and urethral compression from lympho­cele.5,44 Less common etiologies of obstruc­tion include oedema or narrowing at the ureteroneocystostomy, pelvic fibroses, fungal debris, or compression from an extrinsic mass such as adjacent haematoma or lym­phoadenopathy. More than 90% of urethric stenoses occur within the distal third of the urethra and may appear days or years after transplantation.68,69 Once obstruction is sug­gested by US, antegrade pyelography can be obtained in order to confirm the diagnosis, to provide detailed, anatomic definition of the type and level of the obstruction, and to serve as an access route for percutaneous manage­ment. Interventional radiology treatment of urinary tract obstruction consists of percuta­neous nephrostomy, balloon dilatation, inser­tion of double J stents, stent placement, or correction of the source of extrinsic compres­sion of the collecting system, such as a lym­phocele. If obstruction is secondary to ureteroneocystostomy oedema or urethral blood clot, external diversion through a per­cutaneous nephrostomy catheter often pro­vides temporary relief of obstruction until the oedema subsides or the clot has passed spon­taneously (Figure 5).5,44,65 The nephrostomy is removed only after an antegrade nephros­togram has confirmed that the urinary tract is unobstructed. 

Urethral stenosis in the early postrenal transplant period can be safely and effective­ly treated by percutaneous dilatation and stenting, with few side effects and long-term success.70,71 This method is especially effi­cient in patients who develop urethral steno-sis within three months of the transplant. In patients with urethric strictures developing three months after transplantation or later, percutaneous stenting is of limited signifi­cance and most patients require surgical cor­rection. Bhagat et al70 and Fontaine et al71 re­ported a success rate of 69% and 62% of early obstruction (within three months) and 33% and 16% of late obstruction (after three months) in a series of 41 and 44 cases treated percutaneously with urinary diversion by per­cutaneous nephrostomy, balloon dilatation and urethral stenting. We advise the applica­tion of urethral dilatation to short fibrotic strictures, particularly those located at the ureterovesical junction. A high-pressure bal­loon, selected according to urethra and stric­ture size, was inserted and advanced to the stricture and inflated for 1-4 min. When the pressure dents on the balloon disappeared, the stricture had been controlled, and an 8-9 Fr double J stent was passed into the urethra (Figure 6). Usually the stent is kept indwell­ing for 9 to 18 weeks, after which it is re­moved cystoscopically.5 However, surgical re­construction may be required for long or re­current stricture, and strictures refractory to balloon dilatation. 



Urine leaks (urinomas) 
Urine leaks are relatively rare complications following transplantation, occurring at the frequency of approximately 1% to 5%, and ap­pearing in the early postoperative period as pain, swelling, and discharge from the 
wound.65,68,72 
Urethral extravasations pro­ducing urinoma can be caused by graft rejec­tion, urethral necrosis due to ischemia, or in­adequate surgical technique.63 Most urine leaks occur at the ureteroneocystostomy, pos­sibly due to vascular insufficiency, or along the anterolateral surface of the bladder where the ureteroneocystostomy has been per­formed.44,68,70 Leaks may also occur from the proximal urethra, renal pelvis, or calyces sec­ondary to distal urethral obstruction, renal in­farction, or percutaneous renal biopsy. Diagnosis is usually made by US evaluation of the transplant, which reveals perinephric fluid collections that is relatively anechoic but may contain septations. Initial management should include percutaneous aspiration and fluid analysis to distinguish it from a lympho­cele, which reveals an elevated creatinine lev­el. A percutaneous nephrostogram and drainage can be both diagnostic and thera­peutic, and effective in the treatment of urine leaks in renal transplant patients.65,67,70 Definitive therapy can be carried out surgi­cally or percutaneously with urethral stent-ing, double-J stents and urinary diversion by percutaneous nephrostomy.70,71,73 Matalon et al have reported a success rate of 87% in a se­ries of 23 cases of urinary leaks treated per­cutaneously with urinary diversion.74 Fontaine et al treated 17 patients with trans­plant urinary leaks with percutaneous nephrostomy and nephroureteral stent and achieved successful closure of the urinary fis­tula in 10 patients (59%).71 Benoit et al de­scribed successful closure of urinary leaks in all 7 patients (100%) with percutaneous nephrostomy and stent insertion.72 The dura­tion of catheter drainage typically ranges from 6-17 weeks.5,65,71,74 
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Radiol Oncol 2004; 38(4): 323-7. 


case report 


Annular pancreas causing extrahepatic biliary obstruction 
Mateja Ogulin, Breda Jamar 
Clinical Institute of Radiology, University Medical Centre, Ljubljana, Slovenia 
Background. Annular pancreas is an uncommon congenital abnormality, consisting of a flat band of pan­creatic tissue, which encircles duodenum or extrahepatic biliary duct. We present a case of obstructive jaun­dice, caused by annular pancreas. Case report. A 46 years old female was admitted because of a sudden onset of abdominal pain, vomiting and jaundice. For the last six years she occasionally noticed her skin was light yellow, in the last year she felt distension in the upper abdomen, especially after fatty meals. Conclusions. Two US examinations, the first one six months before the admission, showed dilated hepatic ducts. The reason of dilatation was unclear, even after the endoscopic US examination. At operation an al­most complete obstruction of the common hepatic duct was found, caused by a narrow band of pancreatic tissue. 
Key words: pancreas abnormalities; bile duct obstruction, extrahepatic; cholangiopancreatography, en-dosopic retrograde 
Introduction 
Annular pancreas is an uncommon congeni­tal abnormality. It consists of a flat band of pancreatic tissue completely encircling the second portion of the duodenum or the extra-hepatic bile duct.1 
It may manifest clinically in the neonate (52%) or remain asymptomatic until adult­hood (48%).1 It can represent an incidental finding during an endoscopic retrograde cholangiopancreatography (ERCP).2 
Received 3 November 2004 Accepted 23 November 2004 
Correspondence to: Mateja Ogulin, MD, Clinical Institute of Radiology, University Medical Centre Ljubljana, Zaloška cesta 7, SI-1000 Ljubljana, Slovenia. 
In adults, symptoms of annular pancreas usually present at the age of 20-50 years as a duodenal obstruction, rarely as a biliary tract obstruction.2 
Jaundice associated with an annular pan­creas has been presumed to result from pan-creatitis,2,3 but some reports suggest that an annulus is, by itself, capable of causing a sig­nificant biliary obstruction.4,5 
We present a case of obstructive jaundice, caused by annular pancreas, without pancre­atitis. 
Case report 
A 46 years old female presented to the emer­gency room suffering from an acute abdomi­nal pain and vomiting. At physical examina­tion she was jaundiced. Liver function tests were abnormal (AST 7.14, ALT 8.78, bilirubin 57/42, .GT 2.92), but levels of lipase and amylase were normal. The US examination showed thickened gallbladder wall, proximal­ly dilated common bile duct and moderate di­latation of the right and the left intrahepatic ducts. No gallstones or masses were seen (Figure 1). 

For the last six years the patient occasion­ally noticed having light yellow coloured skin. In the last year she felt distension in the upper abdomen after meals, especially in the afternoon, after eating fatty food. She never vomited, had no diarrhoea and was afebrile. Difficulties gradually increased and 6 months ago she underwent the first US examination. A concrement, a few mm in size, was found in the infundibulum of the gallbladder. The common bile duct was dilated up to 1 cm above the ampulla of Vater. The cause of di­
latation was not clear. 
The patient underwent ERCP. 
Duodenum and papilla of Vater were nor­mal. A 2 mm long stricture of the common bile duct with prestenotic dilatation was seen, intrahepatic ducts were also dilated, the cys­tic duct was not obstructed (Figure 2). 
The pancreatic duct opened into the com­mon ampulla and had a normal course. There was no accessory pancreatic duct visible. 
The endoscopic US examination confirmed a short, smooth stenosis of the choledochal duct and a dilatation of the hepatic duct, look­ing benign. Some small concrements were found in the gallbladder. There were no signs of tumour like masses (Figure 3). 
A congenital anomaly was suspected and with the patient in a good condition, despite a long history of symptoms, the surgeon de-


Figure 1. Ultrasound: dilatation of hepatic ducts. 




cided to perform abdominal laparotomy with­out any additional imaging procedures. 
At intraoperative cholangiography, an al­most complete obstruction of the common bile duct was found (Figure 4). It was caused by a narrow band of pancreatic tissue encir­cling the common bile duct. A cholecystecto-my and a hepaticojejunal anastomosis were done. 
Discussion 
Annular pancreas is a congenital anomaly of rotation and fusion of primitive intestine and 
its associated structures, which may cause duodenal obstruction in the neonatal period or remain silent throughout life.2 At post­mortem, the incidence has been quoted as be­tween 5-15/100.000. ERCP has led to a much more frequent diagnosis of annular pancreas in as many as one in 150 patients undergoing this procedure.4 
There are three theories concerning the formation of the annular pancreas: 
a) 
hypertrophy of both, the ventral and the dorsal ducts, resulting in a complete ring, 

b) 
adherence of the ventral duct to the duo­denum before rotation and 

c) 
hypertrophy or adherence of the left bud of a paired ventral primordium.1 


There is a clear distinction between the an­nular pancreas encircling duodenum present­ing in children and that in adults, probably due to different severity of stenosis.6 
In neonates, the symptom of severe duo­denal obstruction is vomiting on the first day of life. There is often previous history of poly­hydramnion. A number of other anomalies such as intestinal malrotation, duodenal atre­sias, and cardiac anomalies are often present as well.1,6 
In older children and adults, the onset is more insidious, with intermittent clinical problems. Nausea, vomiting, and epigastric pain are the main complaints due to the duo­denal obstruction.2,4 Pancreatic stenosis of the duodenum is usually not sufficient to cause symptoms until there the provocating factors - peptic ulcer disease or pancreatitis ­supervene. 

The incidence of associated gastric and duodenal ulcers ranges from 26 to 48%, and pancreatitis develops in 15 to 30% of pa­tients.1,2 
It has been suggested that annular pan­creas may be the cause of extrahepatic biliary obstruction because of pancreatitis in the parenchyma, encircling the duodenum and bile duct, although jaundice is rare.3 
In our case, no laboratory or clinical signs of pancreatitis were present. Laboratory data (AST 7.14, ALT 8.78, bilirubin 57/42, .GT 2.92, normal lipase and amylase) were sug­gestive of biliary obstruction with the abnor­mal liver function. 
The US examination is the first in patients with abdominal symptoms. ERCP is the pro­cedure of choice in patients with biliary ob­struction, especially if the findings at US are equivocal. A diagnosis of annular pancreas encircling biliary tract is not always made pre­operatively.2,7 ERCP fails to make the diagno­sis of annular pancreas if there is the obstruc­tion of the duct leading to annular pancreas, if the duct of the annular pancreas does not empty into the main pancreatic duct or if there is a high grade of duodenal obstruction.2 
In our case, no anomaly of the pancreatic duct was shown at ERCP. 
In reviewing literature, not many cases of annular pancreas, causing biliary obstruction, without pancreatitis or duodenal obstruction, were found. 
Adamo and co-authors reported it as being very interesting because of obstructive jaun­dice being the first symptom of this anom­aly.8 Another article presents three cases of annular pancreas with the obstructive jaun­dice, but the obstruction was due to carcino­ma of ampulla of Vater.4,9 
In another case annular pancreas was causing a dilatation of biliary and pancreatic ducts, without obstructive symptoms and with normal liver tests. This patient under­went CT because of the other suspected dis­ease and the dilatation was an accidental finding.10 
Conclusions 
The prevalence of annular pancreas in Slovenia is not known. In spite of such con­genital anomaly being rare and much rarely being the cause of obstruction of the extra-hepatic biliary tract we should keep it in mind as a differential diagnostic possibility. But, as other authors suggest, an annular pancreas should not be considered a satisfactory expla­nation for the obstructive jaundice until other possibilities have been fully excluded.4 
References 
1. 
Shirkhoda A. Anomalies and anatomic variants of pancreas. In Gore RM, Levine MS, editors. Textbook of gastrointestinal radiology. Philadelphia: WB Saunders; 2000. p. 1754-66. 

2. 
Dharmsathaphorn K, Burrel M, Dobbins J. Diagnosis of annular pancreas with endoscopic retrograde cholangiopancreatography. Gastro­enterology 1979; 77(5): 1109-14. 

3. 
Clifford KMA. Annular pancreas diagnosed by en­doscopic retrograde-choledocho-pancreatography (ERCP). Br J Radiol 1980; 53(630): 593-5. 

4. 
Benger JR, Thompson MH. Annular pancreas and obstructive jaundice. Am J Gastroenterology 1997; 92(4): 713-4. 

5. 
Baggot BB, Long WB. Annular pancreas as a cause of extrahepatic biliary obstruction. Am J Gastroenterol 1991; 86: 224-6. 

6. 
Tolia V, Ramachandra R, Klein M. Annular pan­creas. J Pediatr 1997; 131: 14-5. 

7. 
Maker V, Gerzenshtein J, Lerner T. Annular pan­creas in the adult: two case reports and review of 



more than century of literature. Am Surg 2003; 69(5): 404-10. 
8. 
Adamo M, Bonventre S, Tavarmina A, Ventri G, Di Gesu G. Severe obstructive jaundice in a 90­year-old man caused by a annular pancreas. Report of a case. Minerva Chir 2003; 58(3): 395-7. 

9. 
Shan YS, Sy ED, Lin PW. Annular pancreas with obstructive jaundice: beware of undelying neo­plasm. Pancreas 2002; 25(3): 314-6. 

10. 
Green JD, Fieber SS, Buniak B. Annular pancreas with dilated biliary and pancreatic ducts. Am J Gastroenterol 1993; 88: 467-8. 


