ECR 2018 - BOOK OF ABSTRACTS

Insights into Imaging, Feb 2018

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ECR 2018 - BOOK OF ABSTRACTS

Postgraduate Educational Programme 0 1 2 3 4 5 6 7 8 9 10 11 12 Scientific Sessions 0 1 2 3 4 5 6 7 8 9 10 11 12 My Thesis in 0 1 2 3 4 5 6 7 8 9 10 11 12 Minutes 0 1 2 3 4 5 6 7 8 9 10 11 12 Clinical Trials in Radiology 0 1 2 3 4 5 6 7 8 9 10 11 12 Scientific 0 1 2 3 4 5 6 7 8 9 10 11 12 Educational Exhibits © Satellite Symposia 0 1 2 3 4 5 6 7 8 9 10 11 12 Author's Index 0 1 2 3 4 5 6 7 8 9 10 11 12 List of Authors 0 1 2 3 4 5 6 7 8 9 10 11 12 Co-Authors 0 1 2 3 4 5 6 7 8 9 10 11 12 List of Moderators 0 1 2 3 4 5 6 7 8 9 10 11 12 0 Chairperson's introduction S. Wirth; Munich/DE , USA 1 B. Abdominal trauma R. Basilico; Chieti/IT 2 A. CT M. Rémy-Jardin; Lille/FR 3 Chairperson's introduction G. Brancatelli; Palermo/IT 4 Chairperson's introduction J.A. Reekers; Amsterdam/NL 5 Chairperson's introduction E. Sorantin; Graz/AT 6 Chairperson's introduction A. Mizzi; Msida/MT , USA 7 Oesophagus S. Romano; Naples/IT 8 C. Hyperpolarised MRI F.A. Gallagher; Cambridge/ UK 9 Colon R.G.H. Beets-Tan; Amsterdam/NL 10 Degenerative disorders A. Cotten; Lille/FR 11 Subarachnoid haemorrhage C. Calli; Izmir/TR 12 Chairperson's introduction C. Triantopoulou; Athens/GR - CONTENTS Insights Imaging https://doi.org/10.10P07o/s13244-018-06d03u-8ate Educational Programme stgra Postgraduate Educational Programme EFOMP Workshop (EF) ESR/EFRS meets Sessions (EM) European Excellence in Education (E³) Headline Sessions Joint Sessions Mini Courses (MC) Multidisciplinary Sessions (MS) New Horizons Sessions (NH) Professional Challenges Sessions (PC) Pros & Cons Session (PS) Refresher Courses (RC) Special Focus Sessions (SF) State of the Art Symposia (SA) Wednesday, February 28......... 3 Thursday, March 1 ................ 36 Friday, March 2 ..................... 75 Saturday, March 3............... 117 Sunday, March 4 ................. 168 Wednesday, February 28 08:30 - 10:00 Computed tomography (CT) imaging - often preceded by conventional radiography - represents the major imaging modality for the diagnosis of acute aortic syndromes. This lecture will review the various underlying diseases of acute aortic syndrome, demonstrate typical imaging features enabling the diagnosis and discuss management options depending on the type, extent, and location of the disease. Clinical examples will be shown. Learning Objectives: 1. To understand the different types of acute aortic syndrome. 2. To learn about imaging findings and management options. A-002 09:15 Abdominal traumas can be classified into two categories: penetrating and blunt traumas. Abdominal injuries are more often observed in the setting of polytrauma; in fact, they are present in about 10% of patients admitted to level 1 trauma. However, only 11% of patients with abdominal trauma require laparotomy when a correct imaging-guide approach is performed. In fact, because the management of trauma patients mainly depends on the mechanism and severity of the trauma, it is crucial to choose the correct imaging modality and/or technique when evaluating a trauma patient on the basis of these two parameters. For example, an ultrasound examination, possibly integrated by contrast-enhanced ultrasonography, may be adequate to image a minor blunt abdominal trauma. This modality, however, is not appropriate when evaluating a severe blunt or penetrating abdominal trauma or even a polytrauma patient with a minor mechanism of injury. Multidetector CT is actually the modality of choice for evaluating severe trauma patients, accompanied by an appropriate CT protocol to image these patients so as to avoid missed injuries and to correctly detect abdominal solid organ injuries, mesenteric and intestinal injuries and abdominal vascular traumatic lesions. Moreover, due to the fact that during the past decades there has been a major change from operative to increasingly conservative management of abdominal traumatic injuries, even in patients with higher grades of injuries or those with older age, imaging features together with hemodynamic considerations play an essential role in the treatment choice: surgery, conservative management, and endovascular treatment. Learning Objectives: 1. To identify the signs of trauma. 2. To provide an indication of their clinical significance. 08:30 - 10:00 GI Tract RC 101 GI bleeding: how to solve the problem? A-003 08:30 Sometimes, things may become more difficult and easier at the same time. On one hand advances in imaging allow for very precise and also fast diagnoses in a continuous increasing number of cases. Consequently, even the bleeding of the GI-tract comes even more into radiological play. On the other hand, radiologists have to be more and more aware of clinical entities, pathological patterns, and interdisciplinary networks to quickly and precisely provide our clinical partners with the information they need. Besides that, more and more cases can be managed by minimal-invasive interventional procedures, i.e., by radiologists themselves. Room B Session Objectives: 1. To define acute, overt and occult GI bleeding. 2. To learn about different imaging modalities that can be utilised in the workup of GI bleeding. 3. To define the role of the interventional radiologist in the management of the GI bleeding. Acute gastrointestinal (GI) bleeding is a common medical problem associated with high morbidity and mortality. The clinical presentation of acute GI bleeding varies with the location of the bleeding site, the cause, the amount of blood loss, and the presence of comorbidities. Anatomically, the ligament of Treitz is the border between upper (mouth to Treitz) and lower (Treitz to anus) GI bleeding. However, it is not always possible to differentiate between upper and lower GI bleeding clinically, despite the fact that clinical presentation is different, as is the etiology. In decreasing order, erosions and ulcer, variceal bleeding, Mallory-Weiss tears, vascular lesions, and neoplasms are responsible for upper GI bleeding. In contrast, lower GI bleeding occurs in the elder population, with diverticular disease, angiodysplasia, neoplasms, colitis and benign anorectal lesions being the major etiologies. The main diagnostic objective is the identification of the etiology and site of bleeding. Endoscopy is the initial diagnostic step in upper GI bleeding, but limited in lower GI bleeding due to difficulties in colonic cleansing in an emergency situation. Accordingly, CT is the imaging method of choice [technique: no positive oral contrast, high dose /iodine content/flow of contrast material (e.g.,100-150 ml, 350 mg/ml, 4-6 ml/sec), plain, arterial and parenchymal phases, dual-energy CT with iodine maps if available, multiplanar reformation, high anatomic resolution]. We search for high-attenuation (> 80HU) luminal or wall lesions not seen on unenhanced CT data. Detection rates vary, and an amount of bleeding > 0.350.5 ml/min is required. As bleeding might be intermittent, CT should be performed when active bleeding is present. Learning Objectives: 1. To learn about the common causes of the acute upper and lower GI bleeding. 2. To understand the rationale for different investigative pathways depending on the likely site of bleeding. 3. To appreciate how best to optimise imaging protocols to identify the site and cause of bleeding, and assist with treatment planning. The term obscure gastrointestinal bleeding (OGIB) was traditionally used to include patients with gastrointestinal bleeding who underwent normal upper and lower endoscopic examinations in addition to a small bowel series that did not reveal a source of bleeding. This definition was a sign of the difficulties experienced in small bowel exploration in the past. Given to recent advances in small bowel investigative methods, including endoscopic (video capsule endoscopy, deep enteroscopy) and radiological (CT and MR enterography, CT angiography) techniques, the cause of bleeding is no longer obscure and can now be reached in majority of the patients. For this reason, the term OGIB has been reclassified as “small bowel bleeding”, which corresponds to ~5-10% of all patients presenting with gastrointestinal bleeding. “OGIB” is now reserved for patients in whom a source of bleeding cannot be identified anywhere in the gastrointestinal tract after a comprehensive investigation. Small bowel bleeding can be overt, if patient presents with melena or hematochezia, or occult for patients presenting with iron-deficiency anaemia. Causes of small bowel bleeding are varied and the likelihood to be due to a vascular, inflammatory or mass lesion is related to the patient’s age. Algorithms for investigation of suspected small bowel bleeding include endoscopic and radiological methods, frequently with a complementary role, indicating that an adequate interaction is required among the elements of a multidisciplinary team. Learning Objectives: 1. To learn about the differences between obscure, occult and overt GI bleeding, and the most common causes of each. 2. To understand when imaging is indicated which tests to perform, and the most important diagnoses to look for. 3. To appreciate the interaction between endoscopic and radiologic investigations in managing patients with obscure GI bleeding. W Acute significant gastrointestinal bleeding is generally defined as a bleeding requiring transfusion of at least 4 units of blood within 24 hours or showing signs of hemodynamic instability (hypotension, tachycardia, signs of hypovolemic shock). Most cases are resolved endoscopically, pharmacologically, or by correction of coagulation parameters. Due to its minimally invasive nature, the endovascular solution is currently in most cases, after the previous methods fail, considered the method of choice. The most often used access to undergo embolisation is percutaneous access via common femoral or brachial artery. After reaching the appropriate visceral artery with a diagnostic 4 or 5F catheter, and verification of the source of bleeding, microcatheres are introduced coaxially. The most commonly used embolic materials are microcoils , PVA microspheres and gelatin foam. In the case of more massive bleeding, using of tissue glue (Histoacryl, etc.) may be considered . Upper gastrointestinal tract is characterised by a rich network of collateral supply with lower risk of ischemia. In the risk of rebleeding via collaterals, it is necessary to perform embolisation proximally and distally from the site of bleeding (so-called sandwich method). In the lower gastrointestinal tract, and in particular in the colon, due to the higher portion of terminal branches, ischemia risk is higher and embolisation should be as selective as possible. Learning Objectives: 1. To learn about the role of interventional radiology in the management of acute and chronic GI bleeding. 2. To learn about the variety of techniques available to the interventional radiologist to evaluate obscure GI bleeding and control acute GI bleeding. 3. To understand when interventional radiology is clearly indicated, when it should be considered, and when it should be avoided if possible. 09:44 Panel discussion: Guidelines for management of GI bleeding and real life: why are they different? RC 104 When and how to use perfusion imaging in pulmonary vascular and airway disease? Since the introduction of dual-energy CT (DECT) in clinical practice, great interest has been directed toward analysis of the distribution of iodine in the most distal parts of the pulmonary circulation, often referred to as perfusion imaging. Initially only available with dual-source CT, dual-energy CT has become accessible to single-source CT, with the introduction of rapid kV switching and more recently, dual-layer (sandwich) detectors. Regardless of the difference in the technological approach, perfusion images are generated from the same data set as that used for morphological evaluation, offering the possibility of a simultaneous approach of structure and function in respiratory patients. This combined information provided with CT is a major advantage over scintigraphy and MRI, not only in the field of primary disorders of the pulmonary circulation, like acute pulmonary embolism, but also in the context of bronchopulmonary diseases where perfusion alterations can be interpreted with precise knowledge of the underlying morphologic changes. More recently, this complementarity has also been extended in the field of chronic thromboembolic disease and pulmonary hypertension while a growing interest is reported in oncologic indications. The purpose of this presentation is to make radiologists familiar with the use of CT lung perfusion in clinical practice. Learning Objectives: 1. To learn about the creation of CT perfusion images. 2. To understand the complementarity between morphological and functional information. 3. To learn the various causes of perfusion defects. Author Disclosure: M. Rémy-Jardin: Research/Grant Support; Resaerch grant support from Siemens Heathcare. A-008 09:00 Among functional lung magnetic resonance imaging (MRI) techniques, dynamic contrast-enhanced (4D) perfusion MRI is probably the most robust and widely used method that has entered the clinical arena of routine patient management. Because it delivers temporally resolved datasets, perfusion parameters such as time-to-peak or pulmonary blood flow may be directly quantified by dedicated post-processing. In pulmonary vascular disease it may help to identify arterio-venous-malformations, pulmonary shunts or anomalous venous return. In combination with contrast-enhanced and non-constrast enhanced lung MR angiography, 4D perfusion MRI is now considered an alternative for computed tomography angiography for pulmonary embolism. In case of airways disease such as cystic fibrosis or chronic obstructive pulmonary disease, 4D perfusion imaging exploits the physiological mechanism of hypoxic pulmonary vasoconstriction. This effects a downregulation of perfusion to functional lung units with reduced ventilation, i.e. airway obstruction. Thus, 4D perfusion MRI can directly visualize functional lung impairment associated with airways disease, even when small airways are affected that cannot be otherwise captured with structural imaging. The lecture will summarise technical aspects of performing 4D perfusion imaging with clinical MRI scanners, discuss the most important routine indications incl. implementation into routine workflow, and discuss most relevant imaging findings in vascular and airways disease. Further, future developments and non-contrast-dependent techniques will be reviewed. Learning Objectives: 1. To become familiar with the technical aspects of MRI perfusion. 2. To learn key imaging features. 3. To discuss the most relevant clinical indications. Author Disclosure: M.O. Wielpütz: Advisory Board; Boehringer Ingelheim. Investigator; Boehringer Ingelheim, Vertex. A-009 09:30 C. Nuclear medicine and hybrid imaging E.J.R. van Beek; Edinburgh/UK () Initial management of pulmonary vascular and lung diseases has consisted of lung scintigraphy, enabling the study of both lung perfusion and ventilation. The advent of CT and CTPA has replaced many of the acute indications. Nevertheless, there remains an important role for the use of both lung scintigraphy and the combined use of new hybrid systems (SPECT/CT) to study these disease and facilitate in their management. This presentation will evaluate the historical and current state-of-the-art capabilities of lung scintigraphy to study lung perfusion and ventilation. It will also evaluate the potential best applications in the current diagnostic management, as well as demonstrate some of the pitfalls of this technology. Learning Objectives: 1. To learn about the specificities of perfusion scintigraphy. 2. To understand the advantages of hybrid imaging. 3. To appreciate potential pitfalls of nuclear medicine techniques. Author Disclosure: E.J.R. van Beek: Advisory Board; Aidence BV. Equipment Support Recipient; Siemens Healthineers. Founder; QCTIS Ltd. Owner; QCTIS Ltd. W Learning Objectives: 1. To discuss MRI protocols for MSK-imaging in children. 2. To give an overview of normal development and variations in MR anatomy and signal patterns. 3. To provide an understanding of features indicative of pathology. Arthritis of the temporomandibular joint (TMJ) is common in children and adolescents with juvenile idiopathic arthritis (JIA). Early treatment is warranted to prevent severe growth disturbances and joint deformities. As TMJ arthritis is often clinically silent, MRI with contrast-enhancement has been considered to be the most reliable method to assess signs of inflammation. To reliably guide therapeutic decisions and monitor outcomes, it would be of utmost importance to clearly define the MR characteristics of a normal TMJ as a basis for the assessment of minor pathologies. However, similar to other small joints in children, we are just beginning to understand its developmental, physiological and anatomical characteristics as well as its reaction to inflammatory diseases and their treatment. Recent studies on normal TMJ in children have revealed age dependent changes in shape and angulation of the mandibular condyle as well as typical time-intensity curves of contrast-enhancement in the soft joint tissue and the condyle. To date, the differentiation between normal synovial findings and mild signs of synovitis remains challenging. This lecture presents typical MR images of normal and inflamed TMJs in children and adolescents, including age dependent anatomical variations. It discusses the available data on possible cut-offs between normality and pathology, the impact of the temporal dynamics of contrast-enhancement, and presents findings that can mimic arthritis. It summarizes the minimum requirements of image quality and spatial resolution, the best image orientation, as well as the advantages of fat suppression and subtraction analysis in contrast-enhanced imaging. Learning Objectives: 1. To discuss MRI protocols for imaging of the temporomandibular joints (TMJ). 2. To give an overview of MR imaging finding in arthritis of the TMJ. 3. To highlight the major differential diagnoses of TMJ arthritis and its MR imaging characteristics. Musculoskeletal injuries are common in children. They account for 15-20% of admissions to the ED. Children have an immature skeleton with unique biomechanical features and a stronger, thicker and richly vascularized periosteum. Paediatric fractures may present with unique patterns including plastic deformation, buckled fractures, and greenstick fractures. Fractures in children include the ones involving the physis (epiphysiolysis) and we will review their classification and prognosis after treatment. We will review these injuries making special remarks on the imaging techniques used for their correct diagnosis and treatment planning. Learning Objectives: 1. To become familiar with the types of injuries seen in children. 2. To understand the basic mechanisms. 