Thoracic Imaging 2003 - Society of Thoracic Radiology

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TUESDAY 170 Table 2: Pediatric CT Angiography * mAs slightly higher than body CT protocols ** use 0.5 second rotation time when an option Consider using bolus tracking vs empiric delay of 10-15 seconds after start of injection Applications for Pediatric Chest MDCT • Similar applications for chest MDCT in children and adults: • Evaluation of infection, and cancer. • Different applications in children • Less evaluation of chronic lung disease (eg fibrosis), trauma, pulmonary embolism, and evolving use in lung cancer and CAD screening • Evaluation of congenital abnormalities of the lung, mediastinum and heart are more typical in children. • Applications can be divided into lung, airway, mediastinum, cardiovascular system, and chest wall. • Lung parenchyma: • Applications of MDCT are identical to those of SDCT. • overlapping reconstructions can be obtained for assessment of small or subtle abnormalities such as a pulmonary nodule. • Multiplanar and 3D depictions: can be helpful for clinical services • MDCT provides opportunity for evaluation of bronchopulmonary foregut malformations, especially sequestration • Airway: both functional and anatomic. • Anatomic evaluation is established: • congenital abnormalities • endobronchial or extrinsic processes • postoperative stenosis or dehiscence • trauma. • If only airway evaluation ,consider thin slices (e.g. sub mm thickness), 80-110 kVp, and 20-40 mAs., limiting scan to airway and not the whole chest and upper abdomen. • Functional evaluation: • dynamic assessment of airway narrowing • CT data can be segmented and to display dynamic changes in airway caliber related to respiratory cycle displayed, or adjacent structures such as masses or cardiac abnormalities. • Mediastinum: • MDCT offers improved contrast enhancement of adjacent structures, and multiplanar and 3D depiction of abnormalities • Cardiovascular System: • Improved assessment with MDCT due to CT angiography. • Evaluation of aorta (including vascular rings, post operative changes), and pulmonary arteries, as well as problem solving tool for complex cardiac assessment not sufficiently addressed by echo • Chest wall: • Assesment of structures that may be arise from or secondarily involve the chest wall Recent Developments for Pediatric MDCT • Pediatric protocols • Automatic exposure controls • Innovative filters • More applicable phantom information (CTDIw and DLP). REFERENCES Frush DP, Donnelly LF. Helical CT in children: technical considerations and body applications. Radiology. 1998; 209:37-48. Hollingsworth CL, Frush DP, Cross M, Lucaya J. Helical CT of the body: survey of pediatric techniques. AJR. 2002; In press. Donnelly LF, Emery KH, Brody AS, et al. Minimizing radiation dose for pediatric body applications of single-detector helical CT. AJR 2001; 176:303-306. Frush DP. Pediatric CT: practical approach to diminish radiation dose. Pediatr Radiol. 2002; 32 (10):714-717. Donnelly LF, Frush DP. Pediatric Multidetector CT. Radiographic Clin N Amer. In press 2003. Lucaya J, Piqueras J, Garcia-Peña P, et al. Low-dose high-resolution CT of the chest in children and young adults: dose, cooperation, artifact incidence, and image quality. AJR 2000; 175:985-992. Frush DP, Donnelly LF, Chotas HG. Contemporary pediatric thoracic imaging. AJR 2000; 175(3):841-51. Cohen RA, Frush DP, Donnelly LF. Data acquisition for pediatric CT angiography: problems and solutions. Pediatr Radiol. 2000; 30:813-822. Frush DP, Donnelly LF. Pulmonary sequestration spectrum: a new spin with helical CT. AJR 1997; 169(3):679-682. Denecke T, Frush DP, Li J. Eight-channel multidetector CT: unique potential for pediatric chest CT. J Thorac Imaging. 2002;17(4):306-309.