Radiol Oncol 2004; 38(4): 329-32. 


case report 


Clinical importance of portal venous gas detected by abdominal sonography: a report of two cases 
Primož Gregoric, Alenka Višnar-Perovic 
Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia 
Background. Portal venous gas (PVG) can be a sign of serious disease and a predictor of poor clinical out­come. However, it can also occur as a transient phenomenon with little clinical significance, especially fol­lowing blunt abdominal trauma and various diagnostic and therapeutic procedures. Case reports. We describe two patients with PVG detected on abdominal sonography, who had very sim­ilar sonographic findings but a completely different clinical outcome. The first patient was a 70-year-old man in whom PVG was the consequence of mesenteric infarction; the patient died in hospital shortly after the admission. Our second patient was a 26-year-old man who was injured in a motor vehicle accident. He was clinically stable and needed no aggressive treatment. PVG proved to be a transient phenomenon that cleared spontaneously within a day. Conclusions. Doppler sonography is a sensitive and specific modality for the detection of PVG. In patients with a serious underlying disease, sonography can identify the cause of PVG, so that the appropriate ther­apy may be undertaken without delay. If the aetiology is unclear, the decision to undertake further expen­sive and potentially harmful diagnostic procedures should be based on the patient’s clinical status. 
Key words: portal vein; embolism, air - ultrasonography; ultrasonography, Doppler 
Introduction 
Portal venous gas (PVG) in adults is a rare en­tity. In the past, PVG was regarded as a sign of serious disease (mostly intestinal is-chemia), predicting a poor clinical outcome in most cases. In the recent years, however, the 
Received 3 November 2004 Accepted 23 November 2004 
Correspondence to: Primož Gregoric, MD, Clinical Radiology Institute, University Clinical Centre Ljubljana, Zaloška 7, SI-1000 Ljubljana, Slovenia; Phone: +386 1 839 48 63; E-mail: primoz.gregoric@ guest.arnes.si 
routine use of sonography in the evaluation of a variety of conditions, in particular blunt abdominal trauma, has led to the recognition of a number of clinically unimportant causes of PVG.1 
We describe two patients with PVG de­tected by abdominal sonography who had a completely different clinical outcome. 
Case reports 
Our first patient was a 70-year-old man pre­senting with severe abdominal pain, who had been found lying on the floor in his home a few hours before the admission. On initial evaluation by a traumatologist and an ab­dominal surgeon, he was disorientated and showed signs suggestive of an acute ab­domen. The abdominal sonography revealed PVG, but there was no definitive evidence of bowel ischemia, although the patient’s clini­cal status was compatible with this diagnosis. At the operation, performed on the same day, a necrotic distal ileum and proximal colon were resected. The patient died on the fol­lowing day. The autopsy examination con­firmed bowel ischemia caused by occlusion of the superior mesenteric artery. 

The second patient was a 26-year-old man who was involved as a driver in a traffic acci­dent and was suspected of having blunt ab­dominal injuries. After the initial evaluation by a trauma surgeon, he underwent the ab­dominal sonography, which showed mild contusion of the right kidney and PVG, but there were no definite signs of bowel injury, and no free fluid or gas was detected in the abdomen. CT of the abdomen likewise failed to reveal evidence of bowel injury. The pa­tient was haemodynamically stable and the abdominal pain gradually subsided. The fol­low-up abdominal sonography on the follow­ing day was within the limits of normal. PVG was no longer present, and the patient was discharged from hospital. 
Discussion 
Gas in the portal vein can be visible on a plain radiograph, but newer imaging tech­niques, such as computed tomography and sonography - especially Doppler sonography ­are more sensitive and specific for its detec­tion. Small amounts of PVG detected by Doppler sonography may not be demonstrat­ed by CT.2,3 
Sonography is usually the first diagnostic modality used in the assessment of a patient with suspected abdominal disease. In our hospital, sonography is performed routinely in all patients suffering from blunt abdominal trauma. 
PVG can be diagnosed both with the grey-scale and the Doppler techniques. 
On the grey-scale examination, PVG is seen as small echogenic foci moving rapidly in the direction of blood flow in portal veins. The high acoustic impedance of gas is re­sponsible for this phenomenon.4 Initially the foci are visible mainly in the main portal vein and its major branches. Later, they may be seen also in the periphery of the liver parenchyma. Besides, gas bubbles, red-blood-cell aggregates can also be visualized moving in the lumen of a vein, but gas is readily dis­tinguished from them by its greater echogenicity and velocity (Figure 1).1 
In a Doppler sonogram, gas within a vessel has a characteristic appearance. It produces an artefact of bidirectional, vertical, high-am­plitude spikes, accompanied by a characteris-tic noise that disturbs the normal Doppler tracing of the portal vein (Figure 2).5 



Gas may come into the portal vein by the direct infiltration through the damaged intes­tinal wall (to an intestinal venule or a mesen­teric vein), or it may be produced within the portal vein by bacteria that have traversed a damaged intestinal wall.6 
The causes of PVG can be divided into four groups: 
a. 
intestinal wall alterations (mesenteric is-chemia, inflammatory bowel disease); 

b. 
bowel distension, occurring spontaneously or due to traumatic or iatrogenic causes; 

c. 
intra-abdominal sepsis (diverticulitis, ab­dominal wall gangrene, pylephlebitis, necrotizing enterocolitis, perforation of a gastric ulcer); 

d. 
other causes (transplantation, intestinal pneumatosis, corticosteroid therapy, chronic pulmonary disease).7 The most common cause of PVG is bowel 


ischemia. PVG resulting from bowel ischemia has been shown to have a poor prognosis, with a mortality rate of 75-90%.7 A recent study has suggested that the prognosis may be more favourable if PVG is the result of mesenteric ischemia without associated bow­el necrosis.8 The causes of mesenteric is-chemia include arterial and venous mesen­teric thrombosis, hypoperfusion associated with nonocclusive vascular disease, embolic disease, and disease processes leading to the intestinal obstruction.7 
Most patients with PVG due to bowel is-chemia, as is the case with our first patient, are in a critical condition. The demonstration of PVG on the abdominal sonography should prompt a search for associated abnormalities, such as thickening or ischemia of the bowel wall, occlusion of the superior mesenteric ar­tery, absent peristalsis, bowel distension, mesenteric oedema, ascites, fluid collections or intestinal pneumatosis. If any of these ab­normalities occur in association with clinical signs suggestive of an acute abdomen, la-parotomy must be undertaken without delay. If none of these abnormalities are found and the patient is clinically stable, further imaging studies, such as contrast-enchanced CT or angiography, should be performed before la-parotomy. 
Bowel distension can produce a minimal mucosal disruption that allows intraluminal gas to become intravascular. PVG secondary to bowel distension can occur in association with 
1. 
iatrogenic dilatation of the stomach and bowel (endoscopic procedures, e.g. colonoscopy, sclerotherapy for gastric varices, ERCP or barium enema); 

2. 
paralytic ileus, mechanical obstruction, acute gastric dilatation; 

3. 
blunt trauma and barotrauma. 


7 
Most patients in the first two groups can be managed medically. The mechanical ob­struction of the bowel requires a causal treat­ment. 
PVG has been reported to occur in less than 1% of patients with blunt abdominal trauma.1 In these patients, PVG does not nec­essarily imply bowel perforation or necrosis. Benign PVG in the setting of blunt abdominal trauma is thought to result from acute pres­sure changes that occur at the time of injury and force intraluminal gas into the bowel wall, where it is absorbed into the portal cir­culation. The finding of additional abnormal­ities on sonography, such as an aperistaltic, distended bowel with a thickened, ischemic wall, or the presence of free fluid, calls for ap­propriate therapeutic measures. When no ad­ditional abnormalities are present, the further management should be governed by the clin­ical status. If this is stable and the patient has no major problems, as is the case with our second patient, there is no need to carry out expensive and potentially harmful investiga­tions (contrast-enhanced CT, angiography). Only a plain radiograph of abdomen on the left lateral side should be obtained to rule out a possible perforation of the bowel (free gas), and a follow-up sonography should be carried out after 24 hours to check if the PVG has cleared. 

Several infectious abdominal processes, in­cluding diverticulitis, appendicitis, cholecys­titis and colitis, are associated with PVG. The pathogenesis of PVG occurring in conjunc­tion with the abdominal infection is not fully understood. It can be the result of septi­caemia in the mesenteric and portal veins (pylephlebitis) or increased fermentation of carbohydrates within the bowel.7 If there is no associated liver abscess, the medical treat­ment is sufficient in most cases. 
Another possible mechanism for the de­velopment of PVG is a portosystemic shunt, allowing gas to enter portal veins from the systemic venous circulation, where it may oc­cur as a consequence of penetrating trauma, recent surgery or various procedures, such as central venous catheter placement. 
Conclusions 
Sonography is usually the first diagnostic ex­amination in the evaluation of a patient with abdominal troubles. In our hospital, it is per­formed routinely in all patients suffering from blunt abdominal trauma who do not re­quire an immediate laparotomy. The Doppler mode is particularly sensitive and specific for the detection of gas in the portal vein. The finding of PVG on the abdominal sonography in a patient who appears to be severely ill warrants a careful search for other abnormal­ities. In experienced hands, sonography can reveal a serious abdominal disease underly­ing PVG, thus making it possible to initiate an appropriate treatment without delay. If the cause of PVG is not apparent on sonography, the decision to undertake further, more de­manding and potentially harmful investiga­tions (contrast-enhanced CT, angiography) must depend on the patient’s clinical status. 
We must bear in mind that PVG is not al­ways a sign of serious illness but may occur as a transient, clinically insignificant phe­nomenon, especially following abdominal trauma and various diagnostic and therapeu­tic procedures. 
References 
1. 
Brown MA, Hauschildt JP, Casola G, Goink BB, Hoyt DB. Intravascular gas as an incidental find­ing at US after blunt abdominal trauma. Radiology 1999; 210: 405-8. 

2. 
Chevallier P, Peten E, Souci J, Chau Y, Padovani B, Bruneton JN. Detection of portal venous gas on sonography, but not on CT. Eur Radiology 2002; 12(5): 1175-8. 

3. 
Maher MM, Tonra BM, Malone DE, Gibney RG. Portal venous gas: detection by gray-scale and Doppler sonography in the absence of correlative findings on computed tomography. Abdominal Imaging 2001; 26: 390-4. 

4. 
Strohm WD, Romele UE. Die Bedeutung der sono­graphie bei dem nachweis von gasansammlungen in der pfortader oder in lebervenen. Medizinische Klinik 1994; 89: 538-42. 

5. 
Schultze CG, Blum UK, Haag K. Hepatic portal ve­nous gas: imaging modalities and clinical signifi­cance. Acta Radiologica 1995; 36: 377-80. 

6. 
Lafortune M, Trinh BC, Burns PN, Breton G, Burke M, Dery R, et al. Air in the portal vein: sono-graphic and Doppler manifestations. Radiology 1991; 180: 667-70. 

7. 
Sebastia C, Quiroga S, Espin E, Boye R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings and prognosis. Radiographics RSNA 2000; 20: 1213-24. 

8. 
Ohtsubo K, Okai T, Yamaguchi Y, Watanabe H, Motoo Y, Matsui O, et al. Pneumatosis intestinalis and hepatic portal venous gas caused by mesen­teric ischemia in an aged person. Gastroenterology 2001; 36: 338-40. 


Radial Oncol 2004; 38(4): 333-8. 



case report 

Radiographic, computed tomographic and magnetic resonance imaging appearances of primary V -cutting zone of resorption of lumbar vertebral body in Paget's disease 
Vladimir Jevtic 
Clinical Radiology institute, University Clinical Centre Ljubljana, Slovenia 
Background. Paget's disease of bone typically demonstrates three evolutionary phases with the character­istic radiographic findings. The incipient stage is manifested by an advancing lytic zone of resorption. Unlike the skull and the long bones the primary advancing zone of rarefication has not been clearly demonstrated within the spine and pelvis. Case report. A 62-year-old man with histologically proved polyostotic Paget's disease was admitted to the hospital due to the exacerbation of pain at the toracolumbar junction with deterioration during the night. Due to slight elevation of acid phosphatase and clinical signs indicating prostatic hypertrophy the possibil­ity of metastatic prostatic carcinoma has been raised. A bone scintigraphy with technetium phosphonate showed the expected marked increased uptake affecting numerous bones with the typical radiographic signs of Paget's disease. Besides these findings, there was also moderate focal accumulation within the right dor­sal half of the vertebral body of Ll. Conventional tomography, computed tomography (CT) and magnetic resonance imaging (MRI) demonstrated the primary cutting zone of resorption affecting the same region. Conclusions. We present a unique case of Paget's disease with primary V-cutting zone within the unde­formed vertebral body of L1 and spontaneous progression to the midphase of the disease on a three year fol­low-up. 
Key words: osteitis deformans; spinal diseases -radiography; tomography, x-ray computed; magnetic res­onance imaging 
Introduction 

Received 3 November 2004 Paget's disease of bone typically demon­Accepted 18 November 2004 strates three evolutionary phases with the characteristic radiographic findings. The ini­Correspondence to: Prof. Vladimir jevtic, MD, PhD, tial lytic phase is followed by the midphase 
Clinical Radiology Institute, University Clinical 
with a mixture of lytic and sclerotic changes 
Centre, Zaloska 7, Sl-1525 Ljubljana, Slovenia; 
leading finally to the late sclerotic phase of 