3. To learn about the diagnostic imaging approach. RC 108 Differential diagnoses you don't want to miss Moderator: M.R. Eriksen; Stavanger/NO A-013 08:30 A. Differential diagnoses of orbital masses V. Chong; Singapore/SG () The approach to orbital mass analysis follows two basic rules. The first rule emphasizes the general fact that diseases arise from pre-existing tissues or structures unique to different spaces in the orbit. The second rule highlights exceptions to the general rule. For example, metastatic or other systemic diseases may involve the orbit, while trans-spatial pathological processes such as infiltrative lesions may affect multiple compartments simultaneously or metachronously. The orbit can be divided (by the muscle cone) into an intraconal and an extra-conal compartment. Structures in the intra-conal compartment include the optic nerve/sheath complex and the surrounding fibro-fatty tissues, small vessels and small nerve branches. The contents of the extra-conal space include the lacrimal gland, cranial nerves (V1 and V2) and the periosteum of the orbit. Hence, knowledge of the applied anatomy of the orbit with a working knowledge of commonly seen diseases is a prerequisite for generating lists of differential diagnoses. The analysis of orbital masses should always be carried out in the clinical context of the patient. Tentative as well as definitive diagnosis can often be made with reference to the clinical information. For example, a lesion with unusual morphology or location can be tentatively diagnosed as metastatic disease in the presence of a history of malignancy elsewhere. In conclusion, the integration of knowledge of orbital anatomy, pathology and clinical information provides the basis of sound radiological differential diagnoses for further patient management. Learning Objectives: 1. To become familiar with the anatomy of the orbit. 2. To learn which imaging technique to use. 3. To understand the typical imaging appearance of orbital masses. Cystic and tumorous pathologies of the jaws can be imaged with cone-beam CT, CT and MRI. These pathologies include, e.g. in most cases inflammation or tumours. PET-CT or PET-MR may also be used. CT may be used without or with the i.v. application of iodinated contrast material dependent on the pathology. The images can be documented in soft-tissue- and/or bone-windowlevel setting. Imaging planes are usually axial, coronal or sagittal depending on the pathology. MRI has the advantage of higher soft tissue contrast and the possibility of using different sequences. Depending on the pathology, e.g. fatsuppressed T2-weighted, diffusion-weighted, T1-weighted sequences before and after the i.v. use of gadolinium and T1-weighted contrast-enhanced sequences with fat suppression are used. The imaging planes may be axial, coronal or sagittal. In this refresher course, the normal anatomy of the jaw, variants mimicking osteolytic or osteoblastic lesions, and cystic and tumorous pathologies of the jaws will be shown, and the imaging characteristics will be explained. Learning Objectives: 1. To become familiar with the anatomy of the jaw. 2. To learn which imaging technique to use. 3. To understand the typical imaging appearance of jaw lesions. Soft tissue masses of the supra and infrahyoid neck are a rather heterogeneous group of tumours, classified by WHO in nine categories, based on their histologic differentiation: adipocytic, fibroblastic or myofibroblastic, fibrohistiocytic, smooth muscle, skeletal muscle, vascular, pericytic, and chondro-osseous tumours, and tumours of uncertain differentiation. Based on their clinical behavior and history such tumours may be described as benign, malignant or intermediate, the latter further subclassified as locally invasive or metastatising at distant sites. US is generally the first imaging step in infrahyoid neck lesions; MDCT or MRI are mandatory in suprahyoid masses, but are also needed to better define the deep extent and anatomic relationships of infrahyoid tumours. In many cases, imaging findings are overlapping and insufficient for tumour characterisation; nonetheless, some specific clues may orient the differential diagnosis. Site of origin of the lesion is probably the first brick in the wall; therefore, knowledge of the space-based neck anatomy is essential prerequisite. Patient’s age, size and number of lesions, presence and pattern of calcifications are useful additional details. Some specific density or signal intensity patterns may cut the list of differentials, whereas the potential role of the additional information provided by DWI-MRI or dual-energy CT is far from being fully elucidated. However, it is clearly assumed that imaging diagnosis does not replace pathologic assessment, which in a significant number of cases can be accurately obtained with FNA. Learning Objectives: 1. To become familiar with the anatomy. 2. To learn which imaging technique to use. 3. To understand the typical imaging appearance of soft tissue masses. A B C D E F G W 08:30 - 10:00 Special Focus Session Room E1 SF 1 Hepatocellular carcinoma: diagnosis, staging and current guidelines A-016 08:30 Hepatocellular carcinoma (HCC) is the second leading cause of cancer death worldwide. In this session, the rationale behind the need for screening for HCC will be discussed, and the geographic differences in screening programs will be highlighted. The benefits of using LI-RADS terminology, interpretation, and reporting for both clinical care and research will be presented. Typical and atypical appearance of HCC will be shown, along with common mimickers and useful tips of differentiation of focal hepatic nodules in cirrhotic liver. Finally, the speakers will be exposed to challenging cases in the form of unknown, will share their reasoning with each other, and engage in discussions with the chairperson and the audience. Session Objectives: 1. To become familiar with the international guidelines for HCC screening. 2. To understand why a standardised report facilitates patient management. 3. To learn about the key concepts of diagnosis of typical and atypical HCC with CT and MRI. Author Disclosure: G. Brancatelli: Speaker; Bayer, Guerbet. A-017 08:35 Hepatocellular carcinoma (HCC) is the most common type of liver cancer, accounting for 80-90% of all cases of liver cancer. It is the fifth most common cancer and the third leading cause of cancer-related deaths around the world. As HCC occurs in 90% of the cases in patients with chronic liver disease, screening is indicated in those patients having compensated cirrhosis. Several guidelines have been implemented to help the practitioner to manage the patients during the screening, when a nodule is detected and to decide the optimal treatment in patients with HCC. Among the HCC guidelines which are the most used: AASLD, EASL, Japanese, Korean, and Asia-Pacific ones, there are common features. All agree : (i) on the noninvasive diagnosis of HCC using contrast-enhanced CT or MR imaging with two hallmarks: hypervascularisation on arterial-phase and wash-out on portal and/or delayed phase in lesions larger than one centimeter; (ii) on the role of liver biopsy when diagnosis cannot be achieved with imaging. Yet they differ in many other issues: stratification according to lesion size, first-line imaging modality, role of hepatobiliary MR contrast agents, and role of contrast-enhanced ultrasound. These differences are explained by the different prevalence of HCC worldwide and the different goals of diagnostic performance (high specificity or high sensitivity). Learning Objectives: 1. To be aware of the different guidelines in HCC screening. 2. To know the most striking differences. 3. To understand the consequences in patient management. A-018 08:58 Diagnosis of HCC, LI-RADS 2017: why we need it? C.B. Sirlin; San Diego, CA/US () LI-RADS is a comprehensive system for imaging HCC in adults with cirrhosis or other risk factors for HCC. It provides standardized terminology with precise definitions and illustrations for screening and surveillance using US, diagnosis and staging using CT, MRI, and CEUS, and treatment response assessment using CT and MRI. It addresses the entire spectrum of lesions and pseudo lesions encountered in the cirrhotic liver as well as the full range of malignant neoplasms associated with chronic liver disease. This lecture will review LIRADS terminology, interpretation, and reporting and explain why standardization is needed for clinical care, research, and education. Learning Objectives: 1. To understand the need for standardised terminology, interpretation, and reporting for clinical care. 2. To understand the need for standardised terminology, interpretation, and reporting for research. 3. To become familiar with LI-RADS terminology, interpretation, and reporting. Author Disclosure: C.B. Sirlin: Advisory Board; Bayer. Grant Recipient; Bayer, GE, Siemens, Philips, ACR. Hepatocellular carcinoma (HCC) poses a burden on global health. As HCC typically has a poor prognosis with a 5-year survival rate of only 28.6%, it is of paramount importance to achieve the earliest possible diagnosis of HCC and to recommend the most up-to-date optimal treatment strategy in order to increase the survival rate of patients who develop this disease. HCC is commonly diagnosed using dynamic CT and/or dynamic MRI without histological confirmation, on the basis of a characteristic arterial enhancement and portal venous or delayed phase washout. Indeed, the noninvasive diagnosis of HCC in high-risk patients by typical imaging findings alone is widely adopted in major practice guidelines for HCC. HCC usually presents with typical imaging characteristics but at times can present with a wide spectrum of atypical appearances. Familiarity with unusual presentations and their imaging findings is critical to ensuring prompt, accurate diagnosis and treatment. Moreover, while imaging techniques have markedly improved in detecting small liver lesions, they often detect incidental benign liver lesions and non-hepatocellular malignancy that can be misdiagnosed as HCC. The common mimickers of HCC in the cirrhotic liver include nontumorous arterioportal shunts, rapidly enhancing hemangiomas, intrahepatic massforming type cholangiocarcinoma (CC), angiomyolipomas, focal inflammatory liver lesions and focal nodular hyperplasia-like nodules. Among them, it is important to recognize the suggestive imaging findings for intrahepatic CC as the management of CC is largely different from that of HCC. Recognition of the typical imaging findings of common HCC mimickers can reduce false-positive HCC diagnosis. Learning Objectives: 1. To demonstrate imaging spectrum of hepatocellular carcinoma including typical and atypical appearance. 2. To illustrate common mimickers of hepatocellular carcinoma in cirrhotic liver. 3. To provide useful tips of differentiation of focal hepatic nodules in cirrhotic liver. Author Disclosure: J.M. Lee: Grant Recipient; Bayer, Guerbet, Philips, Samsung Medison, GE Helathcare, Starmed, RF medical, Acuzen, Toshiba. Research/Grant Support; Siemens, GE Healthcare, Philips, Samsung Medison, Toshiba. Speaker; Bayer, GE Healthcare, Siemens, Philips, Samsung Medison, Guerbet. 09:44 Panel discussion: At the plateau of the learning curve: how do experts reason? W B D F Room E2 08:30 - 10:00 Neuro Neck pain is a common problem with many possible causes. The facet joint and the uncovertebral joint are frequently involved in degenerative cervical spine disease. It is important to learn how to differentiate normal and asymptomatic changes that occur with age from abnormal findings that are causing neck and/or arm pain. I will demonstrate the use of plain film, CT, SPECT, and MRI in diagnosing an offending uncovertebral or facet joint. Many of these offending joints can be targeted specifically, leading to easy and fast pain reduction in many patients with aspecific neck pain. Learning Objectives: 1. To learn about the physiological and pathophysiological degeneration of the cervical spine. 2. To understand the role of imaging in the diagnosis and clinical decision making in the degenerative cervical spine. 3. To appreciate the clinical relevance of imaging findings in the degenerative cervical spine. Degenerative changes of the cervical spine occur during the aging process or are caused by segmental mechanical overload. Among the degenerative processes leading to spinal stenosis are marginal osteophytes of the vertebral bodies and joints, intervertebral disc degeneration with herniation and hypertrophy of the ligaments. CT, CT-myelography, and MR imaging are essential in assessing the extent and severity of spinal canal stenosis, especially with a view to guiding conservative or surgical treatment. Next to the assessment of the osseous and soft tissue structures of the vertebral column as well as spinal canal stenoses, T2-weighted MRI imaging is crucial for the assessment of signal changes within the myelon. The differentiation between signs of an acute myelopathy and myelomalacia, caused by an irreversible damage of the spinal cord, is essential to select the appropriate treatment option. Moreover, patients present with a broad spectrum of clinical symptoms ranging from neck pain to spastic paraparesis; therefore, it is crucial to put imaging findings in context with clinical symptoms to assess the potential benefit of different conservative and surgical treatment options. Learning Objectives: 1. To learn about the pathophysiology and imaging findings in spinal stenosis and cervical spondylotic myelopathy. 2. To understand the relation between imaging findings and clinical presentation. 3. To appreciate the importance of imaging findings and the clinical presentation with respect to possible treatment options. Cervical spine surgery is common, so it is important for radiologists to know what the normal imaging findings are to avoid pitfalls. This is not easy as there are substantial imaging overlaps between normal early postoperative findings and surgical complications. Because there are a vast variety of surgical approaches and hardware that can be applied to the spine, it is a challenge for the radiologists to know their anatomical implications and possible complications. The use of a particular imaging technique is dictated by multiple factors including the underlying pathology, surgical approach, device or instrumentation used, and suspected complications. The postoperative imaging should be able to assess progression of osseous fusion, confirm correct positioning and integrity of instrumentation, and detect suspected complications such as new disease or disease progression. Radiographs are most commonly used for assessment of fusion. CT is the modality of choice for the evaluation of graft position, hardware, bone integrity, and fractures. It also provides imaging of bone detail to accurately assess the degree of osseous fusion. MRI is the best option for evaluation of endplates, paraspinal soft tissues, epidural spaces, and intrathecal structures, making it useful for detecting and monitoring infection or postoperative collections. Learning Objectives: 1. To learn about the imaging findings and pitfalls of postoperative cervical spine imaging. 2. To understand the heterogeneity of imaging findings and their clinical relevance. 3. To appreciate the importance of standardised imaging, interpretation and reporting of postoperative imaging findings in the cervical spine. The thyroid gland consists of two lobes which are interconnected by the isthmus. The gland is directly attached to the larynx and trachea. The standard view is axial, visualising the main overlying (strap) muscles, the great vessels and lymphnodes and the oesophagus, as well. The main congenital abnormalities are thyroglossal duct cyst, lingual thyroid gland and aberrant thyroid tissue. Diagnosis of the thyroid masses/nodules is done by sonography using the TI-RADS classification and colour-doppler, lesion size suspicion grade, and fine needle aspiration biopsy (FNAB) reaching an accuracy of 94%. Very important is to differentiate malignancy (papillary / follicular / anaplastic / medullary carcinoma) and inflammatory changes (Hashimoto and DeQuervain thyroiditis). Standard imaging procedures for the parathyroidea are sonography and Sesta-MIBI-SPECT reaching an accuracy of 97%. In unclear cases 4D-CT and/or MRI + contrast may be used additionally. Learning Objectives: 1. To discuss current imaging techniques for evaluation of normal anatomy. 2. To describe common imaging manifestations of inflammatory diseases. 3. To identify and describe the imaging appearance of malignant pathologies. This presentation offers a clinically orientated approach to imaging salivary gland disease in which the alignment between findings and further management is defined. Salivary imaging has been changed dramatically by the development of cross-sectional imaging. Ultrasound, CT and MRI have consigned radiographs and sialograms to a subsidiary role. Scintigraphy offers the best measure of global salivary gland function, but currently is not widely used in practice. Today investigation is closely related to the underlying pathology of salivary disorders and to provide reliable guide to surgical or medical treatment. Masses are well detected by cross-sectional imaging, which provides accurate guidance on appropriate approaches for surgical management. Differential diagnosis cannot always be achieved, but this is rarely a clinical problem because biopsy or resection are usually indicated. Sialography remains a reliable method of showing calculi and ductal changes in sialadenitis, but cross-sectional techniques, especially ultrasound and MRI, have advantages in inflammatory disease and complete sensitivity in detecting ductal disease may not be necessary in practice because patients may be treated symptomatically. A strong case can be made for using MRI as a sole investigation as this has been shown to be sensitive to both surgical and medical conditions. On this basis, the radiologist may be well placed to offer a primary referral service with triage, directing clinical management of patients or A B C D E F G W further referral on the basis of findings on MRI. Salivary interventional techniques have more recently extended the role of the radiologist. Learning Objectives: 1. To discuss current imaging techniques for evaluation of normal anatomy. 2. To describe common imaging manifestations of inflammatory diseases. 3. To identify and describe the imaging appearance of malignant pathologies. In case of a visible or palpated neck mass, lymph node enlargement is routinely included in the differential diagnosis list. Medical imaging can be effectively used to distinguish other causes of cervical swelling, as well as characterizing enlarged lymph nodes. Although commonly used as a criterion, nodal size is not reliable in characterization. Imaging parameters including internal structure, vascularity pattern, degree of enhancement, and perinodal tissue changes may shed light on the etiology of any lymphadenopathy, which may be reactive hyperplasia, infection, inflammation or neoplastic infiltration. Characteristically, reactive hyperplastic lymph nodes have well-defined borders, reniform shape and central fatty hilum contiguous with adjacent cervical fat tissue. In children, and in most of the adult cases with a low risk of malignancy, ultrasound is the first choice of imaging modality owing to its radiation-free nature, and due to practical reasons. However, when further characterization of nodal abnormality or evaluation of sonographically inaccessible anatomic locations is required, use of other cross-sectional techniques, like CT and MRI are mandatory. They provide not only more detailed information including anatomic localization, size, number, internal structure, and enhancement characteristics of lymph nodes, but also important data about perinodal soft tissue and other associated pathologic processes in the region. Although the choice of imaging modalities to be used in the evaluation of cervical lymph nodes changes according to the means, experience, and preferences of institutions, the role of medical imaging remains pivotal and decisive in this common indication. Learning Objectives: 1. To discuss current imaging techniques for evaluation of normal anatomy. 