The Spectrum of Pulmonary Infection in the Immunocompromised Child Richard I. Markowitz, M.D. The Children’s Hospital of Philadelphia & University of Pennsylvania School of Medicine Although respiratory infection is one of the most common childhood illnesses, it can be a signal of an underlying abnormality of the immune system. A high frequency of infection, an infection of unusual severity ,or an infection by an organism usually not pathogenic in a healthy individual should arouse suspicion of an immunodeficiency.1 However, the radiologic and pathologic patterns of disease in imrnunodeficient children are not different from the patterns of infection found in normal individuals.2 These pathologic patterns differ according to the distribution and extent of pulmonary infection and include bronchopneumonia, interstitial pneumonia, lobar pneumonia, lung abscess, empyema, bronchiectasis, and overwhelming pneumonia. Examples of these patterns will be shown demonstrating the wide and variable spectrum of pulmonary infection in the immunocompromi sed child. The most common immune defects in children are not due to rare genetic mutations, but are secondary to common systemic problems such as severe malnutrition,3 debilitating chronic illness, or immaturity of the immune system.. Iatrogenic immunodeficiency is a common side effect of steroids, chemotherapy, and radiation predisposing these children to serious infection. Infants are especially vulnerable to infection because of the immaturity of their immune system, although they do obtain passive immunity from their mothers. Host Defenses Much has been learned concerning the factors and mechanisms that comprise the immune system. Cellular, humoral, and mechanical factors work in concert to prevent microorganisms from literally “eating us alive.” T-lymphocytes, B-lymphocytes, natural killer cells, granulocytes, complement, and antibodies as well as a wide variety of receptors and polypeptide mediators known as cytokines interact in complex ways. The first barrier to infection is the skin and mucous membranes which afford mechanical protection. When these mechanical defenses are impaired as in cystic fibrosis or immotile cilia syndrome ,chronic infection can lead to irreversible tissue destruction, i.e. bronchiectasis. Primary 1mm unodeficiency Disorders Primary immunodeficiency disorders are inherited diseases which affect one or more specific parts of the immune system. Although they have been classified by which cell type is predominantly affected, there is a large overlap in the ways these disorders cause disease.4 First, we will consider T-cell (cellular) immune deficiency, then B-cell (humoral) immune deficiency, and then combined T and B cell deficiency syndromes. Finally, we will discuss some disorders of phagocytic function and complement deficiencies. Although all of these disorders result in increased susceptibility to pathogens, humoral defects, such as Bruton’ s agammaglobulinemia, predispose patents to bacterial infections, while cellular or T-cell defects make the individual more prone to viral, fungal, and parasitic diseases. Disorders of cellular immunity The prototype genetic defect of T-cell immunity is DiGeorge syndrome or congenital thymic hypoplasia. This disease derives from a deletion at the chromosome 22q11 site which inhibits normal development of structures derived from the third and forth pharyngeal pouches. Partial or complete absence of thymic lymphoid tissue results in varying degrees of T-cell deficiency; absence of the parathyroid glands causes hypocalcemia which can lead to tetany; and cardiac and aortic arch anomalies are frequent.5 These patients present in early infancy, and their course is often complicated by severe viral and fungal infections. Radiologic recognition of the absent thymus is a valuable clue in the first day or two of life, but becomes more difficult thereafter because severe stress in infants with other illnesses can cause rapid thymic involution. Disorders of humoral immunity X-linked agammaglobulinemia (Bruton) is a prime example of a defect in humoral immunity caused by a failure of development of B-cell precursors into mature B-cells. This genetic defect of B-cell maturation results from a mutation on the long arm of the X chromosome responsible for the production of a specific tyrosine kinase (Bruton tyrosine kinase or btk) which is necessary for pro B-cells and pre-B-cells to properly develop into mature B-cells capable of producing biologically active gamma-globulin.6 Because of the location on the X chromosome, this X-linked recessive disease presents only in the sons of maternal carriers. Clinical manifestations include absent germinal centers of lymph nodes; underdeveloped tonsils, adenoids, and hilar lymph nodes; absent plasma cells; and severely diminished serum gamma-globulin. Recurrent bacterial infections of the respiratory tract due to Streptococcus pneumoniae, Staphylococcus aureus, and Haemophi/us influenzae are common and may lead to bronchitis, pneumonia, bronchiectasis , and empyema. Radiologic signs of this disease include a paucity of the normal lymphoid structures surrounding the upper airway, i.e. absent tonsils and adenoids, as well as recognition of an increased frequency and severity of infections with common pyogenic organisms. Immunoglobulin replacement is standard treatment. Selective or isolated IgA deficiency is common occurring in approximately 1 in 600 people.7 Both serum and secretory IgA are absent due to a failure of maturation of fgA-positive B-cells. It can be a familial defect or acquired following a viral infection. Most individuals are asymptomatic, but are prone to variable bacterial infections of the sinuses, respiratory tract, and gastrointestinal tract. The term “common variable agammaglobulinemia” denotes a heterogeneous group of disorders characterized by defective B-cell function and frequent bacterial sinus and pulmonary infections. Bronchitis and bronchiectasis may lead to chronic respiratory failure.7 Non-caseating granulomas are often found as well. Gastrointestinal infections are also common. Hyperimmunoglobulin E syndrome, sometimes referred to as Job’s syndrome, is a rare inherited disorder which manifests 171 TUESDAY
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The Society of Thoracic Radiology T
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Dear Friends, Welcome to Miami Beac
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Continuing Medical Education Credit
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Warren B. Gefter, MD University of
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Ernest M. Scalzetti, MD SUNY Upstat
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Registration Hours Saturday, March
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Program Committee Ella A. Kazerooni
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Small Airway Disease Americana 3 Mo
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Benjamin Felson Memorial Lecture Am
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Session 2-B Concurrent Session Clin
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Workshops (choose 1) 1:00 - 1:45 D1
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Sunday
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March 2, 2003 General Session Sunda
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SUNDAY 46 One type of direct-readou
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CT-PET Imaging Suzanne Aquino, M.D.