Phone/Pax: +386 1 23 23 556; Email: vladimir.jevtic@ mf.uni-lj.si the disease. The incipient stage is manifested 
by an advancing lytic zone of resorption. Unlike the skull and the long bones the pri­mary advancing zone of rarefication has not been clearly demonstrated within the spine and pelvis.1 It has been stressed that the most of vertebral lesions reported in literature as the primary lytic phase of the disease actual­ly represent the secondary bone resorption following the compression of the vertebral bodies.2 
In this case report, we describe radi­ographic, computed tomographic (CT) and magnetic resonance imaging (MRI) findings of primary cutting zone of the resorption within the undeformed vertebral body of Ll. A three-year follow-up revealed a progressive transition to the midphase of Paget's disease. 
Case report 
A 62-year-old man with histologically proved polyostotic Paget's disease was admitted to the hospital due to the exacerbation of pain at the toracolumbar junction with deterioration during the night. The physical examination of the toracolumbar spine demonstrated the limited mobility without neurological impair­ment. Pertinent laboratory findings included extremely elevated levels of serum alkaline phosphatase and urine hydroxyproline. Due to slight elevation of acid phosphatase and clinical signs indicating prostatic hyperthro­phy the possibility of metastatic prostatic car­cinoma has been raised. A bone scintigraphy with technetium phosphonate showed the ex­pected marked increased uptake affecting the right frontal area, the vertebras C3, Tl, TS, L2, L3, L4, LS, the left scapula, the pelvic bones and the proximal part of the left femur. Besides these sites, there was also moderate focal accumulation within the right dorsal half of the vertebral body of Ll. The plain films of the affected areas demonstrated fea­tures typical for the midphase of polyostotic Paget's disease with the exception of the Ll 
Radio/ 0 11col 2004; 38(4): 333-8. 
vertebra. A careful analysis of the conven­tional tomography of L1 revealed the discrete triangular osteolytic area affecting the right dorsal part of the vertebral body localized just bellow the lower end plate and the dorsal cor­tex (Figure la). The osteolytic area correlated well with the region of moderately focally in­creased uptake on the bone scintigraphy. MRI of L1 showed the triangular low signal intensity area on Tl-weighted spin-echo im­ages, which was of high signal intensity on T2-weighted images and demonstrated the in­tense Gd-DTPA contrast enhancement on Tl­weighted postcontrast images {Figure 1 b). Since the clinical, scintigraphic and radiolog­ic findings were in favour of the eventual metastatic disease secondary to prostatic car­cinoma CT guided bone biopsy was pro-
Figure la. Lateral conventional tomography of unde­formed L1 vertebral body shows discrete triangular primary cutting cone zone of resorption localised bel­low the lower end plate and the dorsal cortex (small ar­row heads). Note also •picture-frame• appearance of the vertebral body L2 (big arrow heads), typical for the midphase of Paget's disease. 

posed. The CT examination of L1 vertebra showed an oval purely lytic lesion below the dorsal cortex without any enlargement of bone contours (Figure le). The patient ulti­mately refused the bone biopsy and was dis­charged from the hospital. He was lost from our control for one and a half year. During that time the patient was treated intermit­tently with calcitonin and diphusphunates but laboratory examinations demonstrated only slightly decreased levels of serum alka­line phospahatase and of urine hydroxypro­line. The repeated CT examination of L1 ver­tebra (Figure 2a) showed that the lesion pro­gressed centrifugally for approximately 6-7 mm. The lesion, which at the first examina­tion was purely lytic, on the control examina­tion demonstrated mixed lytic/sclerotic fea­tures. The advancing edge of the lesion re-
Figure lb. Sagittal TJ-weighted (500/15) spin-echo Gd-DTPA postcontrast image demonstrates marked contrast enhancement within the primary lytic zone of L1 (small arrow heads) and the central part of L2 ver­tebral body (big arrow head) 
Figure le. Initial Cf scan of L1 reveals an oval purely osteolytic lesion without evident bone enlargement (small arrow heads). 
mained osteolytic and it looked as it was fol­lowed by osteosclerosis. In comparison with the initial examination the most interesting new finding was some enlargement of the bone contour seen along the posterior border of the vertebral body of L1 (Figure 2b). The re­peated bone scintigraphy was similar to the first examination and revealed no additional focal accumulation, which could be expected in case of eventual metastatic disease. On a three year follow-up radiography, CT and MRI demonstrated the further progression of the lesion with a mixture of lytic/ sclerotic findings typical for the midphase of Paget's disease. The slight compression of the lower end plate of LJ was evident reflecting the weakening of the pagetic bone (Figure 3). 

Discussion 
The primary lytic phase of Paget's disease of bone is characterised by an advancing zone of bone rarefication reflecting the intense osteo­clastic activity. The average rate of progres­sion in the untreated patients has been esti­mated at about 1 cm/year {1 mm / month). The focal bone resorption is quickly followed by a marked osteoblastic repair which tends to compensate the loss of the bone3 This focal bone balance between resorption and forma­tion may demonstrate considerable varia­tions.2 Therefore, the sclerotic phase may be quickly changed into the mixed or the lytic appearances of the disease. The advancing zone of rarefication can be easily revealed ra­diographically within the skull as osteoporosis circumscripta or within the long bones as V­shaped cutting cone. However, within the tra­becular bones like pelvis and spine, the pri­mary lytic zone has not been clearly demon­strated.1 The first radiologic evidences in these areas are typically sclerotic features of the disease.3 According to Maldague and Malghem2 most of the vertebral lesions, re­ported in literature as demonstrating the cut­ting cone of primary lytic phase, actually fol­lowed the final sclerotic phase of the disease. The secondary resorption within the sclerotic pagetic bone usually occurs due to some pro­voking factors, most commonly the compres­sion of the vertebras, and has been never ob­served at the level of undeformed vertebral bodies. In this respect our case is unique. An osteolytic zone has been clearly demonstrat­ed by the conventional tomography and CT examination within the undeformed vertebral body of Ll (Figures la, le). Furthermore the primary zone of rarefication affected only a part of the vertebral body of Ll. In other re-ported cases not only the compression of the vertebral bodies was seen, but the rarefica­tion was more diffusely distributed.2.4.5 There are no reasons to believe that in this particu­lar case the zone of rarefication appeared sec­ondarily within the preexisting pagetic bone. At the initial examination the lesion was purely osteolytic and there was no enlarge­ment of the vertebral body which would be present in a case of previous sclerotic phase of the disease. The scintigraphic finding of only moderately increased uptake of tech­netium phosphonate within the primary re­sorption zone seen in our patient has been re­ported in literature at the initial phase of Paget's disease.2 MRI appearances of high signal intensity on T2-weighted images and 

Figure 2a. Follow-up er examination one and a half  
year later shows centrifugal enlargement of the lesion.  Figure 2b. er scan also demonstrates an enlargement  
The advancing lytic cutting cone (small arrow heads)  of bone contour at the dorsal aspect of the vertebral  
is followed by osteosclerosis (big arrow heads).  body of Ll (small arrow heads)  
Radio/ Oncol 2004; 38(4): 333-8.  

Figure 3. A three year follow-up lateral tomography re­veals mixed lytic/ sclerotic features typical for the mid­phase of Paget's disease. The lesion has progressed and affects nearly half of the vertebral body L1 (small arrow heads). Note initial concavity of the lower end plate in the region of weakened pagetic bone (big ar­row heads). 
marked contrast enhancement on Tl-weight­ed postcontrast images (Figure l b) within the primary lytic zone of L1 and the central part of vertebral body of L2 represented oedema and hyperaemia consistent with the replace­ment of fat and haematopoietic elements of normal bone marrow with hypervascular fi­broblastic tissue characteristic of Paget's dis­ease.l The radiologic features on a follow-up examination were also in favour of the exis­tence of primary lytic zone within the verte­bral body of Ll. Two of the four cardinal ra­diographic appearances of Paget's disease were shown, the enlargement of bone con­tours and an advancing resorption zone. A typical bone enlargement not seen at the ini­tial examination appeared only after one and a half year reflecting activation of the sub­peristeal cortex (Figure 2a). At that time there was also the evident progression of primary cutting cone for about 6-7 mm. The primary zone of resorption was quickly followed by secondary osteosclerosis, which may reflect a higher remodelling rate of the trabecular bone. 2 The rapid process of sclerosis could be eventually attributed to antiosteclastic thera­py. However, the influence of treatment was probably limited since the levels of serum al­kaline phospahatase and urine hydroxypro­line were not significantly decreased after one year and a half. 
Without bone biopsy the definite diagno­sis of Paget's disease still remains hypothetic. On the other hand the eventual bone biopsy at the beginning of the lesion of vertebral body of L1 could substantially change the natural evolution of the disease. Anyhow, the diagnosis of metastatic disease after a three year follow-up was not realistic. Relevant clinical, laboratory and scintigraphic findings were all negative. Besides, there were no radi­ologic sings of local cortical destruction and extension of the osteolytic lesion of L1 into the surrounding soft tissues which would be expected in the metastatic disease. The lesion has progressed within the periosteal envelope 
Radio/ Oncol 2004; 38(4): 333-8. 

of bone, findings characteristic of a mid phase of Paget's disease. Finally, the radiological changes of the vertebral body of Ll on the fol­low-up examinations were comparable to the neighbouring vertebras with all typical signs of a midphase of Paget's disease. 
In summary, we presented a unique case of Paget's disease with primary V-cutting cone within the undeformed vertebral body of Ll and spontaneous progression to the midphase of the disease on a three year fol­low-up. Pertinent radiographic, CT and MRI findings were described. 
References 
1. 
Mirra JM, Brien EW, Tehranzahed J. Paget's dis­ease of bone: review with emphasis on radiologic features, part L Skeletal Radio/1995; 24: 163-71. 

2. 
Maldague B, Malghem J. Dynamic radiologic pat­terns of Paget's disease of bone. Clin Orthop 1987; 217: 126-51. 

3. 
Mirra JM, Brien EW, Tehranzahed J. Paget's dis­ease of bone: review with emphasis on radiologic feature, part IL Skeletal Radiol1995; 24: 173-84. 

4. 
Chaouat Y, Aboulker J, Ramadier J, Mazabraud A, Kanovitch B, Faures B, et al. Maladie de Paget vertebrate osteolytique, mono-osh~olytique ou os­teoblastome? Revue du Rlmmatisme 1973; 49: 139­45. 

5. 
Rosenthal DJ, Kevin R. Paget disease (osteoporosis circumscripta) of C3. Skeletal Radio/1981; 6: 205-7. 


Radiol Oncol 2004; 38(4): 339-47. 




case report 

A calcified cervical intervertebral disc in a child and a thoracic 
disc calcification in an adult with posterior herniation-radiographic, computed tomography and magnetic resonance imaging findings 
Vladimir Jevtic 
Clinical Radiology Institute, University Clinical Centre Ljubljana, Slovenia 
Background. Nucleus pulposus calcification in children is a relatively rare but well known clinical syn­drome, usually localized at the level of the cervical spine. The exact aetiology still remains uncertain. Calcifications of the intervertebral discs in adults differ from the childhood variety. They are mainly de­generative in nature and occur at the level of midthoracic and upper lumbar spine. Potentially serious com­plications, posterior herniation of calcified disc may occur in both entities. Case reports. We report two cases of the calcification of the nucleus pulposus in a seven-year-old boy at the level of C7-T1 and a case of calcified intervertebral disc T11-T12 in a forty-five-year-old woman, with massive posterior herniation. Remission of symptoms was achieved with a conservative therapy alone. Clinical, radiographic, computed tomographic and magnetic resonance imaging (MRI) findings were ana­lyzed in an attempt to investigate similarities and differences between both disease entities. Conclusion. Massive posterior herniation of calcified nucleus pulposus in a child was treated conserva­tively with a favourable outcome. A disappearance of symptoms followed quick resolution of herniated cal­cified masses. In adult variety extruded thoracic disc calcification was of a permanent type with no tenden­cy towards spontaneous resolution and remission of symptoms after the conservative therapy. MRI seems to be able to depict disc calcification before a conventional radiography. The widening of affected discs in a paediatric patient was also better demonstrated by MRI. It would seem to support the theory of an increased intradiscal pressure as the precursor of annulus fibrosus ruptures and consecutive calcified disc herniations. 
Key words: intervertebral disc; calcinosis; intervertebral disc displacement; spinal disease - radiography, tomography; x-ray computed; magnetic resonance imaging 
Received 3 November 2004 Accepted 18 November 2004 
Correspondence to: Prof. Vladimir Jevtic, MD, PhD, Clinical Radiology Institute, University Clinical Centre, Zaloška 7, SI-1525 Ljubljana, Slovenia; Phone/Fax: +386 1 23 23 556; Email: vladimir.jevtic@ mf.uni-lj.si 
Introduction 
Nucleus pulposus calcification in children is a relatively rare but well known clinical syn­drome, usually localized at the level of the cervical spine. More than hundred and thirty cases have been reported in the literature with an increasing number of new reports in the last decade.1-4 The disease entity has been attributed to trauma,5,6 inflammation,7,8 or in­creased hydrostatic pressure within the disc,3 but the exact aetiology still remains uncer­tain. The prognosis of discal calcifications in children is good.3,9,10 As a rule pain resolves and there is a spontaneous resorption. Although the benign nature of the disease has been emphasized by many authors, the herni­ation of the calcified nucleus pulposus through the ruptured annulus fibrosus may occasionally occur.1,2,5,6,11-14 This rare but po­tentionally serious complication with radio­logic signs of the extradural space occupying lesion raises the question of an eventual op­erative therapy.12-14 In several cases, which have been reported in literature,1,9,11 the re­mission of symptoms occurred with a conser­vative treatment. 