2. To describe the imaging features of infectious and inflammatory disorders. 3. To describe the imaging appearance of neoplastic disorders. Author Disclosure: S.S. Özbek: Other; Advisory Panelist -Siemens Healthineers Ultrasound Radiology. The immune system is capable of preventing the development of tumour diseases and stimulation of cytotoxic T-lymphocytes can repress existing tumours. A new class of antibody-based medication, the immune checkpoint inhibitors, influences the activation of T-lymphocytes. Immune checkpoint inhibitors are active against a number of tumours. In some cases, such as malignant melanoma and non-small cell lung cancer, the response rates are impressive and exceed those achieved with conventional chemotherapies. Modern immunotherapies in oncology show tumour response patterns differing from conventional chemotherapies including initial pseudo-progression which can occur in up to 10% of cases depending on the immunomodulating drug and tumour entity. Response Evaluation Criteria in Solid Tumours (RECIST 1.1) represent the currently most used response criteria for conventional chemotherapy of solid tumours. However, atypical response patterns of immunotherapies are not correctly classified using RECIST 1.1 so that the effectiveness is also incorrectly interpreted. To correctly interpret these atypical response patterns, special Immune-Related Response Criteria in Solid Tumours (iRECIST) have been published. iRECIST was developed only for usage in trials testing modern immunotherapeutics. In contrast to RECIST 1.1, according to iRECIST an initially unconfirmed progressive disease (iUPD) requires confirmation (iCPD) in clinically stable patients by subsequent control imaging after 4-8 weeks. New lesions are separately assessed within iRECIST. Learning Objectives: 1. To understand the basic principle of immune related therapies. 2. To learn how tumour morphology and functional parameters change with therapy. 3. To appreciate the existing evidence for immune therapy follow-up strategies. Radiomics is an emerging translational field of research, aiming to extract data from clinical images, containing information that may reflect the underlying pathophysiology of tumoural tissue. The extracted information may be associated with clinical data, and can be used to assess prognosis and to support clinical decision. Specific softwares allow the extraction of radiomic features, representative of the entire tumors or defined subvolumes within tumors, from digital images (CT, MR, PET), and convert them into mineable high dimensional data for hypothesis generation, testing, or both. The steps necessary for a radiomic approach to digital radiological examinations include: acquisition of the images; identification of volumes of interest that may contain prognostic value; segmentation of volumes; extraction of radiomic features from the volume; clustering of the features; creation of a database; inclusion of the extracted data to develop models to predict outcomes, possibly in combination with demographic, clinical, comorbidity, or genomic data. Imaging is used in routine practice for oncological patients worldwide, at many stages of diagnosis and treatment. In the current era of targeted therapies, radiomics guarantees a nearly limitless supply of imaging biomarkers over time during and after therapy, to quantify and monitor phenotypic changes many times during treatment. The power of a predictive classifier model is dependent on the amount of data; hence, it is desirable that the radiomic studies will consider sharing of data between different centers, with the creation of databases including radiomics data and covariates, such as genomic profiles, histology, serum markers, patient histories, and biomarkers. Learning Objectives: 1. To learn about the concept of radiomics and individualised medicine. 2. To learn how radiomics can be extracted from standard clinical examinations. 3. To appreciate the consequences of radiomics for radiologists in the future. B D F Room D A-032 09:30 Bone marrow edema is a pattern of marrow alteration frequently observed at MRI. It is defined by the presence of an ill-delimited area of moderate and homogeneous decrease in signal intensity on SE T1 images that converts to high signal intensity on fat-saturated proton density or T2-weighted images. It is non-specific and may be associated with almost any abnormal marrow, bone or joint conditions. Epiphyseal bone marrow edema can be associated with self-limited spontaneously resolutive conditions (overuse, stress insufficiency fractures, transient osteoporosis), or with evolutive disorders including chondropathy or spontaneous osteonecrosis. The main task of the radiologist is to assess the cause for bone marrow edema and to highlight imaging features that contribute to a specific diagnosis and subsequently a prognosis (resolutive versus non-resolutive). The current lecture aims at emphasizing imaging features indicative of bone marrow edema to avoid confusion with systemic osteonecrosis. We will also highlight imaging features of prognostic significance that enable the clinician to tailor the treatment to the patient’s condition. Learning Objectives: 1. To understand the aetiologies of bone marrow oedema syndromes. 2. To learn about the imaging characteristics of avascular necrosis of bone. Bone marrow contusions are frequently identified at magnetic resonance imaging after an injury to the musculoskeletal system. These osseous injuries may result from a direct blow to the bone, from compressive forces of adjacent bones impacting one another, or from traction forces that occur during an avulsion injury. Commonly these injuries resolve without long term sequelae. However, they may also involve the cartilaginous surface with or without an associated fracture line defining these as osteochondral injuries, which may have a different prognostic relevance. Subchondral fractures have been implicated in the genesis of some well-known destructive articular conditions whose cause was previously undetermined, such as rapidly progressive osteoarthritis of the hip or spontaneous osteonecrosis of the knee. Subchondral fractures may ultimately lead to bone collapse, secondary osteonecrosis, and severe articular damage. It should be suspected in the appropriate clinical setting, as in early stages it is usually indistinct on initial plain radiographs and magnetic resonance imaging is required for a definitive diagnosis. The fracture line usually appears as a band of low signal intensity in the subchondral bone plate, adjacent to the articular surface, most often surrounded by bone marrow edema. As these injuries may be occult on radiographs, the differentiation of bone contusions from osteochondral injuries or subchondral fractures is possible only with MRI including fat-suppressed and non-fat suppressed sequences. While purely subchondral lesion may have a good prognosis if diagnosed early, disruption of the articular surface may lead to early degenerative alterations including focal cartilage loss and other features of osteoarthritis. Learning Objectives: 1. To understand the pathomechanisms of osteochondral injury and subchondral fractures. 2. To learn about the imaging techniques and prognostic values. Author Disclosure: F.W. Roemer: Shareholder; Boston Imaging Core Lab (BICL), LLC. Rheumatoid arthritis is the most common inflammatory rheumatic disease. The pathogenesis of RA is subject to ongoing discussion. The traditional concept of inflammatory pannus, in which fibroblast-like synoviocytes provoke cartilage and bone destruction through direct invasion and indirect triggering of catabolic cascades has been termed the outside-in hypothesis. There is also evidence supporting the inside-out hypothesis, in which joint inflammation and destruction originates from the bone marrow. Next to synovium and subchondral bone, another tissue involved in cartilage and bone damage in RA is extra- or intraarticular fat tissue which produces ca. 50 adipo(cyto)kines which may be involved in degradation of all components of the connective tissue, including cartilage. Finally, the hyaline cartilage autoantigens, activated by cartilage damage, may activate and maintain synovitis and lead to joint damage. In everyday practice, the clinical relevance of synovitis and bone marrow inflammation in terms of their role as an erosions precursors is known and ultrasound and MRI are used to detect synovitis, BME, inflammatory cysts, hyaline cartilage loss, and bone erosions. Less in known about inflammatory and destructive potential of intra- and extraarticular fat tissue which may also be evaluated in US and MRI. And only research centers use quantitative MR applications to cartilage to show glucosaminoglycans loss possibly preceeding visible cartilage damage. In this presentation pathomechanisms that result in articular cartilage and bone damage in RA will be presented, including the clinical relevance of synovitis and BME in terms of their role as an erosion precursors, as well as the role of imaging techniques to detect early cartilage damage and bone erosions. Learning Objectives: 1. To understand the pathomechanisms that result in articular cartilage and bone damage in rheumatoid arthritis, including the clinical relevance of synovitis and BME in terms of their role as an erosion precursor. 2. To learn about the role of imaging techniques to detect early cartilage damage and bone erosions. Room G 08:30 - 10:00 Physics in Medical Imaging CT dual energy publications have heavily increased in the last years. The trend seems to be continuing since PubMed has found, from Jan 2015 until Nov 2017, around 1000 peer review abstracts. Publications on phantom simulation (for algorithm verification) and patient's study regarding the most important area of diagnostic have been published sourcing from CT imaging and Hybrid Imaging (PET CT for examples). Bone and high density tissue evaluation are one of the most important application with high density artifact reduction, materials analysis based on attenuation spectra observed, tumor analysis and no contrast imaging application. A lot of technological solutions have been introduced during the last years, but the technique has not yet seen widespread implementation in routine protocols. During the course, the basic principle of dual energy and some new trend of spectral imaging will be introduced both technologically and clinically. To compare image quality and radiation dose of single-energy CT and dual energy, it is very important to quantify the patient risk with the introduction of these new technologies. Quantitative evaluation studies (retrospective and prospective) will be more and more important. During the refresh-course, the basic principle of patient dose in spectral imaging will be presented and attention is paid to the quantitative method of image analysis. Session Objectives: 1. To learn about the basics of dual-energy CT (DECT). 2. To understand today's photon counting detector technology. 3. To learn how DECT is applied in clinical practice. W exploit spectral information regarding attenuation ability of tissues for diagnostic purposes. Despite conceived during ‘70s soon after the first clinical CT, the clinical endorsement and widespread application of DECT was initiated with the advent of dual-source CT systems in 2006. Providing the potential to improve CT image quality through artifact suppression and extracting valuable information regarding tissue composition and function, DECT is the new exciting field for the radiology community and the main driving force for CT technology evolution over the last decade. Currently, all CT vendors put considerable efforts in developing CT systems capable of performing DECT studies, while novel clinical applications of DECT are continuously introduced. However, comprehension of the basic physics of DECT and familiarisation with the advanced technological features of modern DECT scanners is prerequisite to fully exploit the advantages of DECT imaging. Learning Objectives: 1. To learn about the underlying physics and today's technology. 2. To see potential advantages compared to single-energy CT. 3. To appreciate the rationale behind clinical applications. Recent years' advances in room-temperature semi-conductors, especially CZT and CdTe, have enabled the transformation from energy-integrated (EI) detectors to photon-counting (PC) detectors in diagnostic CT, enhancing significantly its clinical benefits. The higher signal per x-ray photon (X10) and the short rise time of ~10 nanoseconds enable spectral analysis of each counted photon, use of adjustable multi-energy bins, K-edge imaging, and increased CNR through different energy weightings, while reducing the dose significantly. The continuous sensitivity of a pixelated sensor and the elimination of electronic noise through a threshold above it enable using much smaller detection pixels than in a conventional EI CT and contribute to further lowering of the dose. Consequently, spatial resolution is improved compared to EI CT (> 20 lp/cm). Reduction of the detection pixel size is essential also for lowering photon rates per pixel to avoid pile-up effects. However, charge sharing and Kα escapes of Te and Cd cause severe distortions to the recorded x-ray spectrum. A forward model of the detector response is used to address it and restore spectral capability, using a projection domain material decomposition. It will be shown that this can be accomplished as long as the peak-to-tail ratio is not too large, namely, detection pixel of about 0.5 mm. HW and SW methods of pile-up corrections will be shown too. Phantom and preclinical verifications on the PHILIPS Spectral Photon-Counting CT (SPCCT) in Lyon demonstrate the capability of such a system achieving spectral results superior to dual-energy CT, and the advantage of dual-contrast injection in a single scan. Learning Objectives: 1. To learn about the underlying physics and technological solutions. 2. To understand the potential advantages compared to dual-energy CT. 3. To appreciate how mature today's photon counting technology is. Author Disclosure: A. Altman: Employee; PHILIPS Healthcare. Radiographers play an essential role in the provision of high quality forensic imaging services. This is recognised in many countries and forensic imaging has been recognised by the European federation of radiographer societies (EFRS) as one of nine specialist areas of advanced practice for radiographers. While the concept of optimisation is at the heart of the profession, there remains room for improvement in further advancing optimisation for forensic applications. As with all specialist areas, or areas of advanced practice, appropriate education and training, and continuous professional development are fundamental. Through international organisations such as the international society for forensic radiology and imaging (ISFRI) and the international association of forensic radiographers (IAFR), together with national organisations and groups, forensic imaging continues to move in the right direction. Session Objectives: 1. To provide insights into the role of imaging, and radiographers, in forensic imaging and mass fatality incidents. 2. To appreciate the key aspects of a quality forensic imaging service. 3. To understand the challenges associated with forensic imaging. W benefit of this technique at the CURML. The indication to perform the MPMCTA is the suspicion of vascular lesions due to natural or traumatic origin, such as traffic accidents, homicides (stab wounds, ballistic), medical malpractice (especially in a post-surgery context), or unexpected adults death. This procedure allows examining vascular anatomy: analyses of the vascular lumen with potential stenosis or dilatation; analyse of the vascular walls with potential dissections or ruptures; characterization of the nature of an arterial and/or venous leakage. It also permits to obtain morphological information of the organs parenchyma. At the CURML, the MPMCTA is fully executed by the forensic radiographer. He is in charge of preparing the body, collecting samples before the angiography, denudating the arterial and venous vessels for the injections and proceeding the CT-scan acquisition. The duration of this technique lasting about 30 minutes won’t disturb the investigation work flow. The MPMCTA is then interpreted by a team involving forensic pathologist and a radiologist. Limitations and pitfalls of this technique should be known to identify artefacts and pitfalls. Learning Objectives: 1. To learn about the development of multiphase post-mortem CT angiography (MPMCTA). 2. To appreciate the benefits and limitations of MPMCTA examinations. 3. To understand the role of the radiographer in the MPMCTA. Forensic imaging is an ever-expanding sub-speciality of both radiology and forensic medicine. The overall role of forensic imaging is to obtain evidence and answer legal questions associated with either living or deceased individuals. Forensic imaging can be utilised in a variety of cases including suspected physical abuse, medical negligence, drug trafficking and mass fatalities incidents. In forensic pathology, forensic imaging has established a role in the assessment of identification and establishment of cause of death, particularly in cases of severely decomposed or burnt remains. The role of radiographers within forensic imaging contrasts significantly with that of the routine clinical environment. Those individuals involved in forensic imaging must understand and be aware of the medico-legal features and professional guidelines that impact their practice. Learning Objectives: 1. To appreciate the role of the radiographer in forensic imaging. 2. To learn about the importance of continuity of evidence and record keeping. 3. To discuss the various situations a radiographer can be exposed to during forensic imaging. 09:44 Panel discussion: Developing a service/getting involved in forensic imaging Room M 1 08:30 - 10:00 Vascular RC 115 Peripheral vascular malformations: what every radiologist should know A-042 08:30 Vascular malformations are rare and therefore the diagnosis is often unknown to a general radiologist. It is important to differentiate a congenital vascular malformation from an infantile hemangioma. Congential vascular malformations a have a specific anamnesis, which is often the major clue to the final diagnosis. There are 3 main types of congenital vascular malformations. Arterial (high flow with direct fistula), venous (low flow) and lymphatic. There are some related vascular tumours like capillary malformation and port-wine stains. There are several syndromes in relation to vascular malformations. The most known is Klippel-Trenaunay-Weber syndrome. For a general radiologists it is important to recognise a vascular malformation. Treatment and further work-up diagnosis should only be undertaken in centres of expertise. Only malformations that give complaints like pain, bleeding or cosmetic issues should be treated. Both embolisation (for high flow) and local sclerotherapy (for low flow) are used to treat vascular malformations. Session Objectives: 1. To review classification and description. 2. To identify the role of imaging modalities. 