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SUNDAY 58 an accompanying decreased
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SUNDAY 60 Radiofrequency Ablation i
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SUNDAY 62 17. Sewell PE, Vance RB.
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SUNDAY 64 cal ventilation will be r
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SUNDAY 66 radiologic, and histopath
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SUNDAY 68 application. The untreate
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SUNDAY 70 The Expanded Spectrum of
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SUNDAY 72 Hypersensitivity Pneumoni
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SUNDAY 74 Small Airway Diseases Mic
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SUNDAY 76 The “Head-cheese Sign
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SUNDAY 78 “Holes” in the Lung:
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SUNDAY 80 Pleural Effusions Gerald
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SUNDAY 82 Asbestos Related Pleural
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SUNDAY 84 Other Pleural Neoplasms S
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SUNDAY 86 Image-Guided Therapy of M
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Notes 88
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March 3, 2003 General Session 7:00
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Cardiac MRI: Established Indication
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Cardiac MRI: New Developments Gauth
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5. The volume of contrast medium re
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Acute Aortic Syndrome Ernest M. Sca
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as well as separation of the cusps
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Pulmonary Veins: Imaging for Radiof
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Imaging of Cardiopulmonary Support
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plied to the hollow fibers by an ex
Page 81 and 82: swelling of the entire leg, calf sw
Page 83 and 84: Multi-channel Pulmonary CTA: New Te
Page 85 and 86: terminate scintigrams, CT correctly
Page 87 and 88: CT Strucural and Functional Imaging
Page 89 and 90: curves (TDCs) are generated by manu
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Page 93 and 94: 80. Fleischmann D, Rubin GD, Bankie
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Page 99 and 100: REFERENCES Bergin CJ, Rios G, King
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Page 103 and 104: March 4, 2003 General Session 7:00
Page 105 and 106: Adult Manifestations of Congenital
Page 107 and 108: will usually display the limbs of t
Page 109 and 110: Imaging of the Pericardium Paul L.
Page 111 and 112: Cardiomyopathy Martin J. Lipton, M.
Page 113 and 114: TUESDAY 150 Nuclear Cardiology Upda
Page 115 and 116: TUESDAY 152 ties. The predominant 1
Page 117 and 118: TUESDAY 154 Imaging protocols: Util
Page 119 and 120: Manpower Shortage in Radiology: Sol
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Page 127 and 128: NIBIB Update for Thoracic Radiology
Page 129 and 130: vertically along the right atrium t
Page 131: Multidetector Pediatric Chest CT: P
Page 135 and 136: Immune deficiency occurs frequently
Page 137 and 138: TUESDAY 180 The Internet and the Pr
Page 139 and 140: TUESDAY 182 Workshop A1: Lymphoma:
Page 141 and 142: TUESDAY 184 Digital Images: Camera
Page 143 and 144: TUESDAY 186 Analysis of Mediastinal
Page 145 and 146: Unusual Manifestations of Lung Canc
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Page 149 and 150: March 5, 2003 General Session Wedne
Page 151 and 152: WEDNESDAY 208 principle is that “
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Page 155 and 156: WEDNESDAY 212 lesions generally mim
Page 157 and 158: WEDNESDAY 214 capable of studying t
Page 159 and 160: WEDNESDAY 216 Small T1 Lung Cancer:
Page 161 and 162: WEDNESDAY 218 REFERENCES Seely JM,
Page 163 and 164: WEDNESDAY 220 Therefore, radiologis
Page 165 and 166: WEDNESDAY 222 sectional area varies
Page 167 and 168: WEDNESDAY 224 Lung Cancer Staging A
Page 169 and 170: Metastatic Disease to Lung Gordon L
Page 171 and 172: Thoracic Metastates from Osteosarco
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Page 177 and 178: WEDNESDAY 236 Pulmonary Arterial Hy
Page 179 and 180: WEDNESDAY 238 pathological process,
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THURSDAY 250 Pulmonary Tuberculosis
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THURSDAY 252 1. Clinical criteria:
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THURSDAY 254 AIDS patients are also
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THURSDAY 256 Viral Infection on HRC
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THURSDAY 258 Imaging of Coccidioido
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THURSDAY 260 from the laryngeal sur
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THURSDAY 262 Inflammatory Diseases
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Virtual Endoscopy in the Thorax: Pr
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Notes 269 THURSDAY
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SECOND LEVEL THIRD LEVEL
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