Calcifications of the intervertebral discs in adults differ from the childhood variety and may reflect numerous systemic diseases. Disc calcifications are more frequent and often af­fect not only the nucleus pulposus but also the annulus fibrosus. In adults calcific de­posits are mainly degenerative in nature and occur at the level of midthoracic and upper lumbar spine which are relatively nonmobile. Therefore, a posterior massive displacement of a calcified intervertebral disc into the spinal canal is a rare complication.1 
Radiographic and computed tomography (CT) findings in herniated disc calcifications are well known. However, magnetic reso­nance imaging (MRI) appearances have not been often reported in the literature.15,16 In the last decade, the significance of MRI as a primary radiologic diagnostic modality in dif­ferent spinal disorders has been increasingly gaining in relevance. Therefore, the radiolo­gists and the clinicians must be aware of the MRI findings of these rare but potentionally serious complications of the intervertebral disc calcifications. 
We report two cases, a case of the calcifi­cation of the nucleus pulposus in a seven­year-old boy at the level of C7-T1 and a case of the calcified intervertebral disc T11-T12 in a forty-five-year-old woman, with the massive posterior herniation. The remission of symp­toms was achieved with a conservative thera­py alone. Clinical, radiographic, CT and MRI findings were analyzed in an attempt to in­vestigate similarities and differences between both disease entities. 
Case reports 
Case I 
A seven-year-old-boy presented with lower neck pain, limited movements and stiff neck, a day following gymnastic activity at school. He could not remember having had any sig­nificant trauma. There were no neurological findings. The patient was afebrile, his ery-throcyte sedimentation rate and a white blood cell count were within normal limits. Initial lateral radiographs demonstrated calci­fications of the nucleus pulposus at the levels C4-C5, C5-C6, C6-C7, C7-T1 and the mild flat­tening of the vertebral bodies C4, C5 and C6 (Figure 1a). MR imaging revealed a signal void within the intervertebral discs C4-C5, C5-C6, C6-C7 and C7-T1, findings consistent with nucleus pulposus calcifications and slight disc expansions most pronounced at the level C7-T1 (Figure 1b). Following the treatment with a cervical collar on an outpa­tient basis he became asymptomatic after four weeks. The patient was admitted to hos­pital for the second time one year later with mild left-sided torticallis. He complained of lower neck pain radiating to the shoulders. There was no history of trauma. Neurological 



Figure 1b. Mid-sagittal PD-weighted spin echo image (TR 2200 ms, TE 20 ms) reveals signal void within the calcified intervertebral discs C4-C5, C5-C6, C6-C7 and C7-T1 (arrow heads) with slight disc expansion most pronounced at the level C6-C7. Note that the signal void at this level extends far posteriorly into the an­nulus fibrosus indicating the possibility of its rupture. 
and laboratory investigations were normal. A control lateral radiograph of the cervical spine showed disc calcifications at the levels of C4-C5, C5-C6 and C7-T1. However, there was no nucleus pulposus calcification of C6­C7 disc which was most pronounced at the initial examination (Figure 2a). CT scan re­vealed minimal calcifications within the in-tervertebral disc C6-C7 and a narrow calcified tract in the midline leading to the rupture of the annulus fibrosus. The calcified nucleus pulposus was nearly completely herniated posteriorly and distributed quite evenly throughout the whole epidural space behind the vertebral body of T1. The narrowing of the spinal canal was slightly more pro­nounced on the left side (Figure 2b). On MR imaging nucleus pulposus calcifications with­in the disc and the epidural space were demonstrated as a signal void (Figure 2c). The signal intensity of the vertebral bodies C6 and C7 was decreased on T1-weighted images and increased on T2 weighted spin echo images, findings consistent with bone marrow oede-ma (Figure 2d). In comparison to radiography and CT examination MR imaging clearly re­vealed that there was no compression of the spinal cord. The patient was discharged from the hospital after a cervical collar was ap­plied. On a control clinical examination six weeks later he was asymptomatic. Control CT showed only minimal remnants of the calci­fied herniated nucleus pulposus in the mid-line, the abundance of epidural masses being resorbed (Figure 3). 
Case II 
A forty-five-year-old female complained of pain radiating from the lower to the upper thoracic region for many years. The pain was aggravated by thoracic flexion but was not in­creased by coughing. There was no preceding history of any significant trauma. She experi­enced hypoesthetic area localized dorsally on the right side at the level of T10-T11. There was no neurological deficit and the laborato­ry findings were within normal limits. Lateral roentgenogram and conventional tomogra­phy of the thoracic spine showed findings typical of haemangioma of the vertebral body T10 and a calcified area in the posterior third of the intervertebral disc T11-T12. The dorsal herniation of the calcified material into the spinal canal behind the vertebral body D12 was also evident (Figure 4a). CT examination revealed the calcification of the nucleus pul­posus and a narrow calcified tract leading to the rupture of the annulus fibrosus. Extruded calcified material was globular in appearance and localized in the midline within the epidural space (Figure 4b). The calcified nu­cleus pulposus and herniated masses were of low signal intensity on all MRI sequences. 



MR imaging showed no compression of the spinal cord. The signal intensity of the neigh-bouring vertebral bodies T11 and T12 was normal (Figure 4c). The patient was treated with analgesics on an outpatient basis and her pain diminished in intensity but did not disappear completely. On a follow-up radi­ographic examination two months later the herniated calcified masses remained un­changed. 
Discussion 
The herniation of the calcified nucleus pulpo­sus in children through the rupture in the an­nulus fibrosus is an unusual complication. Only forty cases including ours have been published to date.1,2,5,6,11-14 The calcified nu­cleus pulposus may be displaced in different directions. However the posterior and pos­terolateral extrusion into the spinal canal with the neurological signs of the spinal cord or the nerve-root compression may occasion­ally occur. This is the most serious complica­tion of disc calcification in children.12-14 Clinical symptoms in our patient did not dif-fer from similar cases reported in literature and included limited movements, stiff neck, mild torticollis and lower neck pain. There was no history of significant trauma or labo­ratory signs indicating the inflammation. With the exception of several patients,12-14 who were treated surgically in majority of cases including ours, the remission of symp­toms was achieved with a conservative thera­py alone. The disappearance of symptoms in our patient coincided with a quick resolution of the herniated calcified nucleus pulposus which occurred during six weeks. Good prog­nosis in children may be attributed not only to a quick resolution but also to a pliability of calcified masses which has been proved sur­gically.14 

The calcific deposits in adults predomi­nantly consist of hydroxyapatite and may be of impermanent or permanent type.15 In our case a longstanding clinical history and a ra­diographic follow-up examination which showed no signs of resolution suggested the permanent type of calcification. The results of the conservative treatment in our adult pa­tient were not favourable. Her pain did not resolve completely, which was in accordance with the radiographic signs of a persistent calcification within the spinal canal. In the absence of the significant neurological im-

Figure 2c. control sagittal MR T1-weighted spin echo image (TR 500 ms, TE 15 ms) reveals disappearance of sagittal void at the level of herniation (small arrow head). Extruded calcified low signal intensity nucleus pulposus cannot be identified since the CSF space is of similar low signal intensity on T1-weighted image. It is of interest to note the decreased signal intensity of the vertebral body C7 (big arrow head) consistent with bone marrow oedema. 

Figure 2d. On T2-weighted spin echo image (TR 2200 ms, TE 80 ms) high signal intensity bone marrow oedema is seen within the vertebral bodies of C6 and C7 (big arrow heads). Low signal intensity extruded calcified nucleus pulposus is clearly demonstrated due to neighbouring high signal intensity CSF on T2­weighted (small arrow heads). 

pairment a surgical treatment was not justi­fied. 
Radiographic signs in our young patient were fairly typical. The usual findings of cer­vical multilevel disc calcifications were demonstrated. However, the distribution of calcified masses throughout the individual disc spaces differed. At the levels of C4-C5, C5-C6 and C7-T1 the calcification appeared to be flattened and more widespread. Since the normal nucleus pulposus lies eccentrical­ly on the border between the medial and pos­terior third of the disc space, the widespread distribution of calcified masses suggests the intradiscal displacement of the calcified nu­cleus pulposus into the fissures of the annu­lus fibrosus, findings clearly demonstrated on CT examination. Radiographic appear­ances were to some extent reminescent of discographic findings in the degenerative disc disease.17 Fragmentation with a tenden­cy towards the anterior displacement was re­vealed at the level C5-C6. The flattening of the vertebral bodies C4, C5 and C,6 seen also in our patient, has been frequently reported in literature.3.9.10 
The mechanical stress is an important fac­tor in modeling of the normal vertebral bod-ies. It has been proved that, in the absence of normal weight-bearing, the height of the ver­tebral bodies increase.18 Conversely, the flat­tening of the vertebral bodies presumably in­dicates that the increased stress has been evenly distributed throughout the whole end-plate reflecting the morphological appear­ance of widespread distribution of the calci­fied nucleus pulposus within the interverte­bral disc. In comparison to other disc calcifi­cations the nucleus pulposus calcification at the level of C6-C7, which ultimately herniat­ed, was more abundant and globular in ap­pearance. The initial MR examination (Figure 1b) revealed not only the expected signal void within the calcified intervertebral discs but also a slight disc expansion, most pro­nounced at the level of C6-C7, consistent with an increased intradiscal pressure, which was not so clearly demonstrated on the plain film radiography. Similar MRI findings have been already reported in discs without visible 


Figure 4a. Conventional tomography of the lower tho­racic spine demonstrates calcified nucleus pulposus of the T11-T12 disc space (big arrow heads) and dorsal extrusion of the calcified material behind the vertebral body of T12 (small arrow heads). Findings typical of cavernous haemangioma of the vertebral body T10 are also seen (arrow) 

calcifications by Swischuk and Stansberry16 who supposed that it could represent the ini­tial phase of the disease entity. In our case the rupture of the annulus fibrosus occurred at the level of C6-C7 in which the disc expan­sion was most pronounced. These findings are in favour of the theory of an elevated in-tradiscal pressure.3 On the basis of the MRI appearances it could be assumed that an ini­tial phase of the disease may be characterized by an expansion of the intervertebral disc, presumably due to the osmotic absorption of water caused by an increased content of cal­cium salts within the nucleus pulposus. An increased intradiscal pressure makes the disc more vulnerable and ultimately leads to rup­tures within the annulus fibrosus with a con­secutive intradiscal displacement and/or ex­trusion of the calcified nucleus pulposus and disc decompression. These MR appearances also suggest that MR is probably more sensi­tive than radiography in depicting a disc widening and possibly that the most expand­ed discs are at highest risk for eventual her­niations. On a follow-up radiography (Figure 2a) the disappearance of disc calcification C6­

Figure 4b. CT examination at the level of T11-T12 disc space reveals calcified nucleus pulposus and narrow hyperdense tract directed to the left para-saggital rup­ture of the annulus fibrosus (small arrow heads). Extruded calcified material is globular in appearance and localized in the mid-saggital plane of the epidural space (big arrow head). 
C7 together with pain distribution suggested the possibility of the dorsal disc herniation, which has been proved on CT examination (Figure 2b). 
The most common site of the calcified nu­cleus pulposus is at C6-C7,19 which as in our case, has also been a frequent location of her­niations.1,2,11 It could be attributed to the in­creased stress at this level produced by the transition of a mobile cervical to a fixed tho­racic part of the axial skeleton. The narrowing of the disc space following the herniation (Figure 2a) indicated a disc decompression. Due to its well known high sensitivity for the 

Figure 4c. Sagittal MR T2-weighted spin echo image (TR 1900 ms, TE 80 ms) shows decreased signal inten­sity of the intervertebral discs T8-T9, T10-T11 and T11-T12 (arrow heads) and normal signal intensity of the neighbouring vertebral bodies. The extruded low signal intensity calcified masses are clearly seen against high signal intensity CSF (small arrow heads). There is no compression of the spinal cord. High sig­nal intensity haemangioma of T10 vertebral body is al­so demonstrated (arrow). 

demonstration of calcified structures CT is the method of choice in suspect calcified disc herniations. In our patient CT clearly showed the posteriorly and caudally extruded calci­fied nucleus pulposus as a hyperdense space occupying lesion evenly distributed within the epidural space. The distribution reflected operatively proved a soft toothpaste like con­sistence of the calcified nucleus pulposus.14 One of the important advantages of MRI is its inherent high contrast resolution which en­ables the noninvasive presentation of the spinal cord and evaluation of the eventual compression in disc herniations. In our case a good demonstration of low signal intensity herniated calcified masses within the epidur­al space without a cord compression was pos­sible only on T2-weighted images due to neighbouring high signal intensity CSF space (Figure 2d). The most interesting MRI appear­ances, which have not been reported previ-ously,1,16 included the low signal intensity of the vertebral body C7 on T1-weighted images and the high signal intensity of the vertebral bodies C6 and C7 on T2-weighte images, the findings which were not present at the exam­ination done before the disc herniation. These findings, consistent with bone marrow oedema and hyperaemia, were similar to those described at the initial stage of the disc degeneration20 and may presumably explain the radiographically proved early degenera­tive changes which occur following disc calci­fications in children.10 Care has to be taken not to misinterpret these MRI appearances as the presence on an infectious discitis. 
In our adult patient the radiographic (Figure 4a) and CT findings (Figure 4b) were similar to changes seen in a child with disc calcification. However, there was a substan­tial difference in morphology of the epidural calcified masses, which were globular in the adult variety, indicating its hard consistence and nonpliability. MRI findings of the low signal intensity disc spaces at the levels of T8­T9 and T10-T11 without radiographic evi­dence of calcifications and degeneration re­sembled to those seen in the case report by Swischuk and Stansberry.16 It seems to indi­cate the high sensitivity of MRI which is able to detect disc calcifications at an earlier stage than the conventional radiography. MRI find­ings of the normal signal intensity of bone marrow within vertebral bodies were in ac­cordance with the absence of significant disc degenerative changes (Figure 4c). 
In summary, the massive posterior hernia­tion of the cervical pediatric nucleus pulpo­sus was treated conservatively with a favourable outcome. A disappearance of symptoms followed the quick resolution of herniated calcified masses. In adult variety the extruded thoracic disc calcification was of a permanent type with no tendency towards the spontaneous resolution and remission of symptoms after a conservative therapy. MRI seems to be able to depict the disc calcifica­tion before the conventional radiography.16 The widening of affected discs in a child was also better demonstrated by MRI. It would seem to support the theory of an increased in-tradiscal pressure as the precursor of annulus fibrosus ruptures and consecutive calcified disc herniations.3 The most interesting MRI findings, which have not been reported, in­cluded bone marrow changes consistent with the beginning of the disc degeneration in a child. Since these MRI appearances may re­semble to early inflammatory changes, care has to be taken not to misdiagnose an infec­tious discitis. 
References 
1. 
Heinrich SD, Zembo MM, King AG, Zerkle AJ, Mac Ewen GD. Calcific cervical intervertebral disc herniation in children. Spine 1991; 16(2): 228-31. 