3. To understand the role of interventional radiologist in management and treatment. A-043 08:35 A. The diagnostic assessment M. Köcher; Olomouc/CZ () Vascular malformations are categorised into the low-flow malformations and high-flow malformations. From imaging methods is expected to distinguish between the low-flow lesions and high-flow lesions, localisation, volume and range of lesion and relationship to the surrounding tissues and organs. Color doppler ultrasonography (DUS) can offer good differentiation between highflow and low-flow lesions. Magnetic resonance (MR) offers good differentiation between high-flow and low-flow lesions also, and moreover good evaluation of volume and extent of lesion, good interpretation of anatomical relationship to the surrounding tissues and organs. On DUS the low-flow malformations are demonstrated as hypoechogenic or heterogeneous lesions with minimal flow inside, flow during augmentation and normal arterial flow volumes and normal high arterial resistance flow. The high-flow malformations are heterogeneous lesions with tortuous feeding arteries, high velocity and low-resistance flow in feeding arteries, multiple arteriovenous shunts and pulsatile flow in draining veins. On MR the low-flow malformations typically have low signal intensity in T1 weighted images in abnormal vascular structures and high signal intensity in T2 weighted images, whereas the high-flow lesions usually demonstrate a signal voids in abnormal vascular structures on most sequences. At follow-up DUS demonstrates thrombosis and fibrosis of the low-flow lesion. In the highflow lesion the waveform will be normalised and the resistive indexes and the flow volumes will become normalised as well. MR demonstrates thrombosis and fibrosis of low-flow malformation by the loss of high signal in T2 weighted images and loss of signal voids in high-flow lesions. Learning Objectives: 1. To learn about classification and terminology. 2. To understand the role of US, CT and MRA in diagnostic assessment. 3. To learn the optimal imaging algorithm for diagnosis and follow-up. A-044 08:58 B. Percutaneous or endovascular treatment: when and how? B. Peynircioglu; Ankara/TR () Vascular anomalies, are divided in two different categories which carry different prognosis and management: "Vascular tumors" and "Vascular malformations" (VM). Their precise identification is crucial and involves a good knowledge of the biological classification published by Mulliken and Glowacki and that has recently been updated by the International Society for the Study of Vascular Anomalies (ISSVA). Vascular malformations are always congenital and grow with the child. They can involve type of vessels solely or combined with others. A rheologic differentiation between low and high flow malformations is essential to characterise the seriousness of the lesion. Interventional radiology (IR) plays major role in both curative and palliative treatments of these VM. Once understanding the nature and high/low flow characteristics of VM, transcatheter/endovascular (transarterial or transvenous) or direct percutaneous puncture under imaging guidance are the 2 main techniques for treating these lesions. Depending on the type, nature, location and surroundings of the VM, one should decide the best strategy for treatment. Another key point is to decide whether to use embolisation or sclerotherapy. Again, the type, location of the VM is vital and the patient based decision is to be made carefully by a multidisciplinary team. Operator’s experience is of most importance in determining all of the above variables, together with the local circumstances. There are many different types of embolic and sclerotherapy agents available around the world. Learning Objectives: 1. To recognise the indications and the real need for treatment. 2. To learn about technical approach and how to plan the intervention. 3. To understand possible limitations and the final result prediction. A-045 09:21 C. Paediatric vascular malformations: diagnosis and treatment A. Barnacle; London/UK () Haemangiomas are by far the most common type of vascular anomaly that present in childhood. Haemangiomas are benign vascular tumours; several subtypes exist. Infantile haemangiomas are the commonest subtype and the vast majority of these require no intervention at all, because they involute spontaneously over the first few years of childhood. These well defined vascular masses have a highly characteristic growth pattern and typical A B C D E F G W imaging features. They can be distinguished from the rarer congenital haemangiomas by their clinical presentation. Rarer benign childhood vascular tumours include kaposiform haemangioendotheliomas (KHEs) and tufted angiomas, both of which are associated with thrombocytopaenia and have characteristic imaging features to distinguish them from haemangiomas. Unlike vascular tumours, vascular malformations are present from birth and grow slowly in childhood. Lymphatic malformations (LMs) tend to present earlier and are encountered much more commonly in children than adults. Macrocystic LMs consist of thin-walled cysts containing lymph or clot and microcystic lesions appear more solid. Ultrasound is often sufficient to make a diagnosis but MRI may be required to determine the extent of deep-seated lesions. Small lesions may not require treatment; larger lesions are usually treated with percutaneous image-guided sclerotherapy, though surgery has an important adjunctive role in debulking larger lesions. Finally, some children present with complex overgrowth, often of just one limb, which is associated with a vascular malformation. These patients require expert input from a multidisciplinary team and imaging is key. Learning Objectives: 1. To understand the specifics of vascular malformations in children. 2. To recognise when to observe and when to intervene. 3. To learn about interventional techniques used and results of treatment. 09:44 Panel discussion: How could we improve diagnosis and optimise the results of our interventions? Progress in imaging technology equipment enables scanning patients in high geometrical and temporal resolution as well as in multidimensional space (e.g. 4D). The amount of resulting data cannot be read any more in 2D as done in the last millennium. Furthermore, advances in computational power enable the use of sophisticated processing algorithms in real time. Thus reading in 2D, as done in the previous millennium, will be gradually replaced by volumetric reading as well as extracting diagnostic information from parametric images. Moreover, for personalized medicine, radiology has to deliver more detailed information, especially to measure tumour volumes or characterize contrast uptake on perfusion imaging. To get familiar with those now really emerging techniques, three well-known speakers will cover essential subtopics and provide a road map on how to migrate from the reading style in the last millennium to that in the current millennium. Session Objectives: 1. To learn about the state of the art in 3D post-processing. 2. To understand how 3D post-processing can most optimally be used in daily clinical practice. 3. To appreciate how automated 3D post-processing and quantification will lead to increased use of 3D visualisations for diagnostics and therapy planning, over 2D viewing. Author Disclosure: E. Sorantin: Advisory Board; ESPR Represenative at WHO. Author; Scientific papers and book contributions. Consultant; Ulrich Medical Inc. Germany. A-047 08:35 One of the most important developments in radiological interpretation is the need for the incorporation of advanced tools to assist the specialist in the study evaluation. Automated segmentation of structures based on convolutional neural networks (CNN) in the frame of deep learning would allow to significantly increase the efficiency of the study evaluation by the radiologist. Although the detailed segmentation of organs is still intricate in the field of abdomen and modalities like MR, current technology allows for the automated detection of the organs' location and identification of most of the tissue using bounding boxes. These applications may be used today in clinics for the automated assessment of tissue properties. A clear example is the automated detection and identification of vertebrae centroids, which allows for the acceleration of the radiologist reading process in spine CT examinations while it also allows for the automated calculation of trabecular bone quality properties in each identified vertebrae, therefore providing a high value to perform osteoporosis population studies without the need for a user interaction. These algorithms have been recently labelled as zero-click solutions and will provide a paradigm shift in 3D post-processing for radiologists, having the results of the 3D assessment already generated in their PACS even before starting review of the study. Learning Objectives: 1. To learn about recent advances in 3D post-processing techniques. 2. To understand how these techniques can be used in clinical practice now. 3. To learn new tips and tricks to use in your daily practice. Author Disclosure: A. Alberich-Bayarri: CEO; QUIBIM SL. Founder; QUIBIM SL. A-048 08:58 B. Making better use of your 3D package: tips and tricks P.M.A. van Ooijen; Groningen/NL () Advanced visualization, simulation and planning software is increasingly used in clinical practice providing a shift from 2D to 3D visualization, processing and interpretation. With this ongoing trend the radiological profession should not only focus on the diagnosis to be made, but also on the utilization of our imaging data in patient simulation, planning, and treatment. Current functionality moves in this direction with providing extensive possibilities for support of surgical interventions and treatment planning in 3D including the advent of Virtual and Augmented Reality. With this 3D is also moving into the operating theater. Although these new possibilities are interesting and exiting one should be very aware of the pitfalls that come with 3D visualization and processing of data. This not only includes the technical but also the procedural pitfalls where image acquisition optimal for diagnosis is not always optimized for the intended use by the referring physician. To adequately use the new techniques and to provide optimal support from radiology to the referring physicians training is required and dedicated staff should be involved in this process. Learning Objectives: 1. To learn about the functionality of state-of-the-art 3D packages. 2. To understand the pitfalls in use of 3D post-processing. 3. To appreciate the need for training in 3D post-processing techniques. A-049 09:21 C. Interpretation of 3D processing results: from image to volume reading T. Frauenfelder; Zurich/CH () The widespread introduction of multidetector computed tomography (MDCT) has revolutionized the field of computed tomography (CT). This revolution can be attributed to three primary properties of MDCT: its ability to produce a vast quantity of volumetric data in a reduced amount of time, the high resolution, and the ability to create isotropic voxel data and, consequently, reliable multiplanar and three-dimensional (3D) reconstructions. Diagnostic approaches that rely solely on axial reconstructions of MDCT data are often insufficient for formulating an accurate diagnosis or for documentation of clinical cases. Specialized 3D reconstruction techniques permit the visualization of anatomical details, which would be difficult to evaluate using axial reconstructions alone. Such details may require the use of oblique or curved reconstructions, or more complex methods, such as maximum intensity projection (MIP), minimum intensity projection (MinIP), surface-shaded volume rending (SS-VRT), and virtual endoscopy. For example, small pulmonary nodules can only be rapidly and reliably identified through the use of MIP Slab slices. The current trend is to merge the routine diagnostic console and 3D reconstruction workstation. The integration of 3D reconstruction utilities into the standard bi-dimensional diagnostic software has increased the number of operations possible on each exam data, greatly increasing the perceived complexity of CT diagnosis. Although many of us believe that the use of 3D reconstructions greatly increases total exam evaluation time, there are reports show how using 3D reconstruction techniques for examining volumetric data are effective and also improve the speed of interpretation, recognition, and description of specific clinical conditions. Many of these reconstruction techniques are of particular importance for the analysis of subspecialty exams, as for example the 3D depiction and quantification of lung emphysema. Learning Objectives: 1. To learn about different developments in creating 3D anatomical and functional models for diagnostic and therapy planning purposes. 2. To understand the pros and cons of such technologies. 3. To appreciate that automated 3D image analysis will lead to new ways in which diagnosis and therapy planning will be performed. A B C D E F G Author Disclosure: T. Frauenfelder: Other; Bayer. 09:44 Panel discussion: Will we still look at 2D images in 10 years' time? Image interpretation of 3D results: from image reading to volume reading. Portal hypertension is characterized by high pressure in the hepatic portal venous circulation. Clinically significant portal hypertension is diagnosed when the hepatic venous pressure gradient (HVPG) exceeds 10 mmHg. It may be caused by hepatic, pre-hepatic or post-hepatic aetiologies. Diagnostic radiology plays a crucial role in establishing the aetiology, identifying complications and in planning management. Interventional radiology (IR) plays a major role in both the diagnostic and therapeutic management of portal hypertension. HVPG measurement is a minimally invasive IR technique that establishes the diagnosis of portal hypertension. Different therapeutic IR procedures may be used in different clinical scenarios and have replaced more invasive open surgical techniques. The hepatobiliary radiologist is a key player in the multidisciplinary team caring for patients with portal hypertension. The imaging findings of portal hypertension and the different IR procedures used in this condition will be discussed during this session. Emphasis will be made on the practical aspects of interventional radiology procedures, including transjugular intrahepatic portosystemic shunt (TIPS), variceal embolization, splenic artery embolization and balloon-occluded retrograde transvenous obliteration (BRTO) - including their indications, methodology, complications, and clinical outcomes. Session Objectives: 1. To appreciate the role of multidisciplinary treatment of portal hypertension. 2. To learn about imaging and intervention in portal hypertension. 3. To discuss outcomes of interventions in portal hypertension. A-051 08:35 A. Imaging of portal hypertension I. Bargellini; Pisa/IT () Portal hypertension (PH) represents a fearful complication of several diseases (most frequently liver cirrhosis), associated with high morbidity and mortality. Definitive diagnosis of PH is based on the measurement of hepatic venous pressure gradient (HVPG). PH is diagnosed by measuring a HVPG higher than 5 mmHg, it is considered clinically significant when HVPG is higher than 10 mmHg and severe when HVPG is above 12 mmHg. A direct relation has been demonstrated between HVPG and risk of variceal bleeding, hepatic decompensation and liver related mortality, and HVPG has become a surrogate endpoint in the assessment of treatment response and reduction of risk of liver-related mortality. However, HVPG measurement is invasive, is not routinely available and it is reliably standardized only in expert centers. Thus, non-invasive methods, such as elastography, are under investigation, in the attempt to diagnose and grade PH, and to predict presence, extent and risk of variceal bleeding. Non-invasive imaging, such as ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MR) may enable diagnosis of PH through the identification of complications (such as varices, splenomegaly, ascites). The anatomic information provided by these imaging modalities becomes essential to identify the causes of PH and when treatment planning is required (such as in patients indicated for TIPS or candidate for liver transplantation). Imaging plays a crucial role also to assess response to treatment and post-treatment complications. Learning Objectives: 1. To appreciate imaging features of portal hypertension. 2. To discuss the appropriate choice and timing of imaging technique in investigation of portal hypertension and its complications. 3. To learn about relevant findings that influence therapy choice in portal hypertension. Author Disclosure: I. Bargellini: Advisory Board; Bayer Spa. Speaker; GE Healthcare, BTG, Sirtex Medical. A-052 08:58 B. Embolisation of varices and splenic artery in portal hypertension I.E. Keussen; Lund/SE () Portal hypertension is most common secondary to liver cirrhosis, however it can also be caused by portal/splenic vein thrombosis or occlusion. A bleeding secondary to portal hypertension, usually originates from esophageal or gastric varices, other sites may be duodenal, stomal or rectal varices. A bleeding from esophageal varices is primarily most often treated endoscopically with sclerotherapy or rubber banding. Gastric varices are less prevalent, but more difficult to treat endoscopically. If medical and endoscopic treatment methods fail, interventional treatment is the next option, which includes embolisation of varices, TIPS, BRTO and partial splenic arterial embolisation. Embolisation of varices may be performed by percutaneous or transjugular-transhepatic approach, but transsplenic route or direct puncture of the stomal varices are also reported. A BRTO may be applied in patients with a splenorenal shunt and secondary gastric varices. Partial splenic embolisation may decrease inflow of blood to the portal vein and secondary decrease the portal hypertension. In most cases a combination of different techniques is necessary to achieve good results. Learning Objectives: 1. To discuss the rationale for embolisation. 2. To learn about the selection of technique and choice of material. 3. To understand outcomes from embolisation techniques. A-053 09:21 C. Transjugular intrahepatic portosystemic shunt (TIPS): critical appraisal of techniques and guidelines for treatment A. Krajina; Hradec Králové/CZ () TIPS is a minimally invasive method of creating a portosystemic shunt for decompression of portal hypertension (PH). A side-to-side shunt of determined diameter is created to shunt blood flow from the portal vein (PV) to hepatic vein or inferior vena cava above the liver using transjugular approach, long needle, balloon angioplasty, and stent-graft. The most often indication for TIPS is cirrhotic ascites, which is sometimes combined with severe hydrothorax. However, TIPS is used in those patients who are intolerant of repeated largevolume paracenthesis. TIPS has been used as a rescue treatment in rare cases of endoscopically uncontrollable variceal bleeding, especially from gastric fundal varices. Emergent TIPS (in 72 hours) performed in patients with severe PH and high risk of early rebleeding, has been proved to have better bleeding control and survival in 1 year. Partial or complete PV thrombosis does not change usual technique of TIPS. TIPS is technically difficult in chronic extrahepatic PV obstruction, in children, and in patients with massive hepatic veins thrombosis (Budd-Chiari Syndrome - BCS). The absence of hepatic veins and distorted anatomy due to the caudate lobe hypertrophy requires sometimes direct transcaval approach to the PV in patients with BCS. Moreover, these patients must be anticoagulated life long due to underlying hypercoagulopathy. TIPS demonstrated good control of ascites and reversal of liver failure in large series of patients with BCS. All patients with TIPS must be followed regularly in specialized multidisciplinary center, and the surveillance of TIPS function is mandatory. Learning Objectives: 1. To discuss the selection of patients for TIPS. 2. To learn about the techniques for TIPS formation. 3. To discuss outcomes of TIPS and role of imaging surveillance. 09:44 Panel discussion: Appropriate selection of patients for IR including the role of balloon-occluded retrograde transvenous obliteration (BRTO) for gastric varices W 08:30 - 10:00 Room M 4 Lung cancer is the most common cause of cancer-related death in Western countries. In the last several years, a number of new drugs have revolutionized systemic therapy in lung cancer. These new therapies can be divided into two major groups, the targeted therapies and the immunotherapies. Targeted therapies, such as EGFR tyrosine kinase inhibitors, or ALK inhibitors, are a class of drugs that specifically target a well-defined molecular pathway. They have been shown to be more effective than classic chemotherapies in patients who harbor the specific mutation and are associated with fewer toxicities. As these drugs target molecules with a specific mutation, patients who harbor this specific mutation need to be identified. In addition to bronchoscopy, imageguided biopsies are the main modality for obtaining tissue for molecular analysis. Imaging may have a potential role in identifying tumors that harbor a specific mutation, and thus, in guiding further pathologic and genetic work-up. Immunotherapy, however, targets immunological pathways to induce an immunological response against tumors. Immunotherapy has been shown to be a very effective treatment in a subset of patients with non-small cell cancer. Imaging plays a major role in the follow-up evaluation of patients undergoing immunotherapy, as immune reactions must be differentiated from disease progression. Adenocarcinoma is the most prevalent type of lung cancer, showing a large spectrum of genetics, histologic subtype, CT appearance, clinical behavior and prognosis. Activating mutations of EGFR are found in 30%-50% of lung adenocarcinomas in East Asian patients and approximately 15% in Caucasian patients. EGFR mutation status is correlated with nonsmoking status, female sex, lepidic subtype, and high response rate to EGFR tyrosine kinase inhibitors (TKI). Some CT findings have shown to be associated with EGFR mutation such as nonsolid or mixed ground-glass opacity, air bronchogram, smaller and peripheral tumors, and pleural retraction. Furthermore, non-smoking patients presenting with diffuse miliary metastatic disease at diagnosis may be diagnosed with adenocarcinoma harboring EFGR mutation and may show dramatic response to EGFR-TKI. The most common resistance mechanism to EGFR-TKI is the T790M mutation, against which new irreversible TKIs have been found to be clinically effective, thus increasing demand for rebiopsy in progressive NSCLC to analyze mutational status. Rebiopsies are feasible and informative in most of patients with acceptable rates of complications. Furthermore, continued EGFR-TKI therapy may be indicated beyond RECIST progression, because these tumors grow slowly and some tumor cells remain sensitive to EGFR-TKI. Radiologists should also be aware of the risk of classeffect toxicity of EGFR-TKI, in particular pneumonitis with an incidence rate of 4-5% in the Japanese population. Finally, European radiologists should keep in mind that a majority of studies dealing with EGFR mutations in adenocarcinomas arise from Asian countries with results that might not be transposable to Caucasian populations. Learning Objectives: 1. To be aware of the importance of detecting EFGR mutation. 2. To learn about demographic and CT features suggestive of EGFR mutation. 3. To learn about the various initial and follow-up CT features. The 2-7% of non-small cell lung cancers (NSCLC) harbor the rearrangement of anaplastic lymphoma kinase (ALK) - an oncogene related to a tyrosine kinase pathway - notably in adenocarcinoma histology and in non-smokers (about 60% of all ALK-rearranged NSCLC). Target therapy by tyrosine kinase inhibitors (TKI) is clinically available for ALK-positive advanced NSCLC and improves progression-free survival (PFS) compared with previous reference chemotherapy. Hence, testing for mutations is paramount for optimal planning of medical treatment of advanced NSCLC. In the face of a better disease control by TKI, however, it happens that ALK-positive tumors are prone to driver mutation with resistance to first-line TKI, in the first months of therapy. In clinical practice, diagnostic imaging, notably computed tomography (CT), has high yield in the management of patients under target therapy. The CT evidence of disease progression, either local or systemic (note: brain metastases are relatively common because first-line TKIs have low trespassing coefficient through emato-encephalic barrier) is paramount for timely adaptation of therapy. Rapid radiologic progression demands prompt TKI swap towards second-line (e.g., ceritinib, brigatinib, or alectinib) or third-line target therapy (e.g., lorlatinib) or otherwise. Re-biopsy is suggested to pitch the optimal second (or further) line therapy by continuous molecular testing. In clinical trials, again, diagnostic imaging has high yield in the assessment of target therapies, namely for definition of PFS. Adverse events occur in a minority of patients under TKI (1% incidence of lung toxicity). Therapy discontinuation is usually sufficient to reduce toxic effects, with only 3-6% of cases lingering after therapy withdrawal. Learning Objectives: 1. To learn about clinicopathologic features characterising ALK-rearrangement. 2. To understand the impact of ALK rearrangement on the prognosis of nonsmall cell lung cancer. 3. To see some illustrative cases. A-057 09:31 C. PD-L1 positive lung tumours O.L. Sedlacek; Heidelberg/DE () Immune checkpoint inhibitors (ICI) are effective in the treatment of many cancers, blocking immunosuppressive pathways; they play a increasing role in the first-line treatment of lung-cancers. This is particularly true when there is evidence for a significant pretreatment tumor lymphocytic infiltration and/or tumors exhibit a positive staining for PD-L1. As ICIs work through a different mode of action there is good reason to use therapy response criteria other than RECIST. In contrast to cytotoxic agents anti-tumour response in immunotherapy may take longer and in the initial phase the response to immune therapies can manifest in a morphologic “progressive disease”, therefore, called “pseudoprogression”. In this situation a early discontinuation of the treatment would not be appropriate, unless PD is confirmed. “Clinically insignificant” PD may even include the detection of new lesions ("unconfirmed progression") that may not lead immediately to a discontinuation of the oncologic regiment and has to be reevaluated. As ICIs act through a different mechanism than cytotoxic agents or tyrosine inhibitors, deblocking the immune system a broad spectrum of auto immune diseases can be triggered. Imaging characteristics of frequent and serious immune-related adverse events (irAEs) will be discussed. Learning Objectives: 1. To know about the impact of PD-L1 positivity. 2. To know how to evaluate the tumour response after immunotherapeutics. 3. To be aware of the imaging features of immune therapy complications. RC 106 Merging the best: hybrid imaging Moderator: G. Antoch; Düsseldorf/DE A-058 08:30 A. Hybrid imaging with SPECT/CT A. Scarsbrook; Leeds/UK () Latest generation SPECT/CT cameras incorporate multi-detector CT and stateof-the-art gamma camera technology in tandem. These scanners improve the efficacy of a wide variety of nuclear medicine tests by providing more accurate localisation of lesions, exclusion of potentially misleading physiological uptake, characterisation of equivocal or indeterminate activity and detection of additional lesions. In addition, they offer the potential for a more efficient "onestop-shop" imaging approach. Iterative reconstruction algorithms and faster processing power facilitate radiation dose reduction and increased image resolution. The clinical utility of SPECT/CT is diverse and a cross-spectrum of applications in musculoskeletal, oncological, cardiological, endocrine, hepatobiliary and GI tract imaging will be presented. Learning Objectives: 1. To learn the basic principles of hybrid SPECT/CT imaging. 2. To understand what complementary information can be given by SPECT/CT. 3. To learn about clinical applications of SPECT/CT. A B C D E F G W A-059 09:00 B. Hybrid imaging with MR/PET F.M.A. Kiessling; Aachen/DE () In this talk an overview on the technological state of the art in PET-MRI as well as an outlook on emerging new technologies will be provided. Concerning the latter in particular new PET-insert solutions will be highlighted that are tailored to specific medical applications and body parts. Besides this, there will be a brief overview on new detector setups providing higher sensitivity and spatial resolution as well as on the methods to improve absorption correction and quantification. In the final part of the talk the focus will be set on the medical applications of PET-MRI. In this context, it will be discussed, which applications inevitably demand for PET-MRI hybrid imaging. Thus, with this talk I will try to convince the audience of the high development potential and clinical value of PET-MRI and its future role in patient management. Learning Objectives: 1. To learn the basic principles of hybrid MR/PET imaging. 2. To understand what new information can be given by MR/PET. 3. To learn about emerging clinical applications of MR/PET. There is increasing evidence to support a role for metabolism in many diseases; for example, deregulation of cellular energetics is now considered to be one of the key hallmarks of cancer. There are a number of imaging methods that have been used to probe this metabolism: the most widely available is 18F-fluorodeoxyglucose (FDG), an analogue of glucose, used in PET. Hyperpolarised carbon-13 MRI (13C-MRI) is an emerging molecular imaging technique for studying cellular metabolism, particularly in the fields of oncology and cardiology. This method allows non-invasive measurements of tissue metabolism in real-time. To date, the most promising probe used in conjunction with hyperpolarised MRI has been 13C-labelled pyruvate: pyruvate is metabolised into lactate in normal tissue in the absence of oxygen, but in tumours this occurs very rapidly even in the presence of oxygen. Results from many animal models have shown that there is a reduction in the metabolism of pyruvate to lactate following successful treatment with chemotherapy. In the heart, pyruvate is also metabolised to carbon dioxide in addition to lactate and this balance between anaerobic and aerobic metabolism alters in many disease states. There are now a small number of sites performing human hyperpolarised carbon-13 MRI imaging. This talk will discuss the progress that has been made in this field within the areas of oncology and cardiology and potential clinical applications. Learning Objectives: 1. To learn the basic principles of hyperpolarisation. 2. To understand what new information can be given by hyperpolarised MRI. 3. To learn about oncological and non-oncological applications of hyperpolarised MRI. Author Disclosure: F.A. Gallagher: Research/Grant Support; GE Healthcare, GSK. 10:30 - 12:00 E³ - ECR Academies: Interactive Teaching Sessions for Young (and not so Young) Radiologists E³ 221 Musculoskeletal radiology: inflammation A-061 10:30 A. Inflammatory and infections in the soft tissues S. Martin; Palma de Mallorca/ES () The diagnosis of infections is based on the presence of clinical symptoms like erythema, swelling, and pain. Also the diagnosis is based on the presence of clinical signs such as fever, tachycardia, shock, and hypotension and laboratory test such as leukocytosis, C protein reactive and Erythrocyte sedimentation rate. However, the clinical symptoms and signs of infection may not be specific, especially in the early stages of the disease. In these cases, imaging tests play a fundamental role in the early diagnosis of infections and in the differential diagnosis. The most important radiological findings for inflammatory and infections soft tissue are: (1) intramuscular fluid collections; (2) soft tissue air; (3) fascial fluid collections; and (4) muscle edema. Potential causes of these radiological findings are diverse, including, infectious, autoimmune, inflammatory, neoplastic, neurologic, traumatic and iatrogenic conditions. Some of these conditions require prompt medical or surgical Room A management, whereas others do not benefit from medical intervention. Necrotizing fasciitis is a rare, life-threatening soft-tissue infection and a medical and surgical emergency that radiologist must know. The presence of gas within the necrotized fascia is characteristic, but may be lacking. The main finding is thickening of the deep fascia due to fluid accumulation and reactive hyperemia. All these findings may be seen in other different conditions. The ability to accurately diagnose these conditions is therefore necessary, and biopsy may be required to establish the correct diagnosis. Clues to the correct diagnosis and whether biopsy is necessary or appropriate are often present on the images techniques, especially when they are correlated with clinical features. Learning Objectives: 1. To learn the key signs for differential diagnosis. 2. To learn about imaging findings and management options. A-062 11:15 Arthritis is a common problem involving the joints in the axial and/or appendicular skeleton across all age groups. Imaging plays a key role in the diagnosis and management of arthropathies, which are generally divided into degenerative, inflammatory, and metabolic categories. Digital radiography is the main imaging tool for joint diseases. Magnetic resonance imaging (MRI), computed tomography and ultrasonography are also used along with digital radiographs in the initial diagnosis and follow-up of joint diseases. The multiplicity and distribution of the involved joints, the pattern of joint space narrowing, and periarticular bone and soft tissue changes are important considerations for radiological diagnosis. The involvement of a single joint with inflammatory arthritis requires the exclusion of infection, whereas c involvement with degenerative arthritis may be due to an identifiable remote trauma. Septic arthritis does not have a pathognomonic radiological finding and, in the presence of clinical suspicion for infection, imaging should not delay joint fluid aspiration for microbiological investigation. This interactive session will cover the radiographic clues of arthropathies and the use of cross-sectional imaging methods, especially MRI, for suggesting the likely diagnosis. Some conditions, such as rotator cuff arthropathy and degenerative disease of the medial compartment of the knee secondary to medial meniscus posterior root avulsion, that have typical MRI findings shedding light on the pathophysiology of arthropathies will also be addressed. Learning Objectives: 1. To explain the key points in the differential diagnosis of common arthropathies. 2. To describe the imaging findings of common arthropathies as they relate to pathophysiology. Room F1 In this presentation focused on the first segment of the alimentary tract, current imaging techniques for evaluation of normal anatomy will be considered and described. From conventional radiography to modern hybrid imaging, essential information regarding the methods will be included. The second part of the lecture will describe the imaging features in most common benign pathologies, to give the attending useful informations for the daily clinical practise. Elective and Emergency conditions for the evaluation of the oesophagus will be considered. Finally, a pictorial guided review of the imaging features of malignant pathologies will be done. Learning Objectives: 1. To discuss current imaging techniques for evaluation of normal anatomy. 2. To describe the imaging features in most common benign pathologies. 3. To review and illustrate the imaging features of malignant pathologies. A B C D E F G W A-064 10:53 Today, the stomach is well accessible for endoscopic evaluation. Therefore, double-contrast barium studies of the stomach have almost completely disappeared from the armamentarium of imaging studies in radiology. However, abdominal computed tomography (CT) - not so much magnetic resonance imaging (MRI) - has become the number one procedure in many scenarios if ultrasonography fails to provide a conclusive diagnosis. As the stomach is always imaged when abdominal CT is performed knowledge of normal anatomy, incidental findings, and the most often benign and malignant gastric pathologies is mandatory. Depending on the clinical request, imaging techniques are slightly different. If the main focus is on a lesion of the stomach, maximum wall distention should be achieved by oral administration of up to 2 L of water shortly before the study and i.v. administration of a hypotonic agent. In addition, i.v. administration of iodinated contrast material is mandatory. The presentation will cover normal anatomy of the stomach including locoregional lymph nodes. Examples of common and uncommon gastric lesions (e.g., carcinoma, lymphoma, GIST, NET, metastases, ulcer, portal gastropathy, pneumatosis, ischemia, pseudocysts) will be shown and discussed. Also examples of postoperative anatomy and potential complications will be part of the presentation. Learning Objectives: 1. To discuss current imaging techniques for evaluation of normal anatomy. 2. To describe the imaging features in most common benign pathologies. 3. To review and illustrate the imaging features of malignant pathologies. Magnetic resonance imaging (MRI) provides excellent soft-tissue contrast without radiation exposure and three-dimensional imaging capabilities, which are important when studying the small intestine. Various sequences and contrast agents have been proposed for MRI examination of the small bowel. The development of high performance gradient systems improved the performance of ultra fast sequences and allowed comfortable breath-hold acquisition times. For a more detailed evaluation of small bowel diseases, MRI examination should be performed in conjunction with duodenal intubation and administration of a suitable contrast agent, i.e., iso-osmotic water solution (PEG) for homogeneous lumen opacification and adequate distention. A comprehensive MR enteroclysis imaging protocol should comprise single shot turbo spin echo (SSTSE), diffusion weighted imaging, true FISP, HASTE and fat suppressed T1 FLASH sequences. SSTSE is utilized for monitoring the infusion process and performing MR fluoroscopy while true FISP and HASTE, classified as sequential ultra fast techniques insensitive to motion, are mainly used for anatomic demonstration and detection of the pathology. T1 FLASH sequences after intravenous gadolinium injection may aid tissue characterization. For the assessment of Crohn’s disease activity other alternative techniques may be used including perfusion and calculation of the magnetization transfer ratio of the bowel wall. These techniques may be useful for differentiating edematous or inflammatory bowel thickening from fibrotic thickening, but a more extensive evaluation is required to determine the clinical utility of these methods. Learning Objectives: 1. To discuss current imaging techniques for evaluation of normal anatomy. 