2. 
Hoeffel JC, Bernard C, Schmit P, Denardaud L. Herniation of calcifying discopathy in chilhood: report of three cases. Eur J Pediatrics 1990; 149(10): 695-7. 



3. 
Sonnabend DH, Taylor TK, Champman GK. Intervertebral disc calcification syndromes in chil­dren. J Bone Joint Surg Br 1982; 64: 25-31. 

4. 
Dias MS, Pang D. Juvenile intervertebral disc cal­cification: recognition, management, and patho­genesis. Nerosurgery 1991; 28(1): 130-5. 

5. 
Bjelkhagen I, Gladnikoff H. Calcified disc protru­sion in children. Acta Radiol 1957; 48: 151-5. 

6. 
Schorr S, Adler E. Calcified intervertebral disc in children and adults. Acta Radiol 1954; 41: 498-504. 

7. 
Eyring EJ, Peterson CA, Bjornson DR. Intervertebral disc calcification in chilhood. J Bone Joint Surg 1964; 46: 1432-4. 

8. 
Wells RG, Sty JR. Comparative imaging: Disc cal­cification in childhood. Clin Nuc Med 1985; 10: 821-2. 

9. 
Wells RG, Sty JR. Comparative imaging: Disc cal­cification in childhood. Clin Nuc Med 1985; 10: 821-2. 

10. 
Wong CC, Pereira B, Pho RW. Cervical disc calci­fications in children. A long-term review. Spine 1992; 17(2): 134-44. 

11. 
Mainzer F. Herniation of the nucleus pulposus. A rare complication of intervertebral-disk calcifica­tion in children. Radiology 1973; 107: 167-70. 

12. 
Mohanty S, Sutter B, Mokry M, Ascher PW. Hernation of calcified cervical intervertebral disk in children. Surgical Neurology 1992; 38(6): 407-10. 

13. 
Oga M, Terada K, Kikuchi N, Oda Y, Sugioka Y. Herniation of cacified cervical intervertebral disc causes dissociated motor loss in a child. Spine 1993; 18(15): 2347-50. 

14. 
Peck FC. A calcified thorarcic intervertebral disk with herniation and spinal cord compression in a child. J Neurosurg 1957; 14: 105-9. 

15. 
Sandström C. Calcifications of the intervertebral disc and the relationship between various types of calcifictions in the soft tissues of the body. Acta Radiol 1951; 36: 217-33. 

16. 
Swischuk LE, Stansberry SD. Calcific discitis: MRI changes in disc without visible calcification. Pediatr Radiol 1991; 21: 365-6. 

17. 
Quinnell RC, Stockdale HR. An investigation of artefacts in lumbar discography. Brit J Radiol 1980; 53(633): 831-9. 

18. 
Gooding CA, Neuhauser EBG. Growth and devel­opment of the vertebral body in the presence and 


absence of normal stress. J Roentgenol 1965; 93: 388-94. 
19. 
Schapira D, Goldsher D, Nahir M, Scharf Y. Calcified thoracic disc with herniation of the mu-cleus pulposus in a child. Postgrad Med J 1988; 64(748): 160-2. 

20. 
Modic MT, Masaryk TJ, Ross JS, Carter RJ. Imaging of degenerative disc disease. Radiology 1988; 168: 177-86. 


Radiol Oncol 2004; 38(4): 349-52. 
case report 

Unusual radiographic changes of a gout patient 
Jelena Markota 
Department of Radiology in Hospital Petra Držaja, Clinical Radiology Institute, University Medical Centre, Ljubljana, Slovenia 
Background. Gout is a metabolic disorder that results in hyperuricemia and accumulation of uric acid crys­tals (urats) in tissues, especially joint cartilage. The gouty arthritis presents as acute attacks of arthritis lead­ing eventually to chronic gouty arthritis. In 80% of cases it first occurs in the matatarsophalangeal (MTP) joint of the great toe and is more frequent in male population. Case report. We present a case of unusual radiographic changes accompanying gouty arthritis. A 63 year old female complained about swelling of the first MTP joint on the right, right knee, about stiffness of feet and hands’digits and about backache. First symptoms started to appear 30 years ago. In the time of exami­nation radiographs displayed degenerative changes of the majority of presented joints, bilateral sacroiliitis and osseous ankylosis of both insteps. Microscopic examination showed urate crystals in the samples of the synovial fluid aspirated from the knee. The histological findings of the synovial tissue after the synovecto-my were also in favour of gouty arthritis. Conclusions. Radiographs are the most important imaging modality in the diagnostic process of gout. However, radiographic differential diagnosis can be difficult, since the findings overlap with other condi­tions which cause arthritis and osteoarthritis especially in longstanding gout, elderly patients and females. The diagnosis must be often confirmed with the help of laboratory and histological findings. 
Key words: arthritis, gout - radiography 
Introduction 
Gout is a metabolic disorder that results in hyperuricemia and leads to monosodium urate crystals being deposited in various sites in the body, especially joint cartilage.1 
The commonly reported overall prevalence 
Received 3 November 2004 Accepted 23 November 2004 Correspondence to: Jelena Markota, MD, University 
Medical Centre, Clinical Institute of Radiology, Department of Radiology in Hospital Petra Držaja, Vodnikova 62, 1000 Ljubljana, Slovenia; Phone: +386 1 522 55 56; E-mail: jelena.markota@kclj.si 
of gout is 6 per 1000 population for men and 1 per 1000 population for women.2 The preva­lence is increasing with age to rates of 24 per 1000 in men and 16 per 1000 in women.3 A part of this increase may be increased physi­cians’ awareness of atypical gout.4 
The classic radiographic findings are asymmetrical soft tissue swelling with or without calcifications (gouty tophi); well-de­fined erosions, often with sclerotic borders or overhanging edges, without marked osteo­porosis.1 Joint space width may appear rela­tively wide.5 It typically affects the first metatarsophalangeal (MTP) joint. 

Case report 
A 63-year-old female has been admitted to the department of rheumatology in our hos­pital for several times over the last few years. She was complaining about swelling of the right great toe and right knee at times, about stiffness of feet and hands’ digits and about a backache. First symptoms started to appear 30 years ago. Laboratory tests showed hyper-uricemia. In the department of radiology we performed radiography of feet, ankles, knees, hands, sacroiliac joints and thoracic spine. The radiograph of feet demonstrated state af­ter bilateral operation of hallux valgus defor­mity, osteoarthritis of metatarsophalangeal (MTP) joints and fibular subluxation of digits. The bone structure of MTP joints of great toes was demineralised. We saw osteophytosis of ankles and osseous ankylosis of both insteps (Figure 1). The radiograph of knees showed effusion and marked hyperostotic osteophy­tosis. Degenerative joint disorders were seen on the radiograph of hands. On the sacroiliac joints the radiograph joint space irregularity could be seen: pseudodilatations, especially of the left joint space, indistinct outlines, fine erosions and juxta-articular sclerosis more pronounced on the side of iliac bone (Figure 2); the finding of sacroiliitis was additionally confirmed by the computed tomography. The thoracic spine radiograph demonstrated Forestier’s ankylosing hyperostosis. 

A diagnostic puncture of the right knee’s effusion was obtained. Intra- and extracellu­lar urate crystals were found in the synovial fluid using a polarizing microscope. The his­tological findings of the synovial tissue after the synovectomy of the right knee pointed to gouty arthritis. 
She also underwent the resection of the subcutaneous node on the left elbow. The hystological findings of the node showed large aggregations of uric acid crystals sur­rounded by abundant macrophages, scat­tered lymphocytes and foreign body type cells. The finding is typical of gouty tophi. 
Despite the unusual radiographic presen­tation, the diagnosis of gout was established with the help of laboratory and histological findings. 
Discussion 
Despite centuries of recognition of gout, the proper diagnosis of gout is still problematic.5 It has been only in the past 35 years that a sig­nificant research in the area of gout has been undertaken.6 The classic presentation of gout is as an acute monoarthritis often in the first MTP joint or in other joints, such as knee. Gout is a common problem in middle-aged males, from the fourth to sixth decade, but has an increasing recognition in elderly ones with unique and often atypical features.7 Acute attacks of gout are less common in eld­erly people, in whom it presents as a chronic polyarticular disease in a much different fash­ion making proper diagnosis less likely.8-10 In these cases gout can be misdiagnosed and confused with other arthritides or os­teoarthritis. 

In younger patients, hyperuricemia and gout are overwhelmingly observed in men. However, it has been recognized with an in­creasing frequency particularly in the elderly female population. Although historically only about 5% of all patients with gout were women, recent observations suggest that fe­male gouty arthritis occurs far more com­monly than previously suspected.6 After menopause, serum uric acid levels in women approach those in men. As many women as men are newly diagnosed as having gout when they are older than 60 years, and more women than men are diagnosed when they are older than 80 years.8 Many of these pa­tients also had underlying osteoarthritis. There is also the increased female-male ratio in atypical gout.4 
Although the location of gout is mostly in the MTP joint of great toe (followed by the other joints of foot, ankles, knees, hands), in case of atypical gout it occurs on uncommon places even for the first time. 
Gout is seldom the cause of backache. Sacroiliitis is a rare manifestation of gout. In the literature there are only a few descrip­tions of gout affecting spine. When lum­bosacral spine is involved, the same radi­ographic changes are described as on the pe­ripheral joints - soft tissue tophi, bone ero­sions with sclerotic borders and overhanging edges. There has been a case report of epidur­al tophus, which caused thoracic myelopathy 


Figure 2. Sacroiliitis shown by radiography; indistinct joint space and sclerosis more pronounced on the side of the iliac bone. 
due to the compression.11 Gout seldom pres­ents with ankylosis. There are some descrip­tions of ankylosis in advanced cases of chro­nic gout beginning in youth.12 
Radiographs are the most important imag­ing modality when diagnosing gout. However, the radiographic differential diag­nosis can be difficult, since the findings over­lap with other conditions which cause arthri­tis and osteoarthritis especially in longstand­ing gout, elderly patients and females.13 Therefore, the radiographic diagnosis of gout remains an important challenge and must of­ten be confirmed with the help of laboratory and histological findings. 
References 
1. 
Helms CA. Crystal-induced arthritis. In: Helms CA, editor. Fundamentals of skeletal radiology. New York.: W.B. Saunders company; 1995. p. 127­31. 

2. 
Arromdee E, Michet C, Crowson C, O’Fallon M, Gabriel S. Epidemiology of gout: is the incidence rising? J Rheumatol 2002; 29: 2403-6. 

3. 
Sturrock RD. Gout. Easy to misdiagnose. BMJ 2000; 320: 132-3. 

4. 
Rott K, Agudelo C. Gout. JAMA 2003; 289(21): 2857-60. 

5. 
Watt J. Basic arthritis diagnosis. In: Syllabus 11. Halley Project 1998-2000 - 2nd Refresher Course se­ries. Ljubljana; 2000. p. 169-71. 

6. 
Lomotan ER, Zimmermann B, Lally EV. Crystal-mediated articular disease in the elderly. Clin Rheum Dis 1986; 12: 97-116. 

7. 
Agudelo C, Wise C. Crystal-associated arthritis in elderly. Rheum Dis Clin North Am 2000; 26(3): 527­46. 

8. 
Agudelo C, Wise C. Crystal associated arthritis. Clin Geriatr Med 1998; 14: 495-513. 

9. 
Gonzalez E, Miller S, Agudelo C. Optimal man­agement of gout in older patients. Drugs Aging 1994; 4: 128-34. 

10. 
Fam A. Gout in the elderly: clinical presentation and treatment. Drugs Aging 1998; 13: 229-43. 


11. 
Yasuhara K, Tomita Y, Takayjama A. The myelopathy due to compression by the epidural tophus. J Spinal Disord 1994; 7: 82-5. 

12. 
Cortet B, Duquesnoy B, Amoura I, Bourgeois P, Delcambre B. La goutte ankylosante. Rev Rhum 1994; 61: 49-52. 

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Seidl G, Fischer W. Gout. In: Bohndorf K, Imhof H, Pope TL Jr, editors. Musculoskeletal imaging. Stuttgard: Thieme Verlag; 2001. p. 364-7. 



Radio/ Oncol 2004; 38(4): 253-67. 

Zgodovina Klinicnega inštituta za radiologijo v Ljubljani ­80. obletnica (1923-2003) 

Historia Magistra Vitae 
Jevtic V 
Izhodišca. Prikazana je kratka zgodovina Klinicnega radiološkega inštituta, Univerzitetnega kli­nicnega centra v Ljubljani od njegove ustanovitve l. 1923. Skozi celotno zgodovino so se na po­ti razvoja Inštituta pojavljali številni problemi. Najpomembnejši, s katerimi se soocamo tudi da­nes, vkljucujejo pomanjkanje strokovne in ekonomske samostojnosti. Posledica tega je nezmo­žnost spremljanja hitrega tehnološkega razvoja svetovne radiologije ter nezadostno število radi­ologov in radioloških inženirjev, ki so cezmerno obremenjeni z rutinskim delom, kar povzroca težave v ucni in raziskovalni dejavnosti. Kljub resnim oviram vodstvo Inštituta ter entuzijazem vseh radiologov in radioloških inženirjev zagotavljata nenehni strokovni in tehnološki razvoj, ki je osnova današnje visoko kvalitetne diagnosticne in intervencijske radiologije. Mnogo izrednih dosežkov ne bi bilo brez nekaj izrednih oseb, ki so položile trdne temelje današnjega Inštituta. Zakljucki. 80 let Klinicnega inštituta za radiologijo v Ljubljani je zgodovina uspešnega razvoja vodilne radiološke institucije v republiki, ki so jo skupaj z vodstvom zagotovili odlocnost, eno­tnost in profesionalnost vseh zaposlenih. 
Radio/ Oncol 2004; 38(4): 353-62. 