2. To describe the imaging features in most common benign pathologies. 3. To review and illustrate the imaging features of malignant pathologies. Author Disclosure: N. Papanikolaou: Advisory Board; Advantis. CEO; MRIcons. A-066 11:38 Ultrasound, CT and MRI has a role in the workup of diseases of the large bowel. Transabdominal US is accurate to detect appendicitis. Contrast enhanced CT identifies the causes of bowel obstruction and dilatation. CT shows postoperative complications such as leakage of surgical anastomosis, internal herniation, bowel strangulations ,and bowel ischemia. Inflammation of the bowel, diverticulitis, epiploic appendagitis are well detected on CT. While endorectal US and MRI have been widely adopted in the staging work up of rectal tumors, the role of imaging in Colon cancer is limited to preoperatively roadmap the extent of the tumor into surrounding structures and to identify distant disease. Nevertheless this role may increase in the near future. This lecture will deal with various diseases of the colon and its imaging features and highlights future direction in imaging of colon cancer. Learning Objectives: 1. To discuss current imaging techniques for evaluation of normal anatomy. 2. To describe the imaging features in most common benign pathologies. 3. To review and illustrate the imaging features of malignant pathologies. Pulmonary vascular disease includes a wide spectrum of disease entities, many of which have overlapping clinical and imaging features. CT of the pulmonary vasculature has become an integral part of the investigation of such entities. In this session we are going to evaluate three distinct disease subcategories of pulmonary vascular disease: pulmonary arterial hypertension, pulmonary vasculitis and Rendu-Osler disease. The first talk will cover pulmonary hypertension, the current clinical classification of pulmonary vasculitis, CT signs suggestive of the diagnosis, and CT signs that help discriminate between different causes. The comprehensive nature of CTPA in evaluating the mediastinum, vasculature and lung parenchyma will be shown. The second talk covering pulmonary vasculitis will emphasise the importance of combining CT signs with the clinical features and laboratory results since vasculitis may mimic other disorders and sometimes the clinical features are the major clue. CT findings in granulomatosis with polyangiitis and eosinophilic granulomatosis with polyangiitis will be shown, particularly emphasising the imaging differences between the two entities. The imaging findings of pulmonary hemorrhage will also be shown alongside the commonest causes. Finally the association between interstitial lung disease and the ANCA associated vasculitis will be discussed. The third talk covering Rendu-Osler disease will show the typical imaging features of this disease with a particular emphasis on those imaging aspects that determine outcome and treatment strategies. The talk will also cover contemporary aspects of endovascular treatment modalities and their complications. Pulmonary hypertension (PH) typically presents insidiously with non-specific symptoms and is usually progressive with poor outcome independent of aetiology. CT plays a vital role both in suggesting the possibility of pulmonary hypertension, whether initially clinically suspected or not, and in identifying a specific cause of pulmonary hypertension. The causes of pulmonary hypertension can be broadly divided into those affecting primarily the small vessels, PH secondary to left heart disease or chronic lung disease / hypoxia (the most common causes), chronic thromboembolic PH, and multifactorial causes. CT is widely available, inexpensive, and permits comprehensive assessment of the heart, pulmonary vasculature and lung parenchyma. CT signs such as dilatation of the proximal pulmonary arteries and right heart chambers can be considered as generic features associated with PH of any cause. Signs of a specific cause may lie in the mediastinum (left heart disease, shunt, oesophageal varices, oesophageal dilatation), vasculature (signs of CTEPH, tumour, large vessel vasculitis, fibrosing mediastinitis) or lungs (parenchymal lung disease, mosaic perfusion in CTEPH, signs of a small vessel vasculopathy). CTEPH is a not uncommon sequela of previous acute embolism. If the distribution is proximal it is potentially cured by surgical pulmonary endarterectomy or by balloon pulmonary angioplasty. Imaging in general and CT in particular play fundamental roles in both identification of CTEPH, its differentiation from acute PE, and in characterising its distribution. Imaging signs in CTEPH can be subtle and systematic evaluation of a CTPA is essential. Learning Objectives: 1. To learn about the CT signs of pulmonary hypertension (PHT). 2. To become familiar with the current classification of PHT. 3. To be aware of the imaging features suggesting a thromboembolic origin. A B C D E F G W A-069 11:03 B. Evaluating the pulmonary vasculitis E. Castañer; Sabadell/ES () We will emphasize the importance of combine CT signs with the clinical features and laboratory results as vasculitis may mimic other disorders and sometimes the clinical features rate the clue. We will describe the findings in granulomatosis with polyangiitis (GPA) and eosinophilic granulomatosis with polyangiitis, highlighting the differences. Diffuse alveolar hemorrhage (DAH) is one of the manifestations of primary pulmonary vasculitis, among other entities (idiopathic alveolar hemorrhage, collagen vascular diseases, drug reactions, anticoagulation disorders). GPA and microscopic polyangiitis are the most common causes of DAH. Radiologic signs of DAH are nonspecific and variable, but must be considered in patients with otherwise unexplained alveolar infiltrates, particularly when seen with new onset renal insufficiency or a connective tissue disease. Finally we will mention the association between interstitial lung disease and ANCA associated vasculitis. Learning Objectives: 1. To learn the common imaging features of granulomatosis with polyangitis (GPA). 2. To learn how to differentiate between GPA and eosinophilic granulomatosis with polyangiitis (Churg-Strauss). 3. To learn about the imaging features and differential diagnosis of pulmonary haemorrhage. Rendu Osler disease (ROD) is an autosomal dominant genetic disorders characterized by the presence of telangiectasias and/or arteriovenous malformations. Pulmonary arteriovenous malformations (PAVM) are observed in up to 80% in ROD patients and it is believed that up to 30% of ROD patients will develop PAVM. During the last decade CT became the standard of reference in assessing pulmonary and associated subphrenic anomalies in patients with ROD. This lecture will focus on current protocols and recommendations for CT depending on the objective of the examination (screening, diagnostic or follow-up). Typically, PAVM is a well circumscribed rounded lesion that is connected to an afferent feeding artery and an enlarged efferent vein. PAVMs can be focal, multiple or diffuse. Imaging features as well as a comprehensive classification is provided. In asymptomatic patients, the risk of complications was reported to be high in PAVMs with an afferent artery diameter of 3 mm or more. The role of CT is then not only crucial in diagnosis, but also in therapeutic decision making process even if the 3 mm threshold concept in matter of debate and controversies. Principles of endovascular management of PVAM are reviewed. The transarterial access is the most common procedure. The modern approach includes the use of coils and/or plugs. CT flow up studies aim diagnosis of early complications, PAVM reperfusion detection, surveillance of small PAVMs, and diagnosis of new PAVMs. Learning Objectives: 1. To become familiar with the CT manifestations of this disease. 2. To identify imaging features determining outcome and treatment strategies. 3. To learn about endovascular treatment modalities and complications. 12:30 - 13:30 E³ - The Beauty of Basic Knowledge: Cardiovascular and Interventional Radiology E³ 24A No time to lose: aortic dissection revisited Moderator: M. Krokidis; Cambridge/UK Aortic dissection is the most common acute emergency condition of the aorta, often resulting in the death of the patient. The overall outcome is determined by the type and extent of dissection and the presence of associated complications; therefore, evaluation of the entire aorta, branch vessels, and iliac and proximal femoral arteries is recommended to aid in treatment planning. Early diagnosis and treatment are essential for improving the prognosis. Patients may present with the classic history of acute onset of tearing central chest pain that radiates to the back. Stanford type A dissection involves the ascending thoracic aorta, and the dissection flap may extend into the descending aorta. Type A dissections account for 60%-70% of cases, requiring urgent surgical intervention to prevent extension into the aortic root, pericardium, or coronary arteries. If untreated, type A dissections are associated with a mortality rate of over 50% within 48 hours. Stanford type B dissection involves the descending thoracic aorta distal to the left subclavian artery and accounts for 30%-40% of cases. Management takes the form of medical treatment of hypertension, unless there are complicazioni due to extension of the dissection. CT imaging of the aorta is fast and widely available, which are the important features in making an accurate diagnosis quickly in unstable patients. Multidetector CT allows imaging of the entire aorta with rapid acquisition and data reconstruction to provide prompt and accurate diagnosis and to help identify relevant complications that may have an impact on treatment and management. Learning Objectives: 1. To learn about definition and classification of aortic dissections and subtypes. 2. To understand the importance of accurate diagnosis for appropriate treatment planning. 3. To appreciate the need for acute diagnosis and treatment indication. A-078 13:00 Endovascular treatment in aortic dissection J.P. Schäfer; Kiel/DE Acute aortic dissection represents a life-threatening condition, which must be diagnosed immediately. CTA is considered the imaging modality of choice, offering all relevant information on the pathoanatomy with highest spatial resolution. Stanford classification is used to distinguish between type A- and Bdissections, whereas the left subclavian artery represents the border in between the two types. Actually, surgical repair is the method of choice and indicated in type Adissection, and endovascular repair is the method of choice in type B-dissection, if indicated. Type Bdissection may be uncomplicated or complicated. For uncomplicated type B, best medical treatment is the method of choice, and it is defined by no further symptoms, relief of symptoms and absence of additional dissection associated findings. For complicated type B, endovascular repair including a variety of interventions is the method of choice, and it is defined by mesenterial, renal, peripheral and spinal malperfusion, progressive dissection, aneurysm forming, uncontrollable hypertension, rupture, progressive periaortic and pleural haemorrhage, severe hypotension and shock. Regarding symptom onset and imaging based diagnosis, type Bdissection is classified as acute (<2 weeks), subacute (2-8 weeks), and chronic (>8 weeks). Endovascular repair usually includes prosthesis placement in the descending aorta, in order to seal the proximal entry tear. This excludes the perfusion of the false lumen along the covered aortic segment and restores the blood flow into the true lumen, maintaining and improving the visceral and peripheral perfusion. Additionally, target visceral artery stenting, membrane fenestrating or embolising may be indicated. Protocolled CTA follow-up is mandatory. Learning Objectives: 1. To learn about endovascular treatment possibilities for aortic dissections. 2. To understand the role of radiology in modern treatment of aortic dissections. 3. To appreciate the need to combine the radiological information with the clinical situation. 12:30 - 13:30 E³ - The Beauty of Basic Knowledge: A Survival Guide to Musculoskeletal Imaging Room D Osteoarthritis is the most common joint disease worldwide. It is a major source of pain, disability, and socioeconomic cost. The epidemiology of the disorder is complex and multifactorial, with genetic, biological, and biomechanical components. Conventional X-ray is the standard diagnostic method to confirm the clinical diagnosis, to evaluate the degree of severity of osteoarthritis and to look for predisposing conditions. CT can be performed for the assessment of A B C D E F G W bone stock, anatomic conditions and bone deformation. MRI can be used to confirm early forms and to clarify possible damage and/or wear and tear, which cannot be seen on X-rays. Finally, intraarticular administration of contrast will be performed in selected cases, when a precise assessment of the cartilage or fibrocartilage is required. This lecture will focus on the role of imaging in clinical practice, the typical and atypical imaging features of OA, the radiological features which should not be read as OA, and the main predisposing factors that have to be known and searched. Learning Objectives: 1. To appreciate the musculoskeletal imaging manifestations of degenerative disorders. 2. To understand the underlying pathomechanisms involved in these imaging abnormalities. 3. To appreciate the strengths and weaknesses of imaging modalities in assessing these disorders. Head injuries are one of the most frequent causes of death and disability. The following presentation will discuss the indications for imaging in patients with traumatic brain injury(TBI), review the role of X-ray examination, computed tomography (CT) and magnetic resonance imaging (MRI) in the management of TBI. CT still remains the method of choice in brain injury diagnosis and allows rapid assessment of the extent and type of brain pathology which ensures us which patients require urgent surgical intervention. There are many CT structural modalities such as MPR, volume rendering and CT angiography important in particular cases of traumatic patients. In addition to above, author will also discuss TBI diagnosis in MRI applications which are newly applied to clinical practice like TDI, fMRI and analyse potential applications of these imaging modalities. Using a complex variety of MR sequences, we can provide data concerning both structural and pathophysiological derangements. Future developments with such imaging techniques could improve understanding of the pathophysiology of brain injury and provide data that improve management and prediction of functional outcome. In this presentation all type of brain injury and its imaging features will be presented. Goals and objectives - to understand the mechanisms of traumatic brain injury - to learn about CT and MR imaging findings in different traumatic lesions of the brain - to be familiar with advantages and disadvantages of different imaging techniques in traumatic brain injury Learning Objectives: 1. To review mechanisms of brain injury. 2. To present current imaging techniques for evaluation of brain injury. 3. To illustrate different types of traumatic intracranial lesions. Subarachnid hemorrhage (SAH) is a very common and life-threatining disease. It occurs most commonly secondary to trauma and intracranial vascular abnormalities. The early diagnosis is very important and imaging modalities have an important role. Non-contrast CT (NCCT) should be the first choice for imaging. It can provide the visualisation of hyperdense blood products in the cisterns and sulci. In cases of negative NCCT scan, MRI may be a choice, especially in patients in the subacute phase using FLAIR and SWI sequences. However, every case with non-traumatic SAH should be examined with digital substraction angiography (DSA) in order to exclude a vascular abnormality, particularly aneurysm. In this lecture both common and uncommon causes of SAH will be discussed and a multi-modality approach to the diagnosis will be reviewed. Learning Objectives: 1. To review the most common pathologies leading to SAH. 2. To present current imaging techniques for evaluation of SAH. 3. To describe the radiological findings of SAH. A-082 15:00 CT is primary imaging modality in patients with acute stroke. The early signs of brain infarction on non contrast CT are insular ribbon sign reflect cytotoxic edema and relates to specificity of of arterial anatomy.Disappearing basal ganglia sign is caused my MCA occlusion proximally to lenticulostriate artery. Early mass effect includes narrowing of Sylvian fissure or loss of cortical sulci. Hyperdense artery sign represent stasis of flow due to arterial thrombus and correlates positively with angiographic finding of occlusion. CTA is essential for evaluation of intra- and extracranial vessels and intravascular thrombi. Conventional MRI finding in acute stroke are hyperintense zones on T2 and FLAIR, mass effect, sulcal effacement, loss of arterial flow voids, and abnormal blooming and parenchymal black dots due to the hemorrhage on T2*GE and SWI. DWI with ADC maps is most sensitive for detection of hyperaute stroke at first 6 hours. In ischemic stroke, reduction of perfusion occurs, typically in an affected vascular territory. Regions with hypoperfusion are shown as decreased CBF, decreased CBV, prolonged MTT, and prolonged measures of contrast transit such as TTP, Tmax or DT. Since these parametric changes are detectable minutes after stroke onset, they are of great use for early diagnosis of ischemic stroke and to differentiate ischemic penumbra from infarct core. There are two perfusion approaches with good application in acute stroke, MR perfusion and CT perfusion. Compared the two methods, CT perfusion (CTP) has the advantage of rapidity and wide accessibility in emergency room together with CTA which may be used to guide thrombolytic treatment and may guide predictions of functional outcome and hemorrhagic complications. Learning Objectives: 1. To become familiar with the most common aetiologies of stroke. 2. To present current imaging techniques for evaluation of stroke. 3. To recognise the imaging signs of stroke. MRI of the lungs is increasingly used for a variety of reasons. In some diseases, it can be used as an escape from harmful radiation, such as in young or pregnant patients with suspected pulmonary embolism. This is being extended by short, focused protocols as a first line test in some centres. In other diseases, it is the "go to" modality; for instance, in patients with superior sulcus tumours or where difficult anatomical structures need to be evaluated before treatment decisions can be made. Lastly, airway imaging and evaluation of dynamics of breathing can be assessed using novel methods. This session will go into detail for the three areas described. Author Disclosure: E.J.R. van Beek: Advisory Board; Aidence BV. Equipment Support Recipient; Siemens Healthineers. Founder; QCTIS Ltd. Owner; QCTIS Ltd. Twenty-five% of patients suspected of PE may present with contraindication to iodinated CM which indicates a potential role for MR. Recent MR technical refinements have been substantial in this field with faster sequences, larger coverage, lung perfusion imaging and high-resolution pulmonary MR angiography (MRA). Basic sequences for PE include unenhanced SSFP and 3D GRE pulmonary MRA. Technically inadequate examinations are reported in 25-30%, mainly due to poor vascular opacification and artifacts. MR direct signs of acute PE are similar to those of CT, including partially occluding endoluminal filling defects and complete arterial obstruction showing a meniscus termination outlining the clot. Reported sensitivity and specificity of MRA in large series were around 80% and 95-100%, respectively. Sensitivity decreases from central to lobar level (close to 100%), segmental level (7090%) and subsegmental level (30%). Unenhanced MRA has 82% sensitivity and 90% specificity in the 50% interpretable examinations, showing a similar decrease of sensitivity from proximal to distal level. Perfusion also showed 75% sensitivity and 90% specificity in the 50% interpretable examinations. Similar to CT, MR can provide alternative diagnoses or ancillary findings A B C D E F G W altering the management of the patient. A comprehensive assessment of the venous thromboembolic disease may be achieved by the addition of a MR venous phase without further injection of Gadolinium CM. The sensitivity of the combined test may however be increased at the expense of a higher rate of technically inadequate examinations. It is expected that newer 3D MR angiography sequences will increase yield in the field of venous thromboembolism. Learning Objectives: 1. To learn about the various MR sequences for pulmonary arteries imaging. 2. To become familiar with the MR signs of pulmonary embolism. 3. To understand the current limitations of MR for PE diagnosis. The purpose of this presentation is to review the currently available MR techniques useful in thoracic oncology and to provide an overview of present and emerging clinical applications of oncologic thoracic MRI. Although many studies have advocated a valuable role for thoracic MRI, it has currently limited clinical utilization with the exception of cardiovascular imaging. However, new technical developments and MRI sequences have continuously improved the quality and broadened the clinical indications for thoracic MRI, especially in thoracic oncology. Furthermore, due to its high soft tissue contrast and the lack of radiation exposure, MRI allows for repeated measurements of the lung structures and, therefore, appears to be appropriate for functional investigation of lung. Learning Objectives: 1. To review the role of MR for assessing the T status. 2. To learn about MR diffusion sequence performance for N staging. 3. To review the persisting limitations. Due technical difficulties related to motions and susceptibility artifacts, MR imaging has long been considered out of the scope of routine application in the field of imaging of airways, except in a few expert centers. However, recent improve and simplification in MR acquisition techniques have enabled MRI to reach high resolution imaging for morphological evaluation of both large and small airways. In addition, acute and chronic airway diseases are largely misunderstood by far, so that the ability of MRI to combine both morphology and functional information in a single radiation-free examination will eventually make MRI a modality of choice for better understanding, improving patient care and long term follow up requiring iterative examinations. Finally, recent advances in treatment are also prone to make radiologist reconsider the role and place of imaging in chronic diseases (cystic fibrosis, idiopathic pulmonary fibrosis, etc) to assess sensitively and specifically response to treatment. Learning Objectives: 1. To review the role of MR for evaluating the large and small airways. 2. To learn about the current state-of-the-art MR sequences. 3. To learn about the current role of MR in cystic fibrosis. 14:00 - 15:30 E³ - ECR Academies: Update on Hepatobiliary Imaging Room M 5 The session is focused on the different aspects of diffuse liver disease. An update in non-invasive imaging will be offered in detail, pointing mainly to fat, iron, and fibrosis deposition and the accuracy of quantitative methods in disease grading and severity assessment. Non-alcoholic fatty liver disease is the most common cause of chronic liver disease in Western countries. US, CT and MRI are used to evaluate the disease, to assess severity, and quantify the amount of fat deposition. Despite advances in imaging techniques accurate measurements are still challenging, and new evolving methods are applied on US and MRI. MRI remains the gold standard and the method of choice, answering the clinically important questions. Congenital diffuse liver diseases comprise some rather uncommon conditions, while iron overload is related to a variety of congenital and hereditary conditions. Differential diagnosis is of outmost importance for patients’ management. MRI is the method of choice to evaluate and quantify iron overload provided that specific imaging protocols are used and the standardized techniques together with validated acquisitions are applied. Diagnosis and staging of liver fibrosis is one of the most challenging aspects of non-invasive imaging. Current application of US and MRI are nowadays able to provide accurate measurements based on US and MRI elasticity tools. “Virtual biopsy” refers to the possibility of imaging techniques to depict, map and measure fibrosis minimizing the need for liver biopsies in chronic diffuse liver diseases. MR allows an accurate determination of steatosis, iron overload and fibrosis, even if they coexist. A. Assessment and quantification of fat in NAFLD M. Ronot; Clichy/FR () The diagnosis of steatosis in patients with NAFLD is historically based on histological examination of a tissue specimen obtained by liver biopsy. However, liver biopsy has well-known limitations (invasiveness and sampling variability) and cannot be proposed for all patients, especially given the high prevalence of NAFLD worldwide. Several imaging techniques can be used for the non-invasive diagnosis and quantification of steatosis. Ultrasonography and computed tomography are useful for the detection of marked steatosis, but of limited use for precise quantification of mild to moderate fat deposition. MR proton spectroscopy (MRS) is the most accurate technique, but it is not feasible in routine use and is time consuming. Chemical shift sequences offer now an accurate alternative and have been shown to be very well correlated to MRS and liver biopsy. As a consequence, they are progressively accepted as a reference technique for detection and quantification of hepatic fat deposition. Recently, novel parameters, such as the controlled attenuation parameter (CAP), or the speed of sound estimation have been proposed and offer promising results. As for liver fibrosis, the diagnostic strategy should rely on the combination of several non-invasive techniques. Learning Objectives: 1. To be familiar with the pathogenesis of NAFLD. 2. To recognise current non-invasive imaging methods used to evaluate hepatic steatosis. 3. To realise the clinical applications, diagnostic accuracy and limitations of each method. A-089 14:33 B. Congenital diffuse liver diseases and iron overload M.M. França; Porto/PT () Congenital and inherited hepatic diseases, like congenital hepatic fibrosis, Wilson disease or hereditary hemochromatosis, are rare diffuse liver diseases that may progress to cirrhosis. Liver imaging, particularly magnetic resonance (MR) imaging, provides important information on diffuse parenchymal abnormalities, but may also reveal focal liver lesions. Iron overload is found in hereditary hemochromatosis, but also in transfusional hemosiderosis and iron loading anemias, and chronic liver diseases. Quantification of liver iron concentration by MR imaging is crucial for the diagnosis and treatment monitoring of iron overload diseases. MR quantification of liver iron can be performed with signal intensity ratio (SIR) methods or relaxometry techniques. Both R2 and R2* values are increasingly being used for quantification of liver iron concentration, but they must be performed with validated acquisition and analysis protocols. Hereditary hemochromatosis will be presented as an example of a clinical scenario, to emphasize the relevance of MR for detection and quantification of liver iron deposits and its role in patients’ management and treatment monitoring. Learning Objectives: 1. To recognise specific imaging findings in patients with congenital hepatic diseases such as Wilson's disease and congenital hepatic fibrosis. 2. To be able to determine iron content in liver by MRI. 3. To be able to differentiate common focal lesions found in storage disease of the liver. A-090 15:01 C. Diagnosis and staging of liver fibrosis L. Martí-Bonmatí; Valencia/ES () Chronic liver disease is a major public health problem with an increasing prevalence and an emergence clinical interest. Fat, inflammation and iron deposits induce an oxidative stress on the liver with synergistic effects in the progression of fibrosis and cirrhosis. In this sense, it is well known that around 7% of the adult population without known liver disease have liver fibrosis, mostly associated with NAFLD. The up-till-now gold standard biopsy is limited by sample size (≈1/50.000); sample quality; sampling variability errors (3040%); inter- and intraobserver variability (>30%); morbidity (1%); and not being A B C D E F G W A B C D E F G Johnson G.: A-353 Johnson K.J.: A-731 Johnson K.S.: B-1006 Jolles B.: B-1425 Jonczyk M.: B-0446 Joo I.: B-1524 Jordaan M.: B-0969 Jordan D.W.: B-0125, B-1017 Jorge C.L.: B-1400 Jørgensen S.H.: B-0556 Joseph J.: B-1094 Jost G.: B-0995 Jost L.: B-1534 Joudiou N.: B-0424 Jouve de Guibert P.-H.: B-0386 Jovicich J.: B-1033 JPND Working Group SRA-NED: B-1033 Juaneda M.: B-0992 Juárez-García M.S.: B-1551 Juhee K.: B-1052 Jukema J.W.: B-0335 Juluru K.: B-0705 Jung C.S.L.: B-0990 Jung E.-M.: B-0055, B-0207, B-0208 Jung S.C.: B-0693 Jung S.I.: B-0195 Jungmann P.M.: A-469 Jurgilewicz D.: B-0278 Juskanic D.: B-0924 Jussila A.-L.: B-0351 Jutte P.C.: B-1345 K Kaatee M.: B-0566, B-0571 Kabaalioglu A.: B-0433 Kabbasch C.: B-0511, B-0515, B-0927 Kabin Y.: B-0702 Kachelrieß M.: A-654, B-0542, B-0733, B-0736, B-1432, B-1434, B-1435, B-1437 Kacimi O.: B-0941 Kacso G.: B-0453 Kadir T.: B-0868 Kadivar S.: B-1221 Kadoya M.: B-1315 Kaelin A.: B-1001 Kafrouni M.: B-1057 Kahl G.G.: B-1309 Kahn J.: B-0292, B-0412, B-0894, B-0899, B-0961, B-1056 Kahn J.-E.: B-1654 Kahn T.: B-1564, B-1566 Kaireit T.: B-0235 Kaiser C.: SY 1d Kaissis G.: B-0900, B-0988 Kala P.: B-0260 Kalashnikova L.: B-0215 Kalcan S.: B-1324 Kaleci S.: B-0855 Kalender W.A.: A-146, A-230 Kalesnik A.: B-0406 Kalkan A.: B-0511 Kallemose T.: B-0747 Kallenbach K.: B-1105 Kallur K.: B-0270 Kalovidouri A.M.: B-0466, B-0499 Kaltenbach B.: B-0258, B-1054, B-1091 Kamalasanan A.: B-1182 Kamble A.: B-1282 Kamble A.N.: B-0100, B-1282 Kaminaga S.: B-0403, B-1581 Kamis M.F.A.K.: B-0105 Kamo M.: B-1472 Kamolov B.: B-1561 Kämpgen B.: B-1582, B-1583 Kanavaki A.: B-0430 Kandiloglu A.R.: B-1291 Kandolf R.: B-0979 Kang B.C.: B-0062 Kang E.-Y.: B-0241, B-0639, B-1132 Kang H.: B-0089 A B C D E F G A B C D E F G A B C D E F G C D E F G C D E F G C D E F G Ostojic J.: B-1673 O'Sullivan G.J.: B-0828 Ota H.: B-1306 Otaduy M.C.G.: B-1400 Otani K.: B-0752, B-1049, B-1454 Othman A.E.: B-0791 Otto G.: B-0210 Oudard S.: B-0476 Oudkerk M.: B-0566, B-0571, B-0757, B-0825, B-1109, B-1152, B-1155, B-1458 Overbosch J.: B-1345 Owczarczyk K.: B-1080 Owens C.: A-609, A-954 Oyar O.: B-1429 Oyen R.: B-0362 Oyen R.H.: A-832 Ozalp Ates F.S.: B-1618 Özbek S.S.: A-026 Ozcelik C.: B-0052 Özdemir H.O.: B-0769 Özdemir M.: B-0733 Ozdemir O.: B-1324 Özenirler S.: B-0205 Ozer T.: B-0722 Ozgen Mocan B.: A-168 Ozhan Oktar S.: B-0205 Özmen M.N.: A-834 Oztuna D.: B-0952 Ozturk M.: B-0674, B-1505 Ozturk M.H.: B-0305 P Paalimäki-Paakki K.: B-1310, B-1452 Pacciardi F.: B-1320 Pacella C.M.: B-1545 Pacella G.: B-0627, B-0820 Pacifici S.: B-0136 Pacile S.: B-1416 Padberg F.: A-828 Padhani A.R.: A-197, A-316, B-0244, B-1361, SY 1b Padoy N.: B-0119 Paech D.: B-0363, B-0933, B-0934 Pagan E.: B-1377 Paganelli G.A.: B-1545 Pages M.: B-1520 Pagniez J.: B-1654 Pagonidis K.: A-599 Pahn G.: B-0544, B-0983 Paiman E.H.M.: B-0335 Paiusco M.: B-0773 Paladini A.: B-0861 Palao Errando J.: B-0101, B-1394 Palczewski P.: B-0882 Palfrey R.M.: B-0746, B-0751 Palkhi E.Y.A.: B-0908 Palkó A.: A-241 Pallas R.J.: B-0714 Pallisa E.: B-1551 Palmer Sancho J.: B-0116 Palmisano A.: B-0782, B-0847 Palmucci S.: B-0045, B-0049, B-0420, B-0873 Palumbo P.: B-0300, B-0729, B-1344, B-1539 Pameijer F.A.: A-313 Pamminger M.: B-0572 Panagiotopoulos N.: B-0793 Pancewicz S.: B-0278 Panebianco V.: B-0244, B-1068, B-1547 Panes J.: B-1537 Panfili M.: B-0348 Pang H.: B-1482, B-1483 Panizza P.: B-1390, B-1440, B-1441 Pankowska A.: B-0553 Panopoulou E.: B-1662 Panourgias E.: B-0468 Panov V.: B-1248, B-1369, B-1561 Pansini V.M.: B-1122 Panteleakou E.: B-0430 Panvini N.: B-0357, B-0358 Panyaping T.: B-1199 Qanadli S.D.: A-070 Qechchar Z.: B-0941 Qi R.: B-0147 Qian T.-Y.: B-0364, B-1261 Qu J.: B-0353, B-0810 Quaia E.: B-1532 Quan X.: B-0233 Quarchioni S.: B-0300, B-0612, B-0725, B-0729, B-0960, B-1344, B-1427, B-1539 Quäschling U.: B-0359 Quentin M.: B-0252, B-1363, B-1364 Quere J.-B.: B-0301 Querques G.: B-1513 Quick H.H.: B-0796 Quilez A.: B-0915 Quiney H.: B-1416 Quinn E.: B-0344 Quiros-Gonzales I.: B-1094 Quitzke A.: B-1327 Qureshi A.: B-1080 Q R Ra J.C.: B-1265 Raabe P.: B-0007 Raafat T.: B-1503 Rabelink T.: B-0204 Rabenalt R.: B-0248, B-0252, B-1363, B-1364 Racine D.: B-1135 Raciti M.V.: B-1336 Radbruch A.: B-0363, B-0933, SY 9 Raddatz J.: B-0544 Radder A.: SY 5 Rademacher J.: B-0051 Radhakrishnan S.: B-1500 Radicci V.: B-0549 Radovanovic Z.: B-1632 Radu P.: B-0453 Radzina M.: B-0814, B-1622 Rafaelsen S.R.: B-1660 Raffaelli C.-P.: B-1027, B-1043 Raftopoulos C.: B-0438 Ragab Y.: B-0470, B-0950 Ragot E.: B-0293 Rahmat K.: B-0084, B-0105, B-0617 Rai B.: B-1270 Raimann A.: B-0345 Raimondi E.: B-0209, B-0588, B-1083, B-1202 Raimondi S.: B-0382 Rainford L.: B-1148 Rainford L.A.: A-142, A-391, A-552, A-661, B-0554, B-1300, B-1646 Raininko R.: B-1401 Raissaki M.: A-141, A-192, A-658, B-0771 Raja A.Y.: B-0731 Raja S.: B-0982, B-1476 Rajan S.: B-1397 Rajani H.: B-1373 Rajgopalan N.: B-0261 Ralla B.: B-0061 Ramalho L.: B-0269 Ramirez Girlando J.C.: B-0881 Ramli Hamid M.T.: B-0105 Ramli N.: B-0091, B-0617, B-1597 Rammelsberg P.: B-0264 Ramo E.: B-1219 Ramos Botelho Antunes P.: B-0391 Ramos I.M.: B-0137, B-1314 Rampoldi A.: B-0128 Ramsden W.: A-462 Rana A.: B-1509 Rance B.: B-0476 Rancoita P.M.: B-0847 Rangari A.: B-1601 Ranieri A.: B-1545 Ranjan R.: B-1675 Ranschaert E.R.: A-363 Rao L.: B-1097, B-1098, B-1103, B-1104 Rozalli F.I.: B-0617 Rozhkova Z.: B-1236 Rubbert C.: B-0252, B-1037, B-1235, B-1237 Rübenthaler J.: B-0055, B-0057 Rubin C.: A-461 Rubini A.: B-0221, B-0668, B-1633 Rubins A.: B-1622 Rubins S.: B-1622 Rubtsov R.: B-0402 Rudas G.: B-0659, B-1680 Rudel A.: B-1025 Ruder T.: A-839 Rudolph M.: B-1357 Rudolph T.: B-0976 Rudolph V.: B-0976 Rueppel S.: B-0973, B-0974 Ruff C.: B-0764 Ruffion A.: B-0245, B-1074 Rühaak J.: B-0238 Ruhlmann V.: B-0652 Ruhnke H.: B-0023 Ruibal A.: B-0501, B-0992, B-1395 Ruiter S.J.S.: B-0825 Ruiz Salmeron R.: B-0145 Rukhlenko M.: B-1003 Rummeny E.J.: B-0149, B-0529, B-0543, B-0900, B-0988, B-1120, B-1121, B-1136 Runge V.: A-139, SY 9 Rupreht M.: B-0864 Rusandu A.: B-1297 Ruschi F.: B-0298 Ruschke S.: B-0441 Russo A.: B-1071 Russo F.: B-0378, B-0383, B-1064, B-1244, B-1246, B-1592 Russo G.: B-0049, B-0295, B-0420, B-0873 Ryan A.G.: A-587 Ryan D.: B-0574 Ryan J.: B-0176 Rybczinsky M.: B-0022 Rychina I.: B-1557 Rychkova I.: B-1335 Rymaszewska J.: B-0920 Ryu H.: B-0005, B-0575 S Sá dos Reis C.: B-0130, B-1146 Saal L.H.: B-1006 Saar S.: B-0296 Saba L.: B-0216, B-0374, B-0608, B-0611, B-0840 Sabate Rotes A.: B-0769 Sabatino V.: B-0077 Sabet H.A.S.: B-0473 Sabet S.: B-0379, B-0581 Sabetrasekh P.: B-0212, B-0998 Sabino S.: B-0138 Sachs C.: B-1665 Sack I.: B-0001 Sadat U.: B-0219 Saddekni S.: B-0034, B-1055 Sade R.: B-0712 Sadik J.-C.: B-0514 Saeedi-Moghadam M.: B-1668, B-1669 Safa G.: B-1429 Safina M.: B-1292, B-1614, B-1630 Sah B.-R.: B-0708 Sahakyan D.: B-1548 Sahan M.H.: B-0954 Sahani D.V.: B-0016 Sahbee P.: B-0569 sahin G.: B-0952, B-1618 Sahm F.: B-0933 Saidon T.: B-0705 Sakahara H.: B-0028, B-0720 Sakai M.: B-0416 Sakuma H.: B-0350 Sala E.: A-352, A-575, A-751, A-865 Salamon J.: B-0932 Salapura V.: A-689 Salem A.: B-1138 Salem J.: B-1473 Salemi I.: B-0897 Salerno S.: B-1165, B-1495 Salgado R.: A-195, A-484, A-875 Sali L.: B-0521 Salman S.: B-1045 Salminen P.: B-0744 Salomon G.: B-1569 Saltybaeva N.: A-506, B-0123, B-0310 Saltz L.: B-0167 Salvatore M.: B-1533 Salvesen Ø.: B-1368 Salvioni M.: B-0230, B-0629, B-1205 Salvioni R.: B-0625 Salvo V.: B-1068 Samara E.: A-923 Samei E.: A-785 Sammartano K.: B-1032 Sampangi S.: B-0270 Samreen N.: B-0504 Sanaat A.: B-0740 Sánchez Mateos D.: B-0006 Sanchez J.: B-1610 Sanchez Martinez A.L.: B-1551 Sánchez N.: B-0494 Sánchez Nava D.A.: B-0397 Sanchez S.: B-1520 Sanchez-Montanez Garcia-Carpintero A.: B-0769 Sanchez-Salas R.: A-396 Sanders S.N.: B-0748 Sanderud A.: B-0742, B-0748 Sandford Z.: B-0868 Sanghavi P.S.: B-0872 Sangma S.: B-1334 Sani F.: B-0855 Sanje S.: B-1450 Sankaranarayanan S.: B-1500 Sansone M.: B-1190 Santalco A.: B-0024 Santiago I.: A-382 Santini V.: B-0821 Santoro A.: B-1009, B-1625 Santos A.L.: B-1275 Santos J.: A-495, B-0326, B-0328, B-0557, K-07 Santos J.M.M.M.: B-0902 Santos R.A.M.: B-0964, B-0966, B-0967, B-1313 Santucci D.: B-0627, B-0632, B-0820 Sanz-Rodrigo E.: B-1465 Sapena V.: B-0610 Šaponjski D.: B-1527 Sarabhai T.: B-1367, B-1371 Sarah P.: B-0856 Saranga B.K.: B-1516 Sardanelli F.: A-554, A-931, B-0029, B-0332, B-0503, B-0786, B-1093, B-1651 Sarin D.: B-0673 Sartor H.: B-1006 Sartoris R.: B-0427 Sasaki M.: B-0720 Sasiadek M.: A-302, B-0920, B-1679 Sastoque.g. J.M.: B-0823 Sato M.: B-0451 Sato Y.: B-1550 Satta S.: B-1493, B-1494 Sauer M.: B-1569 Saukko E.: B-0342, B-0744, B-1442, B-1447 Saunavaara J.: B-0342 Sauppe S.: B-1432, B-1434 Saut O.: B-0698 Sauter A.: B-1121, B-1136 Sauter A.W.: B-1381 Savaş R.: B-1219 Savatovsky J.: B-0514 Savlovskis J.: B-0814 Sawall S.: B-0733, B-0736, B-1435 Sawicki L.M.: B-0584, B-0652, B-0706 Sayıt A.T.: B-0256 Sbarra M.: B-0471 Scaglione M.: A-120, B-0295 Škrk D.: B-0745 Skrypets T.: B-0703 Slater J.: B-0492, B-0667 Slowinski T.: B-0055 Smedby Ö.: B-0096 Smeets D.: B-1489 Smeets P.: B-0540 Smidt M.: B-0274, B-1409 Smiechowicz J.M.: B-0160 Smirnova A.V.: B-1003, B-1220 Smirnova E.: B-0406 Smit E.: B-0356 Smit E.J.: B-0695 Smit L.: B-1213 Smith A.: B-0602 Smith J.T.: B-0844 Smith R.A.: B-0685 Smith-Bindman R.: B-1010 Smithuis F.: A-255 Smits M.: A-764, A-910, B-1039 Smyth A.E.: B-0070 Snaith B.: B-0969 Snene F.: B-0531, B-0949 Snoeckx A.: B-0181, B-1558 Soares F.A.P.: B-0748 Soares L.: B-1638 Sobral D.M.: B-1645 Sofia C.: B-1167 Sofikitis N.: B-1662 Sohn J.S.: B-0718 Sokhi H.K.: B-1361 Sokolowski F.C.: B-0777 Solanki R.K.N.: B-0904 Solbiati L.: B-0452, B-1209 Solbiati M.: B-1209 Sollid B.: B-0140 Sommer G.: B-1381 Sommer W.H.: B-0088, B-0513, B-0517, B-0922, B-1076, B-1582, B-1583 Son E.J.: B-0102 Son Forget J.: B-0996 Son J.-Y.: B-1524 Sonck J.: B-1459 Song B.: B-0199, B-1266 Song C.: B-0074 Song D.E.: B-1191 Song J.: B-1171 Song L.: B-0781 Song Y.: B-1238, B-1279 Soni S.: B-0951 Soo S.W.: B-0084 Sood S.: B-1022 Soong S.I.: B-1370 Sorantin E.: A-046 Sorbo A.: B-0295 Sørensen J.S.: B-0435 Soria J.-C.: B-0368 Soricelli A.: B-1533 Sorochan O.: B-1499 Soroush H.: B-0998 Sosna J.: A-820, B-0457 Souchon R.: B-0245, B-1074 Soultatos A.: B-0430 Sousa A.F.C.: B-0557 Sousa Neto J.A.: B-0269 Sousa P.: B-1445 Souto S.: B-1640 Souza Guatelli C.: B-1285 Souza J.A.: B-1285 Soyer P.: B-0448 Spadarella G.: B-1189 Spadavecchia C.: B-0127, B-1129 Spallanzani A.: B-0855 Spanakis K.: B-0771 Spångeus A.: B-1589 Sparano A.: B-0295 Spatafora L.: B-1292, B-1630 Späth L.: B-0932 Specchio N.: B-1404 Spencer N.: B-0969 Spiliopoulos S.C.: A-590, B-0865 Struthers A.D.: B-0214, B-0562 Studzinski J.: A-776 Stumpp P.: B-1564, B-1566 Sturm T.: B-0234 Su K.