Radio/ Oncol 2004; 38(4): 269-73. 

Dezinvaginacija s hidrokolonsonografijo pri otroku 
Vidmar D, Višnar Perovic A 
Izhodišca. Invaginacija je najpogostejši vzrok crevesne obstrukcije pri otrocih, mlajših od dveh let. Proksimalni del crevesa in njegov mezenterij (intususceptum) se uvihata v distalni del (intu­suscipiens), nato ju peristaltika vlece naprej, pri cemer se komprimira mezenterialno žilje. Naj­pogostejša je ileokolicna invaginacija. Diagnozo lahko postavimo z irigografijo ali ultrazvokom. Ultrazvocni znaki so t.i. »kokarda v kokardi«, zadebeljena stena z ali brez znakov prekrvavitve ter prestenoticna dilatacija z ojacano peristaltiko. Dezinvaginacijo lahko izpeljemo s kontra­stnim sredstvom ali z zrakom pod rentgensko kontrolo ali s fiziološko raztopino pod ultrazvo­
cno kontrolo. Bolniki in metode. Pri treh deklicah v starosti 15,16 in 18 mesecev smo ob tipicni klinicni sliki ultrazvocno diagnosticirali ileokolicno invaginacijo in nadaljevali z dezinvaginacijo pod ultra­zvocno kontrolo. S pomocjo sistema za uvajanje barija pri irigografiji smo v široko crevo dova­jali fiziološko raztopino, ogreto na telesno temperaturo. Posoda s tekocino je bila 1 m nad prei­skovalno mizo. Kolicina uporabljene tekocine je bila vec litrov, ker je zaradi nepopolne okluzije rektuma precej tekocine odteklo. Ultrazvocno smo opazovali potovanje vrha invaginata nazaj v proksimalni smeri. Poseg smo zakljucili, ko je izginila tipicna slika »kokarde v kokardi« in je pri­šlo do refluksa tekocine v terminalni ileum. Rezultati. Poseg je bil uspešen in je potekal brez komplikacij pri vseh treh deklicah. Bolecine so takoj po posegu prenehale. Ob kontrolnih pregledih po 2 in 12 urah ni bilo vec znakov invagi­nacije. Nekoliko edematozna je bila stena valvule Bauchini in terminalnega ileuma. Klinicno sta­nje deklic je bilo normalno, tako da so bile odpušcene v domaco oskrbo neposredno po drugi ul­trazvocni kontroli. Zakljucki. Dezinvaginacija s hidrokolonsonografijo je zaradi visoke ucinkovitosti in odsotnosti ionizirajocega sevanja metoda izbora. Zapleti doslej niso opisovani. 
Radio! 011col 2004; 38( 4): 2 75-84. 

Prikaz napredovanja hemisfericne spondiloskleroze s slikovno magnetno resonanco in paramagnetnim kontrastnim sredstvom Gd-DTPA 
Jevtic V, Majcen N 
Izhodišca. Namen študije je bil ugotoviti vrednost slikovne magnetne resonance (MRI) s para­magnetnim kontrastnim sredstvom Gd-DTP A v prikazu napredovanja hemisfericne spondilo­skleroze (HSS). Bolniki in metode. Pri 18 bolnikih s kronicno bolecino v križu in tipicnimi radiografskimi znaki HSS smo opravili Gd-DTPA MRI lumbalne hrbtenice. Primerjali smo morfološke spremembe in spremembe intenzitete signala z radiografskimi znaki HSS. Rezultati. Na podlagi MRI smo primere razdelili v tri skupine. V prvi skupini je bilo radiograf­sko podrocje osteoskleroze hipointenzivno na Tl-poudarjenih spin-eho slikah, hiperintenzivno na T2-poudarjenih slikah in je kazalo difuzno nabiranje paramagnetnega kontrastnega sredstva. Opisane spremembe so bile združljive s kostnim edemom in hiperemijo. V drugi skupini so bi­li robovi vretenc na vseh slikovnih sekvencah hiperintenzivni, obdani s hipointenzivno cono in se v njih ni nabiralo kontrastno sredstvo. Opisano je izražalo kombinacijo mašcevja in kostne skleroze. Pri preostalih bolnikih so MRI znaki predstavljali kombinacijo sprememb vidnih v pr­vi in drugi skupini. Zakljucki. Gd-DTP A MRI kaže zapletene histološke spremembe v teku napredovanja HSS. Spremljanje znacilnih MRI znakov ima lahko klinicni pomen pri sledenju bolezni. 
Radio/ Oncol 2004; 38(4): 353-62. 

Radio/ Oncol 2004; 38(4): 285-90. 

Radiološka diagnostika akutnega pankreatitisa 
Glušic M, Brencic E, Popovic P 
Izhodišca. Akutni pankreatitis zajema širok spekter vnetnih sprememb parenhima pankreasa, najpogostejša vzroka sta alkoholizem in žolcni kamni, drugi pa so redkejši. V clanku obravnavamo diagnosticne metode, povezavo med morfološkimi ugotovitvami, labora­torijskimi testi in nacinom zdravljenja. Zakljucki. Moderne diagnosticne metode, ki so danes na voljo, so pripomogle k boljšemu pozna­vanju morfoloških sprememb, ki jih akutni pankreatitis povzroca. 
Radio/ Onco/ 2004; 38(4): 291-7. 

Magnetnoresonancna angiografija splenoportalnega sistema 
Berden P 
Izhodišca. Splenoportalni venski sistem moramo prikazati pri razlicnih klinicnih stanjih. Tridi­menzionalna (3D) magnetnoresonancna angiografija (MRA) s kontrastom splenoportalni sistem dobro prikaže. Uporabljamo hitre sekvence z gradientnim odmevom ter najkrajšim možnim ca­som ponovitve in odmeva. Skozi periferno veno injiciramo do 40 ml paramagnetnega kontra­stnega sredstva. Za zaznavanje kontrasta v aorti je najbolje uporabiti avtomatiziran sistem, ki nato tudi sproži slikanje. Slikanje opravimo v zadržanem dihu in dvakrat ponovimo, da prikaže­mo arterijsko in vensko fazo. Za obdelavo slik po preiskavi najveckrat uporabljamo tehniko pro­jekcije maksimalne intenzitete (MIP). Zakljucki. Pri bolnikih s portalno hipertenzijo MRA dobro prikaže kolaterale ter prehodnost portalne vene ali portosistemskega šanta. MRA pokaže mesto in dolžino zapore portalne vene pri trombozi portalne vene in pomaga pri odlocitvi o nacinu zdravljenja. Je ustrezna tehnika pri sindromu Budd-Chiari, kjer je pomembno dolociti mesto in dolžino zapore jetrnih ven. MRA je zelo dobra metoda pred presaditvijo jeter, saj odlicno prikaže anatomijo in prehodnost portalne vene, in tudi po presaditvi za odkrivanje morebitnih zapletov. Omejitev MRA predstavljajo me­talni vsadki (npr. srcni vzpodbujevalnik), nezadovoljiv prikaz pa lahko dobimo pri nepravilni na­stavitvi podrocja slikanja in premikanju zaradi dihanja. 
Radio/ Oncol 2004; 38(4): 299-308. 
Intervencijska radiologija pri hemodializnih fistulah 
Šurlan M, Popovic P 
Izhodišca. Namen clanka je podati pregled vloge intervencijske radiologije pri obravnavanju he­modializnih žilnih pristopov. Obravnava bolnika, preden oblikujemo žilni pristop za hemodiali­zo, vkljucuje radiološko ali ultrazvocno diagnostiko perifernega žilja zgornje okoncine in ugotav­ljanje prehodnosti centralne vene. Kasneje pa vkljucujeodkrivanje in zdravljenje zožitev ali tromboz v slabo delujocih dializnih fistulah. Predoperacijski pregled omogoca izbiro ustreznih žil za oblikovanje dobro delujoce dializne fistule. Klinicno in radiološko odkrivanje hemodinam­sko pomembnih zožitev ali zapor vkljucuje fistulografijo, ki ji po potrebi sledi endovaskularno zdravljenje. Razširitev zožitev, ki so vecje od 50%, je upravicena, ker podaljšuje prehodnost žil­nega dostopa. Tehnicni uspeh razširitve je 90%. Enoletna primarna prehodnost razširjene fistu­le na podlahti znaša 51 %, pri graftih pa 40%. Žilne opornice postavljamo le v izbranih primerih; rutinsko pa v centralno veno po razširitvi, v primeru raztrganja vene ali prekomerne elasticne zožitve po razširitvi. Zakljucki. Prehodnost tromboziranih fistul ali graftov lahko zagotovimo z mehanicnimi postop­ki ali v kombinaciji s tromboliticnim zdravljenjem. Tehnicni uspeh dosežemo v 89% -90%, pri­marno enoletno prehodnost pa le v 8% -26%, vendar sekundarna prehodnost dosega 75%. 
Radio/ On col 2004; 38( 4): 353-62. 

Radio/ Oncol 2004; 38(4): 309-21. 

Radiološka diagnostika in zdravljenje zapletov presajene ledvice 
Popovic P, Šurlan K 
Izhodišca. Namen clanka je podati pregled vloge intervencijske radiologije v diagnostiki in zdravljenju zapletov po presaditvi ledvic. Zapleti nastanejo na žilah, secnih izvodilih ter v ledvi­ci in njeni okolici v obliki patoloških tekocinskih formacij. Diagnostiko, nacrtovanje in vodenje znotrajžilnega zdravljenja žilnih zapletov opravljamo z Dopplerskim ultrazvokom (UZ), magne­tno resonanco (MR) in z digitalno subtrakcijsko angiografijo (DSA). Zakljucki. Najpogostejši žilni zaplet presajene ledvice je zožitev ledvicne arterije, ki se pojavi pri 1 % -12% bolnikov. Nezdravljena zožitev je lahko razlog za arterijsko hipertenzijo in odpoved le­dvice, ceprav je zaplet potencialno ozdravljiv. Zožitev zdravimo s perkutano transluminalno le­dvicno angioplastiko (PIRA) z uporabo žilne opornice ali brez nje, ki je za hipertenzijo uspešna v 82% -92% primerov, ohranitev presajene ledvice pa je možna v 80% -100%. Zapleti, kot sta ar­terijska in venska tromboza, so redki. Po biopsijah se obcasno pojavijo znotraj ledvicne arterio­venske fistule in psevdoanevrizme, ki jih zdravimo s superselektivno embolizacijo. Najpogostej­ši urološki zapleti so zožitve, zapore in fistule secevodov, ki jih zdravimo s perkutano nefrosto­mo, balonsko dilatacijo, vstavitvijo dvojne J kateterske opornice ali kovinske opornice. Tekocin­ske patološke kolekcije, kot so limfokele, abscesi, hematomi zdravimo s perkutano drenažo. 
Radio/ Oncol 2004; 38(4): 323-7. 

Anularni pankreas, vzrok izvenjetrne zapore: prikaz primera 
Ogulin M, Jamar B 
Izhodišca. Anularni pankreas, redka prirojena anomalija, je trak pankreaticnega tkiva, ki obkro­ža dvanajstnik ali izvenjetrni žolcni vod. Prikazujemo primer anularnega pankreasa, ki je po­vzrocil izvenjetrno zaporo odtoka žolca. Prikaz primera. 46-letna ženska je prišla v urgentno ambulanto zaradi nenadnih bolecin v trebu­hu, bruhanja in zlatenice. V zadnjih šestih letih je obcasno opazila rumenkasto obarvanje kože, v zadnjem letu pa je obcutila napetost v zgornjem delu trebuha, predvsem po mastnih obrokih. Zakljucki. Dve ultrazvocni preiskavi, prva pred šestimi meseci, sta pokazali razširitev glavnega izvenjetrnega voda in jetrnih žolcnih izvodil. Vzrok za razširitev je ostal nejasen, tudi po endo­skopski ultrazvocni preiskavi. Pri operaciji so našli skoraj popolno zaporo izvenjetrenega žolcne­ga voda, ki jo je povzrocal tracek pankreaticnega tkiva. 
Radio/ Oncol 2004; 38(4): 329-32. 