-H.: B-1017 Su T.: B-0496 Su Y.: B-0004 Su Y.-Y.: B-0194 Subbanna I.: B-1058 Subbotin Y.: B-1247 Subramanian P.: B-1079 Sudarkina A.: B-0641, B-1576 Sudarshan T.A.: B-1182 Sudarski S.: B-0459 Sudhakar K.: B-1675 Südmeyer M.: B-1235, B-1237 Sudoł-Szopińska I.: A-032 Suehiro E.: B-0767 Suetens P.: A-981 Sugawara H.: B-1048 Sugihara N.: B-0043 Sugiyama M.: B-0028 Suhai F.I.: B-0150, B-1657 Suhling H.: B-0235 Sulkowska K.: B-0882 Sullivan C.J.: B-0443 Suman S.: B-0054 Summers P.: B-1000 Summers R.M.: B-1587 Summersgill J.: B-0214, B-0562 Sun C.: B-1593, B-1596 Sun C.C.: B-1535 Sun D.-P.: B-0194 Sun J.: B-0387 Sun K.: B-0774 Sun R.: B-0737 Sun Y.: B-0635, B-0800, B-1021, B-1596 Sun Z.-Y.: B-0364, B-1259, B-1261 Sung C.-M.: B-0534 Sung D.J.: B-0854 Sung J.S.: B-1409 Suntharalingam S.: B-0450, B-1138 Suo X.: B-0662 Suponeva N.: B-1407 Suranyi P.: B-1046, B-1047 Suren C.: B-1120 Surov A.: B-0359 Sutter R.: A-415, B-1430 Sutto M.: B-0128 Suutari H.: B-1452 Suzuki S.: B-0324, B-1048 Suzuki T.: B-1258, B-1315 Svahn T.M.: B-0640 Svedström E.: B-1447 Svensson A.: A-851 Svensson S.F.: B-1137 Sverzellati N.: A-880, B-0045, B-0333, B-0787, B-1349 Swami V.: B-0947 Swamy S.S.: B-1058 Swart L.E.: B-1649 Sweeney J.A.: B-0656 Swoboda B.: B-0621 Syrgiamiotis V.: A-223 Syväri J.: B-0441 Szabo A.G.: B-0659, B-1680 Szabó L.: B-1657 Szatmari P.: B-0129, B-0183 Szczepura K.: B-1303, B-1444 Szczerbo-Trojanowska M.: A-474 Szczesniak D.: B-0920 Szemplinska B.: B-1106 Szeszkowski W.: B-0882, B-1106 Szikora I.: Szilveszter B.: B-0150, B-0754, B-0761, B-1655 Szuba A.: B-0920 T U Uberoi R.: A-240, A-589 Ublinskiy M.: B-0156, B-0806 Uchida M.: B-0272, B-1116 Uchigashima T.: B-0416 Uchio E.: B-0361 Uder M.: B-0621, B-0901, B-1260, B-1629 Udeshi U.: B-1359 Udodov V.: B-0728 Udwadia Z.: B-0872 Uhlig J.: B-0563 Ujlaki M.: B-0605 Ukkola L.: B-0351 Ulaner G.A.: B-0705 Ullrich T.: B-0248, B-0252, B-1363, B-1364 Uluc M.E.: B-1429 Ulus S.: B-0763 Umathum R.: B-0934 Umutlu L.: B-0355, B-0584, B-0652, B-0706, B-0796, B-1367, B-1371, B-1534, B-1621, SY 1a Ünal N.G.: B-1538 Unlu Y.: B-1418 Unno N.: B-0028 Upponi S.: B-0970 Uprimny C.: B-1570 Uras C.: B-1293 Urbani L.: B-1320 Us R.: B-1448 Usanov M.S.: B-1591 Useche N.: B-0694 Ushinsky A.: B-0361 Usman A.: B-0219 Usta E.B.: B-0661 Uzun C.: B-0098 V Vacirca F.: B-0444 Vacondio R.: B-0083 Vael R.: B-0290 Vafaee H.: B-1669 Vafiadis I.: B-0430 Vágó H.: B-1657 Vahldiek J.L.: B-1340 Vaiani M.: B-0625 Vaidya S.: A-121 Vaidyanathan S.: B-0593, B-0908 Valbusa G.: B-0479, B-0481 Valdés Solís P.: A-464 Valdora F.: B-1613 Válek V.: A-438 Valenti M.: B-0410 Valentini A.L.L.: B-0471 van Tulder G.: B-0485 van Urk J.: B-0917 van Zwam W.: A-914, B-0512, B-1008 Vanacker P.: B-0858 Vancheri A.: B-0873 Vancheri C.: B-0049, B-0420, B-0873 Vancoillie L.: B-0682 Vande Berg B.: A-030, B-0438 Vande Vyvere T.: B-1594 Vandecaveye V.: B-0362, B-1075 Vandemeulebroucke J.: B-1050 Vandereyken F.: B-0290 Vandermosten M.: B-1489 Vane M.L.G.: B-0274 Vanhoenacker F.M.H.M.: A-840, A-961 Vani V.: B-0519, B-0520, B-0522 Vaño E.: A-502 van't Sant-Jansen I.: B-1085, B-1376 Vanzulli A.: B-0008 Vardhanabhuti V.: B-0075, B-0603 Vargas H.A.: B-0254 Vargas M.I.: B-0466 Varga-Szemes A.: B-0569, B-0752, B-0776, B-1046, B-1047, B-1232, B-1454, B-1455 Varona Porres D.: B-1551 Varoquaux D.-A.: A-543 Varotto A.: B-1486, B-1492 Varrassi M.: B-1539 Vas D.: B-1537 Vasco Aragão M.D.F.: K-19 Vasilevska Nikodinovska V.: B-0535 Vassallo L.: B-0107, B-1114, B-1592 Vassileva J.N.: A-420 Vassiou K.: B-0304 Vaz Touret M.A.: B-0331 Vazhenin A.: B-1497 Vázquez Caruncho M.: B-0501 Vázquez E.: A-338 Vazquez Mendez E.: B-0769 Vecsey-Nagy M.: B-0150 Vedovo F.: B-1664 Vedsted P.: B-1660 Veeramuthu V.: B-1597 Vega de Andrea N.I.: A-789 Vegar-Zubovic S.: B-1163 Vegt E.: B-0893, B-1274 Veillon F.: B-0067, B-0069, B-0257 Veiss A.: B-0814 Veit-Haibach P.: B-0708 Velasco S.: B-0694 Veldhoen S.: B-0022 Veliou K.: B-1118 Velthuis B.K.: B-0785, B-1656, K-17 Veltman J.: B-1277 Veltri A.: B-0185 Venancio J.: K-27 Venkatasamy A.: B-0067, B-0069, B-0257 Venkatesh S.K.: A-807 Venkatraghavan V.: B-0794 Vento Torres M.: B-1162 Ventrella E.: B-0144 Ventura E.: B-1001 Ventura L.: B-0521 Ventura S.R.: B-0137 Venturini E.: B-1390, B-1440, B-1441 Venturini M.: B-0230, B-0626, B-0629, B-1205 Venugopal V.: B-0872 Verardo I.: B-0837 Verbeken E.: B-1574 Verbist B.: A-594 Verdonschot N.: B-0957 Vergesslich Rothschild K.A.: B-0155 Verhoef G.: B-0362 Verkaik N.J.: B-1649 Verma A.: B-0270 Verma M.: B-1022 Verna S.: B-0056 Verna V.: B-0263 Vernhet Kovacsik H.: B-1133 Vernooij M.W.: B-0118, B-0794, B-0795, B-0797, B-1038, B-1039, B-1678 W Waade G.G.: B-0132, B-0133, B-0134 Wachabauer D.: B-0317 Wacker F.: B-0051, B-0235, B-0237 Wagner M.: B-0273, B-0426 Wagner P.M.: B-0777 Wagner R.: B-1222 Wagner W.: B-0240 Wakayama T.: B-0028 Waldt S.: A-291 Walecki J.: A-080 Walker C.: B-0970 Wallis M.G.: A-635, B-0275, B-1094 Walsh C.: B-0972 Walsh D.: A-697 Walter S.: B-0791, B-0909 Walter W.R.: B-0538 Walton L.A.: B-1303 Waltrich N.K.: B-1435 Wang C.: B-0502, B-1175, B-1178 Wang C.-K.: B-0619 Wang D.: B-0848, B-1271, B-1276, B-1323, B-1480 Wang F.: B-0063, B-0658, B-1280 Wang G.: B-0279 Wang H.: B-0472, B-0878, B-1663 Wang J.: B-0171 Wang K.: B-0600 Wang K.Y.: B-0277 Wang L.: B-0442, B-0889, B-0986, B-1018, B-1276, B-1485 Wang L.-J.: B-0297, B-1250 Wang M.: B-0390 Wang M.-L.: B-1034, B-1599 Wang R.: B-0463 Wang S.: B-0171, B-0360, B-1257, B-1593, B-1596 Wang W.: B-0475, B-0497, B-0935, B-1084, B-1211, B-1479, B-1490, B-1496, B-1526 Wang W.T.: B-1256 Wang X.: B-0404, B-1593 Wang X.-Y.: A-950 Wang Y.: B-0389, B-0467, B-0800, B-1010, B-1298, B-1323 Wang Z.: B-0781, B-0879, B-1193, B-1417, B-1596 Wareing A.: A-930 Warier P.: B-0872, B-1378, B-1379 Warnking J.: B-1676 Warntjes J.B.: B-0096 Waryn M.-J.: B-0313 Washizuka F.: B-0962 Wassef S.: B-1331 Wasser M.: B-0011 Watanabe A.: B-1283 Watanabe H.: B-0451 Watson Y.: B-0165 Wattjes M.P.: A-210 Watts C.: B-1672 Wawrzyniak P.: B-1107 Weber M.: B-0079, B-0155, B-0506, B-0620, B-1168, B-1486 Weber M.-A.: A-370, A-417, A-894, B-0437 Weber T.F.: B-0014 Weber W.: B-0705 Weckbach S.: A-200 Weder W.: B-1355 Wegner F.: B-0793 Weidekamm C.: A-871, A-873, K-20 Weigel U.: A-320 Weikert T.: B-0482, B-1381 Weinheimer O.: B-0240, B-0402, B-0413, B-0871, B-1549, B-1588 Weinmann A.: B-0196 Weinrich J.M.: B-0025, B-0780 Weinstein S.: B-1632 Weir A.: B-0177, B-0670, B-0671 Weir-McCall J.: B-0214, B-0562 Weiser M.: B-0167 Weishaupt D.: A-450, A-879 Weiß C.: B-0243 Weiß J.: B-1208 Weiss K.: B-0727, B-0790, B-0976 Well L.: B-0932 Wells J.: B-1126 Welte T.: B-0051 Wen J.: B-0094, B-0799, B-0807, B-0938 Weng Q.: B-1171 Wengert G.J.: B-0506, B-0507, B-1281 Wenkel E.: B-1629 Wenz H.: B-1582 Wenzel F.: B-1678 Werlen S.: B-0303, B-0539 Werner Reyes M.F.: B-0827 Westbrook C.: B-1144 Westenend P.J.: B-0913 Westerlaan H.E.: B-0907 Weston M.: A-813 Westphalen A.C.: B-0879 Wetscherek A.: B-0405 Wetter A.: B-0450, B-0836, B-1138, B-1367, B-1371 Whitby E.H.: B-0987 Whittle C.: B-0494, B-0667 Wibmer A.G.: B-0254 Wichmann J.L.: B-0258, B-0289, B-0346, B-0439, B-0460, B-0753, B-1026, B-1052, B-1515 Wick M.C.: B-1341 Widya R.L.: B-0330, B-0335 Wiech D.: B-0373 Wielema M.: B-1109 Wielpütz M.O.: A-008, A-608, B-0240, B-0413, B-1588 Wieners G.: B-1056 Wiesinger B.: B-0918 Wiesmüller M.: B-0901 Wiestler B.: B-0088 Wietek B.: B-0918 Wiggermann P.: B-0207 Wildberger J.E.: A-256, A-725, B-0220, B-0222, B-1051, B-1409, B-1410 Wilkinson L.S.: B-0680 Wille M.M.W.: B-0870 Willemink M.J.: B-0026 Williams D.: B-0857 Williams M.: A-258, B-0097 Williams T.M.: B-1079 Willwacher S.: B-0727 Wilman H.R.: B-0002 Wilson D.J.: A-135 Windfuhr-Blum M.: B-0081 Windhager R.: B-1428 Windschuh J.: B-0933 Winfield J.: B-1080 Winklhofer S.: B-1031 Winter-Warnars G.: B-0917 Winzler S.: B-1069 Wirtanen M.: B-1442 Wirth S.: A-003, A-836 Wit E.: B-1565 Wohlfahrt P.: A-885 Woie K.: B-1368 Woisetschlager M.: B-1589 Woitek R.: B-0104, B-0498 Woitek R.A.: B-0079, B-1094 Wojtkiewicz G.R.: B-1175, B-1178 Wolf N.: A-336 Wolter P.: B-0362 Wolterink J.M.: B-0568 Wolters van der Weij E.: A-660 Won S.Y.: B-1563 Wong E.M.F.: B-1370 Wong H.Y.F.: B-0193 Wong J.H.D.: B-0091, B-1597 Wong M.C.Y.: B-0580 Wong Y.-C.: B-0297 Woo K.: B-1424 Woo O.H.: B-1415 Woo S.: B-0649 Wörtler K.: A-485, B-0529, B-1120 Woznitza N.H.: A-788 Wressnegger A.: B-0633 Wright C.L.: B-0888, B-1218 Wu B.: B-0432, B-0781, B-0849 Wu C.-H.: B-0297 Wu F.: B-0811 Wu F.-Z.: B-1352 Wu G.: B-0063 Wu H.-K.: B-1607 Wu H.-M.: B-1099 Wu J.: B-1483 Wu K.: B-0573 Wu K.-H.: B-0534 WU L.: B-1158 Wu M.-H.: B-1590 Wu R.: B-0792, B-1158 Wu V.: B-1533 Wu W.C.V.: B-0217 Wu W.-P.: B-1607 Wu X.: B-0417 Wu Y.: B-1279, B-1483 Wurnig M.: B-0273 Wüst W.: B-0901 Wyttenbach R.: B-0482 X Xi Y.: B-0071, B-1126 Xia C.: B-1648 Xia Y.: B-0390 Xiao Y.: B-0073, B-0656, B-0657 Xie L.: B-0339, B-0389 Xie Q.: B-0878, B-1483 Xing W.: B-0387 Xing Z.: B-0989 Xiong F.: B-1171 Xiong Y.: B-1110, B-1111 Xu G.: B-0421, B-1572 Xu H.: B-0431, B-1153, B-1154, B-1593 Xu H.M.: B-0686 Xu H.-Y.: B-0338 Xu J.: B-0800 Xu J.-M.: B-1560 Xu J.-R.: B-1158 Xu K.: B-0658, B-1475 Xu L.: B-1180 Xu R.: B-1153 Xu W.: B-0938, B-1617 Xu X.-M.: B-1185 Xu X.R.: B-0989 Xue H.: B-0792, B-1181, B-1264 Xue H.-D.: A-948, B-0364, B-1259, B-1261 Xue Y.: B-0223 Xuesong D.: B-0937 Y Yadav A.: B-1362 Yadav M.: B-1334 Yadav T.: B-1334 Yagami K.: B-0324 Yaguchi A.: B-0403 Yamada A.: B-1315 Yamada K.: B-1081 Yamada T.: B-0720 Yamaguchi T.: B-1306 Yamamoto Y.: B-1048 Yamamura J.: B-1317, B-1319 Yamanouchi S.: B-0451 Yamauchi F.I.: B-0877 Yamazaki A.: B-0350 Yan F.-H.: A-947 Yan H.: B-0713 Yan Z.: B-0657 Yang D.H.: B-0337 Yang F.: B-0654 Yang H.: B-1403 Yang H.-C.: B-1099 Yang H.K.: B-1524 Yang J.: B-0570 Yang L.: B-0709, B-0756, B-0759, B-0849, B-1256, B-1318 Yang Q.: B-0004, B-0811 Yang S.: B-0999, B-1323 Yang X.: B-1079, B-1171, B-1172 Yang Y.: B-0689 Yang Z.: B-0339, B-0735, B-0783, B-0788, B-1097, B-1098, B-1100, B-1103, B-1104, B-1153, B-1154, B-1230 Yang Z.-G.: B-0338 Yankaskas B.: B-0685 Yao J.: B-1587 Yao L.: B-0656 Yao Z.: B-1482, B-1483 Yardimci A.H.: B-1206 Yazdani N.: B-1215 Yazicioglu Y.: B-1036 Ye Q.-H.: B-1256 Ye Z.: B-0170, B-1280 Yeh B.M.: B-1021 Yel I.: B-0258 Yeung M.W.R.: B-1370 Yildirim Donmez F.: B-1004 Yılmaz Ö.: B-1330 Yilmaz P.: B-0797 Yilmaz R.: B-0582 Yim J.-H.: B-0197 Yim Y.: B-0693 Yin B.: B-1593, B-1596 Yin X.: B-0279 Yin Z.: B-0658 Ying T.-C.M.: B-0217, B-1214 Yip S.P.: B-0217 Yiqun S.: B-0163 Yokoo P.: B-0283 Yokoyama K.: B-1081 Yoneda N.: B-0198 Yoneda T.: B-0738 Yoon C.J.: B-0032 Yoon D.Y.: B-0724 Yoon J.-H.: B-1321 Yoon K.-H.: B-0005 Yoon S.H.: B-0044 Yoon S.J.: B-0672 York H.: B-1147, B-1643 Yoshida K.: B-1472 Yoshida M.: B-0106 Yoshikawa T.: B-0043, B-0403, B-0767, B-1348, B-1573, B-1578, B-1579, B-1581 Yoshinaga S.: B-0738 Yoshioka K.: B-1457 You H.: B-0810, B-1002 Young K.: B-1083 Young L.K.: B-1585 Younis A.: B-1503 Yousry T.A.: A-561, A-761, B-1039 Youssef A.: B-1503 Yperzeele L.: B-0858 Ytre-Hauge S.: B-1368 Yu M.H.: B-0195 Yu M.L.: B-0193 Yu Q.: B-0233 Yu S.: B-0792 Yu T.: B-0004 Yu Y.: B-1482 Yu Z.: B-0428 Yuan B.: B-0456 Yuan C.: B-0217 Yuan H.: B-0075, B-0686 Yuan Q.Q.: B-0636 Yüceege M.: B-0495 Yucel C.: B-0205 Yue Y.: B-0454, B-0464 Yuekao L.: B-0418 Yui M.: B-1348, B-1573, B-1578, B-1579, B-1581 Yun G.: B-0020, B-0032, B-0664 Yusuf G.T.: SY 11 Yveborg M.: B-1438 Z Zabitova M.: B-1677 Zaccagna F.: B-1672 Zacharzewska-Gondek A.: B-1679 Zackrisson S.: A-175, A-325, B-1006, B-1628, SY 1b Zafeiropoulou K.: B-0468 Zagdanski A.M.: B-0422 Zahirifard S.: B-0500 Zaiss M.: B-0363, B-0933 Zajkowska J.: B-0278 Zajkowska O.: B-0278 Zakharova N.: B-0086 Zambon P.: B-0549 Zamboni G.: A-674, B-0018, B-0166, B-0834, B-1065, B-1519, B-1521, B-1522, B-1523 Zamyshevskaya M.: B-0728 Zanardi S.: B-0038 Zanca F.: B-0314, B-0316, B-0318 Zanconati F.: B-0678, B-1416, B-1439 Zanelli E.: B-0046 Zanetti I.: B-1492 Zanetti M.: A-134, A-511 Zangos S.: B-0030 Zanirato M.: B-0017, B-0978 Zanirato Rambaldi G.: B-0407, B-0579 Zannoni S.: B-1189 Zanotel M.: B-1294 Zaottini F.: B-0615, B-0616 Zapf A.: B-0189 Zappa M.: B-0521, B-1528 Zarb F.: A-140 Zare Mehrjardi M.: B-0599 Zarea A.: B-0592 Zarei F.: B-1668 Zarqane H.: B-1133 Zatońska K.: B-0920 Zavadovskaia V.: B-0728 Zawadzki R.: B-0278 Zdesar U.: B-1443 Zech C.J.: A-095 Zeilinger M.: A-425, A-427 Zeinali B.: B-1668, B-1669 Zekry W.: B-1503 Zeltzer G.: B-0268 Zeng M.: B-1318 Zeng M.-S.: B-1256, B-1270 Zeng Q.: B-0417 Zenouzi R.: B-1317 Zerunian M.: B-0162, B-0164, B-0169 Zeynalova A.: B-0687 Zghaib T.: B-1656 Zhai X.: B-0638 Zhan S.: B-0999 Zhang C.: B-0811, B-0848, B-1271, B-1323, B-1403, B-1412, B-1603 Zhang D.: B-0792 Zhang F.: B-1171, B-1172 Zhang G.: B-1431 Zhang H.: B-0367, B-1483, B-1670 Zhang J.: B-0286, B-0432, B-0888, B-0993, B-1179, B-1218 Zhang L.: B-0638, B-0653, B-1126 Zhang L.J.: B-1487 Zhang M.: B-1596 Zhang W.: B-0456, B-0464, B-0656, B-0937, B-1174, B-1298, B-1617 Zhang X.: B-0502 Zhang X.: B-0389, B-1295 Zhang X.M.: B-0015 Zhang Y.: B-0475, B-0497, B-0935, B-0986, B-0991, B-1095, B-1475, B-1479, B-1485, B-1490, B-1496, B-1580 Zhang Z.: B-0065, B-1187, B-1479, B-1535 Zhao C.: B-0663, B-0817 Zhao H.: B-0758 Zhao L.: B-0781, B-1172 Zhao P.: B-1193 Zhao Q.: B-0788 Zhao S.: B-1172 List of Moderators (G) Abeyakoon O.: SS 1416 Abeyakoon O.: SS 1802b Achten E.: SS 1811a Adam E.J.: IIQ Adda O.: SY 2 Agnello F.: SS 1001a Agostini A.: SS 301b Agrawal A.: SS 317 Ahuja B.: SS 1907b Alberich-Bayarri A.: SS 605 Alexopoulou E.: RC 412 Antoch G.: RC 106 Aringhieri G.: SS 1007 Arkun R.: SS 210 Aukland S.M.: SS 212 Avni F.E.: SS 1412 Aydingoz U.: ESR/ESOR 1 A B C Caceres J.: RTF Quiz Cademartiri F.: SS 1903 Cantisani V.: SY 23 Cappendijk V.: SS 601b Carbonaro L.A.: SS 1902a Carrino J.A.: SY 25 Cartes-Zumelzu F.: RC 1711 Casado Lopez A.M.: SS 1811a Caseiro Alves F.: EM 2 Cassar-Pullicino V.N.: E³ 25A, E³ 25B, E³ 25C, E³ 25D, E³ 25E Castillo J.: SS 614 Catalano C.: SS 614 Cavedon C.: SS 713 Chianca V.: SS 1809 Chidambaranathan N.: BS 3, SS 608 Chodorowska A.: RC 1704 Choi B.I.: SS 1001a Cianfoni A.: RC 111 Claudon M.: WG/EFSUMB 1, SY 19 Clauser P.: MY 16, SS 1402a Claussen C.D.: SS 603 Clément O.: ESR Research, SY 17 Clevert D.A.: WG 1 Colin C.: SS 702 Collettini F.: SS 1509 Cornud F.: SS 1407 Curvo-Semedo L.: SS 1001b Damilakis J.: ESR/EFOMP D'Anastasi M.: SS 207 de Lange C.E.: RC 512 de Rooij M.: SS 1407 de Roos A.: SS 303 Demaerel P.: SS 1511 Denecke T.: SS 301a Denys A.: SY 3 Dewey M.: CT 2, CT 6, CT 10, MY 15 Dioguardi Burgio M.: SS 1409 D'Ippolito G.: SS 301a Dixon A.K.: MY 4 Djilas-Ivanovic D.: SS 1902a Dolic K.: SS 1811b Donati O.F.: JIIQ Dondelinger R.F.: MY 9 Dosa E.: SS 1415 Drapé J.-L.: SS 1010 Dubourg B.: SS 1903 Dzaye O.: C 14 Ehman R.L.: CT 2, CT 6, CT 10 Elmas N.Z.: SS 1801 England A.: SS 1014 Epermane M.: SS 610a Eriksen M.R.: RC 108 Erturk S.M.: RC 1601 Esen G.: SS 302 Esposito A.: SS 1006 Fanelli F.: E³ 526b Farchione A.: SS 316 Fatehi M.: SS 205 Fernandez-Bayó J.: SS 1805 Fernandez Hernando M.: SS 1810 Filippone A.: SS 201a Fontaine L.: SY 10 Forrai G.: SS 1002 Fösleitner O.: SS 1911b Franchi P.: MY 5 Francone M.: SS 703 Freeman S.: SS 707 Friedrich K.M.: CB 1, CB 2 Frigerio A.: SS 202b Frija G.: EU 1 Froeling M.: SS 1410 Gallagher F.A.: SS 1406 Gangemi E.: SS 1411a Gangi A.: RC 509 Garcia G.C.T.E.: SS 208 Gardarsdottir M.: E³ 24C Gersing A.S.: SS 1911a Gheonea I.-A.: SS 602 Giganti F.: SS 1907b Golding S.J.: MY 14 Goldsher D.: SS 1911a Gourtsoyianni S.: ESR/ESOR 2, MY 3 Gourtsoyiannis N.: ESOR H I J K L Grainger A.J.: TC 1328, TC 1428, TC 1528, TC 1628 Granata C.: RC 912 Grehan J.: SS 1814 Gremion I.: EM 4 Grenier P.A.: SS 204 Gruber H.: SS 710a Gubskiy I.L.: SS 701a Guerra A.: SS 307 Haliloglu M.: MY 18 Hamm B.: EM 1, EM 2, EM 3 Hanna S.: SS 207 Hausegger K.A.: SS 1509 Healy N.A.: SS 702 Helmberger T.K.: SS 1416 Henninger B.: SS 210 Hermoye L.: SS 1016b Hernandez-Giron I.: SS 1413 Herold C.J.: RC 104 Herzog C.: SS 203, SS 1415 Hinzpeter R.M.M.: SS 1017 Hodler J.: SS 1410 Hrabak Paar M.: RC 1603 Husseiny Salama D.: C 11 Huyskens J.: RC 408 Ichikawa S.: SS 201a Iliadis K.: SS 612 Ilic D.: SS 709 Inarejos E.: SS 1910 Ivanac G.: SS 1802a Jacob J.: SS 1004 Jacobi-Postma L.: SS 1016b Jäger H.R.: SS 1011b Jin Z.Y.: EM 3 Johnson T.R.C.: SS 604 Jovanovic S.: SS 1416 Kaltenbach B.: SS 601a Katsifarakis D.: MY 17 Kaya T.: RC 410 Kettenbach J.: SS 1909 Kilburn-Toppin F.: E³ 1726a, SS 1002 Kinner S.: SS 1901c Kitrou P.M.: MY 9, SS 215 Kljucevsek D.: SS 612 Klompenhouwer E.G.: SS 716 Klontzas M.: RC 910, S 3 Knapp K.: SS 1414 Kondratyev E.: SS 201b Kortesniemi M.: SS 613 Krokidis M.: E³ 24A Kuhl C.K.: SS 602 Kurz K.D.: SS 1011a Lamot U.: SS 308 Lawler L.P.: RC 903 Leander P.: PI 2 Lebovici A.: SS 216 Lee J.M.: SS 601a Lehotska V.: SS 1402a Leiner T.: ESR/ESMRMB 1 Lell M.: SS 1008 Ley-Zaporozhan J.: SS 1804, SS 1904b Loewe C.: E³ 24B, E³ 24D Mahesh M.: EF 2 Malagari K.: BS 4 Mann R.M.: SY 1b Manoharan T.: SY 1d Marincek B.: BS 2 Marino M.A.: SS 302 Markiet K.: SS 608 Marolt Music M.: SS 214 Massmann A.: SS 309 McGinty G.: PI 3 McNulty J.: EM 4, PI 1 Meder J.-F.: RC 911 Merhemic Z.: MY 8 Mildenberger P.: C 12, PI 3 Miletić D.: SS 1414 Mintert S.: SY 22 Mirón Mombiela R.: SS 610b Moerup S.D.: SS 314 Mordasini M.: EM 4 Mordasini P.: SS 611 Morozov S.: PI 2, SY 18 Mostbeck G.: SS 301b Mück F.: SS 317 Mueller-Lisse U.G.: SS 1516 Samara E.: SS 213 Sánchez M.: SS 616 Santos J.: EM 4 Sappey-Marinier D.: ESR/ESMRMB 1 Sardanelli F.: ESR Publication Savolainen S.: SS 714 Scapin E.: SS 708 Schlett C.L.: SS 703 Schmidt Kobbe S.: SS 701b Schönberg S.O.: SS 1914 Screaton N.J.: SS 1815 Secchi F.: SS 1403 Seidensticker M.: SS 1016a Seimenis I.: RC 1613 Semple T.R.: SS 712 Shahabpour M.: SS 1810 Sidhu P.S.: WG/EFSUMB 1, SY 6, SY 13 Simic M.: SS 616 Sinitsyn V.E.: SS 1803 Smits M.: SS 1811b Snoj Ž.: TF 1 Sommer G.: SS 613 Sommer W.H.: SS 605, SS 1815 Squarza S.A.C.: SS 711b Steinfelder E.: ESR/BBMRI-ERIC Stiller W.: SS 213 Struffert T.: SS 611 Studniarek M.: E³ 1526b Stukalova O.: SS 1003 Sudoł-Szopińska I.: SS 1910 Tack D.: ESR/EFOMP Tacke J.: SS 209 Tamandl D.: SS 201b Tan S.: SY 26 Tanner J.: SS 202b Tardaguila de la Fuente G.: SS 1901a Teneva T.G.: TF 1 Thomassin-Naggara I.: SS 1402b Thurnher M.M.: SS 211 Toia P.: SS 603 Tolan D.J.M.: SS 1017 Tomà P.: MY 18 Tóth A.: MY 7 Traykova N.I.: SS 1508 Trianni A.: EF 1, SS 205 Tsitskari M.: SS 609 Tsougos I.: SS 1911b Tyurin I.E.: SY 18 Tzalonikou M.: RC 1710, SS 310 Radbruch A.: SS 1011b Radeleff B.A.: SS 1809 Radzina M.: SS 701b Ramos-Andrade D.: SS 601b Rampado O.: SS 1413 Ratib O.: ESHI Reijnierse M.: RC 810 Reiser M.F.: E³ 526a, MY 13 Reiter U.: RC 503 Revel M.-P.: SS 304 Riibak M.-L.: SS 1816 Riklund K.: ESR/ESHI, ESHI Ringl H.: SS 1901a Robinson S.: RC 808, CB 1, CB 2 Rockall A.G.: SS 1816 Romei C.: SS 204 Roos J.E.: E³ 1526a Rosendahl K.: E³ 426 Rovira-Cañellas A.: PS 1227, SS 311 Roy C.: SS 1807b Runge V.: SY 9 Uberoi R.: SS 609 W Y Z Tsiflikas I. : B-0764, B-0766 Tsili A.C.: B-1662 Tsogkas I. : B-0923 Tsougos I. : B-0304 Tsuchiya M.: B-0720 Tsuruda K.: B-0684 , B-1606 Tsurumaru D.: B-0716 Tucci Jr S.: B-0879 Tudisca C.: B-1495 Tulay C.: B-1015 Tunariu N.: B-0393 Tunlayadechanont P.: B-1199 Turan Bektas C.: B-1206 Türk S.: B-1219 Turnaoglu H.: B-1004 Turowski B.: B-1037, B-1235, B-1237 Tuscano B.: B-0008 Tutar B.: B-1293 Tyczynski B.: B-0450 Tysnes O.B.: B-0798 Tyurin I.E. : A-529, B-1369, B-1561 Tzedakis A.: B-0771 Tzimas C.: B-1284 Tzschätzsch H.: B- 0001


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ECR 2018 - BOOK OF ABSTRACTS, Insights into Imaging, 2018, 1-642, DOI: 10.1007/s13244-018-0603-8