Klinicni pomen odkritja plina v portalnih venah jeter pri ultrazvo­
cnem pregledu trebuha: prikaz dveh primerov 
Gregoric P, Višnar-Perovic A 
Izhodišca. Dokaz plina v veni porte je ponavadi znak resnega obolenja v trebuhu in pomeni sla­bo prognozo. Z napredkom ultrazvocne diagnostike v zadnjih letih odkrijemo zrak v portalni veni tudi kot pre­hoden pojav brez klinicnih posledic in sicer pri topi poškodbi trebuha in nekaterih diagnosticnih in terapevtskih postopkih. Prikaz primerov. Predstavljamo dva bolnika. Obema smo pri ultrazvocni preiskavi trebuha od­krili znake plina v portalnih venah, potek bolezni pa je bil diametralno nasproten. Prvi bolnik je bil star 70 let. Utrpel je infarkt mezenterija, cigar posledica je bil plin v portalnih venah. Umrl je nekaj ur po prihodu v bolnišnico. Drugi bolnik je bil star 26 let. Poškodovan je bil kot voznik v prometni nesreci. Med hospitalizacijo je bil klinicno stabilen in ni potreboval invazivnega zdrav­ljenja. Ugotovili smo, da se je pojavil plin v portalni veni prehodno zaradi tope poškodbe trebu­ha. Zakljucki. Ultrazvocna preiskava trebuha z uporabo Dopplerja je obcutljiva in specificna meto­da za dokaz plina v portalnih venah. Z ultrazvocno preiskavo lahko tudi odkrijemo obolenje v trebuhu, ki je vzrok za ta pojav in skrajšamo cas do potrebnega zdravljenja. Ce z ultrazvocno preiskavo ne odkrijemo jasnega vzroka za plin v portalnih venah, se moramo o nadaljnih, poten­cialno nevarnih diagnosticnih in terapevtskih postopkih odlocati glede na klinicno sliko, ker je pojav plina v portalnih venah lahko tudi prehodnega znacaja. 
Radio/ Oncol 2004; 38(4): 333-8. 
Radiograf ski, racunalniškotomografski in magnetnoresonancni znaki primarne cone kostne resorpcije v korpusu ledvenega vretenca pri Pagetovi bolezni 
Jevtic V 
Izhodišca. Potek Pagetove bolezni kosti ima tri razvojne faze z znacilnimi radiografskimi znaki. V zacetni fazi je prisotna napredujoca cona kostne resorpcije. Primarna napredujoca cona oste­olize ni bila nikoli jasno prikazana na hrbtenici in medenici, kot je bila na lobanji in dolgih ko­steh. Prikaz primera. 62-letni bolnik s histološko potrjeno diagnozo poliostotske Pagetove bolezni je bil sprejetv bolnico zaradi bolecin v višini torakolumbalnega prehoda, ki so se ponoci stopnje­vale. Zaradi zmerno zvišane kisle fosfataze ter klinicnih znakov hipertrofije prostate je bil po­stavljen sum na karcinom prostate. Kostna scintigrafija s tehnecijevim fosfonatom je pokazala pricakovano nabiranje radiofarmaka na številnih kostnih elementih s tipicnimi radiografskimi znaki Pagetove bolezni. Razen omenjenega se je pokazalo zmerno žarišcno nabiranje radiofar­maka tudi v desni dorzalni polovici korpusa vretenca L1. V istem podrocju so klasicna tomogra­fija, racunalniška tomografija (CT) ter magnetnoresonancna tomografija (MRI) prikazale primar­no cono kostne resorpcije. Zakljucki. Prikazan je edinstven primer Pagetove bolezni s primarno cono kostne resorpcije v morfološko nespremenjenem korpusu vretenca Ll. Po treh letih zasledovanja je prišlo do spon­tanega napredovanja v srednjo fazo bolezni. 
Radio/ Oncol 2004; 38(4): 339-47. 

Kalcifikacija medvretencne plošcice vratne hrbtenice pri otroku in prsne hrbtenice pri odraslem z dorzalno hernijacijo -radiografski, racunalnoškotomograf ski ter magnetnoresonancni znaki 
Jevtic V 
Izhodišca. Kalcifikacije nukelusa pulposusa pri otroku so sorazmerno redek, vendar dobro znan klinicni sindrom, ki se obicajno pojavlja na vratni hrbtenici. Natancen vzrok še vedno ni znan. Kalcifikacije medvretencne plošcice odraslega so vecinoma posledica degeneracije in se pojav­ljajo v višini spodnje prsne in zgornje ledvene hrbtenice. Pri obeh entitetah lahko nastane resna komplikacija, posteriorna hernijacija kalcificiranega diskusa. Prikaz primera. Prikazana sta dva primera kalcificirane medvretencne plošcice, prvi pri 7-letnem otroku v višini C7-Tl ter drugi pri 45-letni ženski v višini Tl1-Tl2, oba z razsežno dorzalno her­nijacijo. V prvem primeru je dosežena remisija s konservativnom zdravljenjem. Na podlagi ana­lize radiografskih, racunalniškotomografskih ter magnetnoresonancnih (MRI) sprememb smo ugotovili podobnosti in razlike med obema entitetama. Zakljucki. Masivna dorzalna hernijacija kalcificiranega nukleusa pulposusa pri otroku je uspe­šno zdravljena konzervativno. Izginotje klinicnih znakov je sledilo hitri resorpciji kalcificirane duskus hernije. Pri odraslem po konzervativnem zdravljenju ni prišlo do resorpcije kalcificirane diskus hernije in klinicnih znakov izboljšanja. Z MRI je možen zgodnejši prikaz kalcifikacij. Tu­di razširitev prizadetih medvretencnih plošcic pri otroku je boljše prikazana z MRL Razširitev kalcificiranih medvretencnih plošcic podpira teorijo zvišanega intradiskalnega pritiska kot vzro­ka rupture anulusa fibrozusa in posledicne hernijacije nukleusa pulposusa. 
Radio/ Oncol 2004; 38(4): 353-62. 

Radio/ Oncol 2004; 38(4): 349-52. 
Nenavadne radiografske spremembe pri bolnici s putiko 
Markota J 
Izhodišca. Putika je metabolna motnja, ki je povezana s hiperurikemijo in nalaganjem kristalov secne kisline (uratov) v tkiva, zlasti v sklepni hrustanec. Za uricni artritis so znacilni ponavljajo­ci se napadi akutnega artritisa, ki se lahko nadaljuje v kronicno obliko. V 80% primerov se bole­zen zacne v metatarzofalangealnem sklepu nožnega palca in je pogostejša pri moških. Prikaz primera. Prikazali smo primer nenavadnih radiografskih sprememb pri uricnem artritisu. 63-letna bolnica se je pritoževala nad obcasnim otekanjem bazalnega sklepa desnega nožnega palca in desnega kolena, okorelostjo stopal in prstov rok ter bolecinami v hrbtu. Prve težave so se pojavile pred tridesetimi leti. Rentgenogrami so pokazali degenerativne spremembe vecine slikanih sklepov, obojestranski sakroiliitis in kostno ankilozo obeh nartov. Pri pregledu sinovij­ske tekocine kolena s polarizacijskim mikroskopom so ugotovili uratne kristale. Tudi histološki izvid sinovije po sinovektomiji je potrdil uricni artritis. Zakljucki. Radiografija je najpomembnejša slikovna metoda pri diagnostiki putike. Diferencial­na diagnostika pa je lahko težavna, kadar se spremembe prekrivajo z drugimi artritisi ali osteo­artrozo, zlasti pri dolgotrajni putiki, starejših bolnikih in ženskah. V teh primerih koncno dia­gnozo potrdimo z laboratorijskimi in histološkimi izvidi. 


Notices 
Natices submitted far publicatian shauld cantain a mailing address, phane and/ ar fax number and/ ar e-mail af a Contact persan ar department. 
Thoracic oncology 
]a1111ary 14-16, 2005 
The »4th Annual Clinical Cancer Update« will be 
held in North Lake Tahoe, USA. 
Contact UCSF Office of Continuing Medical Educa­tion, P.O. Box 45368, San Francisco, CA 94145-0368, USA; or call +1 415 476 4251; or fax +1 415 502 1795; email info@ocme.ucsf.edu; or see http:// www.cme. ucsf.edu 

Radiation oncology 
March, 2005 
The ISRO international teaching course on »Palliati­ve Care in Cancer Treatment« will take place in Dar es Salaam, Tanzania. 
See http://www.isro.be 

Brachytherapy 
May 5-7, 2005 
The Annual Brachytherapy Meeting GEC-ESTRO and pre-meeting workshop on breast cancer will take place in Budapest, Hungary. 
Contact ESTRO office, Avenue E. Mounier, 83/12, B-1200 Brussels, Belgium; or call +32 775 93 40; or fax +32 2 779 54 94; or e-mail info@estro.be; or see http://www.estro.be 

Clinical oncology 
May 13-17, 2005 
The ASCO Meeting will be offered in Orlando, USA. E mail enews@asco.org; or see http://www/asco.org 

Lung cancer 
July 3-6, 2005 
The »llth World Conference on Lung Cancer« will be offered in Barcelona, Spain. 
Contact Heather Drew, Imedex, !ne., 70 Technology Drive, Alpharetta, GA 30005 USA; or call +1 770 751 7332, or fax +1 770 751 7334; or e-mail h.drew@ imedex.com, or see ,,vww.imedex.com/calenders/on­cology/htm 

Radiotherapy 
September 24-29, 2004 
The »8th Biennial ESTRO Meeting on Physics and Radiation Technology for Clinical Radiotherapy« and »Pre-Meeting Workshop on Image-Guided Radiothe­rapy« will take place in Lisboa, Portugal. 
Contact ESTRO office, Avenue E. Mounier, 83/12, B-1200 Brussels, Belgium; or call +32 775 93 40; or fax +32 2 779 54 94; or e-mail info@estro.be; or see http://vvww.estro.be 

Radiation oncology 
September -October, 2005 
The ISRO international teaching course on »Ratio­nal Developments from developing to developed Co­untries« will take place in Lombok, Indonesia. 
See http://www.isro.be 


Lung cancer 
October 17-19, 2005 
The IASLC workshop »Biology and Prevention of Lung Cancer« will be offered in Woodstock, Vermont, USA. 
Contact Taryn Klocke at Envision Communications; call +1 770 763 5690; or see www.lungcancerpreventi­on.net 
Radio/ Oncol 2004; 38(4): 363-4. 

364 Notices 
Oncology 

October 30 -November 3, 2005 
The ESTRO 24 / ECCO 13 Conference will take pla­ce in Paris, France. 
Contact FECS office, Av. E. Mounier, 83/4, B-1200 Brussels, Belgium; or call +32 7759340; or fax +32 2 7795494; or e-mail info@estro.be; or see http://wvvw. fecs.be 
As a service to our readers, notices oj meetings ar courses will be inserted free o f charge. Please send infomzation to the Editorial office, Radiology and Oncology, Zaloška 2, SI-1000 Ljubljana, Slovenia. 

Author Index 2004 
Atanasova S: 1/21-6 
Badowska-Roslonek: 2/137-44 Balta S: 2/145-51 Banev S: 2/131-5 Bartoli F: 2/101-9 Berden P: 4/291-7 Bešlic Š: 1/5-13 Biermann J: 2/111-9 Borštnar S: 1/15-9 Brencic E: 4/285-90 Brkljacic B: 3/171-5 
Casar B: 1/55-60 Cerar A: 3/227-34 Cukjati D: 1/49-54 Czarnomska A: 3/217-25 
Corovic S: 1/49-54 Cufer T: 2/85-92 
Decorti G: 2/101-9 Demant P: 3/217-25 Dizdarevic Z: 2/145-51 Duric O: 2/145-51 
Ehrlich V A: 3/205-16 Eynard N: 2/121-9 
Farthmann J: 2/111-9 
Ganeva V: 2/121-9 Garaj-Vrhovac V: 1/43-7 Gavrankapitanovk F: 2/145-51 Giraldi T: 2/101-9 Glušic M: 4/285-90 Godlewska J: 2/137-44 Grasl-Kraupp B: 3/205-16 Gregoric P: 4/329-32 
Holzscheiter L: 2/111-9 Huber W: 3/205-16 Huzjan R: 3/171-5 
Ihan Hren N: 3/187-92 Ilievska Poposka B: 1/21-6; 2/131-5 
Jamar B: 4/323-7 Janevska V: 3/165-9 Jeraj M: 3/235-40 Jereb B: 3/181-5 Jevtic V: 4/Editorial, 4/253-67, 4/275-84, 4/333-8, 
4/339-47 Jezeršek Novakovi<' B: 1/15-9 Kaczmarek L: 2/137-44 Kagohashi K: 2/153-4 KnasmLller S: 3/205-16 Kocijancic I: 3/177-80 Kotzsch M: 2/111-9 Kovac V: 1/27-34 Kralj B: 1/27-34 Kramar P: 1/49-54 Krysiak E: 3/217-25 
Lipovec A: 3/187-92 Luther T: 2/111-9 
Magdalen V: 2/111-9 Majcen N: 4/275-84 Malusa N: 2/101-9 Markota J: 4/349-52 Martelossi S: 2/101-9 Marušk P: 3/171-5 Metodieva M: 1/21-6 Meye A: 2/111-9 Miklavcic D: 1/49-54; 3/165-9 Miladinova D: 3/165-9 Moscatello I: 1/1-4 
Nakaš B: 2/145-51 Nersesyan A: 3/205-16 Novakovi<' S: 2/73-83 
Obralic N: 2/145-51 Ogulin M: 4/323-7 Ohara G: 2/153-4 Opalski A: 2/137-44 
Pavliša G: 1/1-4 Pavlovic I: 1/49-54 PeczyUska-Czoch W: 2/137-44 Petrusevska G: 2/131-5 Piskorowska J: 3/217-25 Plesnicar A: 1/27-34 Popeska Ž: 3/165-9 Popovic M: 3/181-5 Popovic P: 4/285-90, 4/299-308, 4/309-21 
Ramza J: 2/137-44 Robar V: 1/55-60; 3/235-40 Rols MP: 2/121-9 
Samardziski M: 3/165-9 Satoh H: 2/153-4 Schmitt M: 2/111-9 Sekizawa K: 2/153-4 Selak I: 2/145-51 Sjekavica I: 1/1-4 

Radio/ Oncol 2004; 38(4): 365-6. 
Skurzak H: 3/217-25 Smickova S: 2/131-5 Span P: 2/111-9 Spirovski M: 1/21-6 Spirovski Z: 2/131-5 Stefanovski T: 1/21-6 Stocco G: 2/101-9 Strojan P: 2/93-100; 3/181-5 Sweep F: 2/111-9 Szymariska H: 3/217-25 
Šeronja-Kuhar M: 1/1-4 Šišic' F: 2/145-51 Šoštaric M: 1/35-42; 3/193-203 Šprah L: 1/35-42; 3/193-203 Štern-Padovan R: 1/1-4 Šurlan K: 3/181-5; 4/309-21 Šurlan M: 4/299-308 
Teissie J: 2/121-9 Tomšic-Demšar R: 1/15-9 Trajkov D: 1/21-6 
Veceric' Ž: 3/227-34 Ventura A: 2/101-9 Vernhes MC: 2/121-9 Vidmar D: 4/269-73 Višnar-Perovic' A: 4/269-73, 4/329-32 Vovk M: 1/15-9 Vukelic'-Markovic' M: 3/171-5 
Zafiroski G: 3/165-9 Zdešar U: 1/55-60 Zeljezic' D: 1/43-7 
Supplement V2004 
Casselman J: Sl/153-7 Chersevani R: Sl/139-51 
Cavlek M: Sl/9-20 Cebulj K: Sl/35-49 Cufer T: S1/105-10 
Hertl K: S1/9-20, Sl/51-7, Sl/87-92, Sl/115-26 Hudales B: Sl/115-26 
Jereb B: Sl/9-20, S1/51-7 Jokan E: Sl/115-26 
Kadivec M: Sl/9-20, Sl/51-7, Sl/115-26 Kirar-Fazarinc I: S1/21-5 Kokot A: Sl/115-26 Krajnc Z: S1/35-49, S1/115-26 
Locatelli M: Sl/139-51 
Radio/ Onco/ 2004; 38(4): 365-6. 
Marolt Mušic M: Sl/9-20, S1/51-7 
Novak G: S1/35-49 
Podkrajšek M: Sl/9-20, S1/51-7, S1/83-6 Pogacnik A: S1/93-7 Primic Žakelj M: S1/1-7, Sl/21-5 
Rataj A: Sl/35-49 Rener M: SI/Uvodnik, S1/9-20, Sl/35-49, S1/59­
68, S1/69-78, Sl/79-82, Sl/87-92 Rizzatto G: S1/139-51 Rusjan P: Sl/35-49 
Sardo A: S1/127-30 Schwarzbartl-Pevec A: Sl/99-103 Steyaert L: S1/153-7 Strojan Fležar M: Sl/93-7 
Škrk D: S1/27-33 
Van Kerkhove F: Sl/153-7 Vargazon T: Sl/9-20, Sl/59-68, Sl/69-78, 
Sl/79-82, S1/87-92 Vidergar-Kralj B: S1/99-103 
Weismann Ch: Sl/131-8 
Zadnik V: Sl/1-7 
Žagar I: Sl/99-103 Žgajnar J: S1/111-3 

Subject Index 2004 
acute disease: 4/285-90 adjustment disorders: 3/193-203 adrenal gland neoplasms: 3/177-80 angioplasty, balloon: 4/309-21 aortic coarctation-diagnosis: 1/5-13 arthritis, gouty-radiography: 4/349-52 azathiopurine: 2/101-9 
bile duet obstruction, extrahepatic: 4/323-7 biological: 1/21-6 biopsy, needle: 3/177-80 bone neoplasms-pathology: 3/165-9 Bosnia-Hercegovina cancer incidence: 2/145-51 breast neoplasms: 2/85-92 -breast neoplasms-prevention and control: 1/27-34 
calcinosis: 4/339-47 cancer patients, coping strategies psychosocial prob­
lems, psychosocial support: 1/35-42 carcinoma small celi: 1/21-6 carcinoma, squamous celi: 2/93-100 cathepsins, cystatins: 2/93-100 catheters, indwelling: 4/299-308 cell membrane permeability: 2/121-9 chemotherapy, adjuvant: 3/181-5 child: 4/269-73 cholangiopancreatography, endoscopic retrograde: 
4/323-7 choroid plexus neoplasms: 3/181-5 colonic neoplasms: 3/205-16 comet assay: 1/ 43-7 
DNA damage: 1/43-7 DNA topoisomerases, type II-antagonists and in­
hibitors: 2/137-44 diagnosis, computer-assisted: 3/165-9 distress, intervention, screening: 3/193-203 dosimetry: 1/55-60 drug delive1y systems: 1/49-54 
electron beams: 1/55-60 electroporation: 2/121-9 -electroporation-instrumentation: 1/49-54 embolism, air-ultrasonography: 4/329-32 esophageal diseases, rupture, spontaneous: 1/1-4 
gadolinium DTP A: 4/275-84 genotype: 2/101-9 
haematoma, tomography, X-ray computed: 3/171-5 head and neck neoplasms: 2/93-100 health promotion: 1/27-34 hemodialysis: 4/299-308 IAEA TRS-398: 1/55-60 immunohistochemistry: 2/131-5 incidence: 2/145-51 indols: 2/137-44 inflammatory bowel diseases-drug therapy: 2/101-9 internet: 1/49-54 intervertebral <lise: 4/339-47 -intervertebral <lise displacement: 4/339-47 intestinal neoplasms-chemically induced: 3/227-34 intussusception-therapy-ultrasonography: 4/269-73 
jaw cysts-pathology: 3/187-92 
kidney diseases: 3/171-5 kidney failure, chronic: 4/299-308 kidney transplantation: 4/309-21 
!iver neoplasms: 3/205-16 lung neoplasms: 1/21-6 -lung neoplasms-pathology: 2/131-5 -lung neoplasms-secondary-ultrasonography-patholo­
gy: 3/177-80 lymphocytes-radiation effects: 1/43-7 lymphoma, nonHodgkin's: 1/15-9 
magnetic resonance angiography: 4/291-7 magnetic resonance imaging: 1/5-13; 4/275-84, 
4/333-8, 4/339-47 models, mice: 3/217-25 mood disorders: 3/193-203 multileaf collimator, field shaping: 3/235-40 
neoplasms: 2/111-9 -neoplasms-epidemiology: 2/145-51 -neoplasms-diagnosis: 2/73-83 -neoplasms-drug therapy: 1/49-54 neoplasms-psychology: 1/35-42 -neoplasms-radiotherapy-psychology: 3/193-203 neuron specific enolase: 1/21-6 
odontogenic cysts-epidemiology: 3/187-92 1,2 dimethylhydrazine: 3/227-34 osteitis deformans: 4/333-8 osteosclerosis: 4/275-84 
pancreas-abnormalities: 4/323-7 pancreatitis-radiography: 4/285-90 phenotype: 2/101-9 plasminogen activator inhibitor 1: 2/85-92 Plastic Water: 1/55-60 portal vein: 4/291-7, 4/329-32 preneoplastic lesions: 3/205-16 prognosis: 2/85-92, 2/93-100, 2/131-5 

Radio/ Onco/ 2004; 38(4): 367-8. 

quinones: 2/137-44 

radiology department, hospital: 4/253-67 radiology-history-trends: 4/253-67 radiology, interventional: 4/299-308, 4/309-21 radiotherapy: 3/181-5, 3/235-40 -radiotherapy dosage: 3/235-40 rats, inbred F344: 3/227-34 rats Wistar: 3/227-34 receptors »erb-2«: 2/131-5 renal artery obstruction: 4/309-21 reverse transcriptase polymerase chain reaction: 
2/111-9 rituximab: 1/15-9 RNA, messenger: 2/111-9 RNA splicing: 2/111-9 
6-mercaptopurine: 2/101-9 social support: 1/35-42 spina! diseases: 4/275-84 -spina! diseases-radiography: 4/333-8 -spina! diseases-radiography, tomography: 4/339-47 survival analysis: 3/181-5 
T-cell lymphoma, B-cell lymphoma: 3/217-25 tomography, X-ray computed: 1/1-4; 4/333-8 tumor markers: 1/21-6 -tumor markers, biological: 2/73-83 
ultrasonography, Doppler: 4/329-32 urinary plasminogen activator: 2/85-92, 2/111-9 
vascular patency: 4/291-7 
X-ray computed: 4/339-47 
Supplement V2004 
anatomija dojke: S1/51-7 aspiracijska biopsija s tanko iglo: S1/93-7 
bolecina: S1/115-26 bolezni, rak dojk: S1/87-92 breast: S1/131-8, S1/139-51, S1/153-7 
ciste: S1/69-78 citopatologija: S1/93-7 
diagnostika: S1/79-82, S1/93-7 digital: S1/127-30 dojka: S1/79-82, S1/87-92 -dojka, netipne lezije, lokalizacija: S1/99-103 
elastography: S1/139-51 epidemiologija: S1/1-7 
four dimensional: S1/131-8 
Radio/ Oncol 2004; 38(4): 267-8. 
intervencijska radiografija: S1/87-92 ionizirajoce sevanje: S1/27-33 
kirurško zdravljenje: S1/111-3 klasifikacija: S1/59-68, S1/69-78 kontrola kakovosti: S1/35-49 
limfoscintigrafija: S1/99-103 
mammasonography: S1/131-8 mammography: S1/127-30 mamografija: S1/9-20, S1/27-33, S1/35-49, S1/51-7, 
S1/59-68, S1/115-26 mamomat: S1/153-7 MRI: S1/153-7 
netipljive lezije: S1/93-7 netipljivi invazivni rak: S1/105-10 nevarnostni dejavniki: S1/1-7 nonpalpable lesions: S1/139-51 
optimizacija: S1/27-33 
perfusion imaging: S1/139-51 PET: S1/99-103 pozicioniranje: S1/35-49 preiskava pazduhe: S1/83-6 presejalni program odkrivanja raka dojk: S1/27-33 presejanje: S1/1-7, S1/9-20, S1/21-5, S1/59-68 primarna preventiva: S1/1-7 prognoza: S1/105-10 program: S1/21-5 
radiofarmaki: S1/99-103 
rak dojk: S1/1-7, S1/9-20, S1/21-5, S1/59-68, S1/69-78, S1/83-6, S1/87-92, S1/93-7, S1/105-10, S1/111-3 
scintimamografija: S1/99-103 screen-film: S1/127-30 sekundarna preventiva: S1/9-20, S1/21-5 stereotactic guidance: S1/153-7 
three-dimensional: S1/131-8 tipljiva lezija: S1/79-82 
ultrasound: S1/131-8, S1/139-51, S1/153-7 ultrazvocno vodena tankoigelna biopsija: S1/83-6 ultrazvok: S1/51-7, S1/69-78, S1/83-6 upravicenost: S1/27-33 
vacuum biopsy: S1/153-7 varovalne bezgavke: S1/111-3 


FONDACIJA "DOCENT DR. J. CHOLEWA" JE NEPROFITNO, NEINSTITUCIONALNO IN NESTRANKARSKO ZDRUŽENJE POSAMEZNIKOV, USTANOV IN ORGANIZACIJ, KI ŽELIJO MATERIALNO SPODBUJATI IN POGLABLJATI RAZISKOVALNO DEJAVNOST V ONKOLOGIJI. 
MESESNELOVA 9 1000 LJUBLJANA TEL 0 1 51 9 1 2 77 FAKS 01 251 81 13 
ŽR: 50100-620-133-05-10331 15-214779 

Activity of »Dr. J. Cholewa« Foundation for Cancer Research and Education -A Report for the Last Quarter of 2004 
The Dr. J. Cholewa Foundation for Cancer Research and Education has continued to support various activities associated with cancer research and education in Slovenia throughout the last quarter of 2004. Several other initiatives were examined and care­fully thought of in the aforementioned tirne period. The topics discussed included the possibility of the Foundation co-sponsoring the publication of the book dedicated to children survivors of various cancer diseases, the cooperation with the Emergency Ward at the Clinical Centre in Ljubljana and the problems associated with the public calls for Dr. J. Cholewa Foundation for Cancer Research and Education grant applica­tions. Several other problems associated with all these ideas and endeavours were thoroughly discussed during the course of 2004 and also during the last tirne period mentioned previously. It is worth mentioning that many study and research grants have been already bestowed to researchers from various scientific fields associated with oncology in Slovenia and that many of them were also given grants and means to attend scientific meetings, congresses, conferences and symposia dealing with on­cology worldwide. The Foundation is also determined to continue to support the reg­ular publication of I'.,Radiology and Oncology« international scientific journal, which is edited, published and printed in Ljubljana, Slovenia, as it has done over the last cou­ple of years. 
In one of the meetings of the Supervisory and Executive Boards of the Foundation held previously in the year 2004 the financial situation was thoroughly evaluated and discussed. It has to be acknowledged that various public and privately owned enter­prises find it ever more difficult to contribute financially to help running day to day operations of the Foundation and its many scopes of activity. Several new initiatives and suggestions were discussed and evaluated during the recent meetings of the Foundation to address this serious problem. It is important to note that many public companies and private individuals remain committed to support the Dr. J. Cholewa Foundation for Cancer Research and Education and its activities. 
Tomaž Benulic, MD Borut Štabuc, MD, PhD Andrej Plesnicar, MD 


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Stranski ucinki: Lahko se pojavijo slabost, napenjanje, bruhanje, bolecine v trebuhu, driska. Možni so glavobol, krti in alopecija. Zelo redke so preobcutljivostne reakcije. Pri bolnikih s hudimi glivicnimi obolenji lahko pride do levkopenije, trombocitopenije, povecane aktivnosti jetrnih encimov ter hujše motnje v delovanju jeter. 
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Radiology a11d Oncology 

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Dent RAG, Cole P. In vitro maturation of monocytes in squamous carcinoma of the lung. Br J Cancer 1981; 43: 486-95. 
Chapman S, Nakielny R. A guide to radiolog­ical procedures. London: Bailliere Tindall; 1986. 
Evans R, Alexander P. Mechanisms of ex­tracellular killing of nucleated mammalian cells by macrophages. In: Nelson DS, editor. Immunobiology oj macrophage. New York: Academic Press; 1976. p. 45-74. 
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