HRCT of interstitial lung disease (ILD): The basic ingredients of the alphabet soup

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1 HRCT of interstitial lung disease (ILD): The basic ingredients of the alphabet soup Poster No.: P-0061 Congress: ESTI 2015 Type: Educational Poster Authors: J. Broncano, F. Gutierrez, R. Reyna, S. E. Rossi, A. Luna ; Córdoba/ES, Saint Louis/US, Panama/PA, Buenos Aires/AR, 5 Jaen/ES Keywords: Inflammation, Edema, Drugs / Reactions, Computer ApplicationsGeneral, Biopsy, CT, Thorax DOI: /esti2015/P-0061 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 91

2 Learning objectives 1. Introduction Akin to cooking different recipes with the same basic ingredients but obtaining different flavors, in cases of ILD we may encounter similar basic patterns in different combinations which can result in totally different disease entities. The pulmonary parenchyma, when subject to different insults, will frequently respond in a somewhat predictable and stereotypical fashion. As a result, totally different disease entities (ground glass can be seen in infection, inflammation, hemorrhage) can have very similar appearances on HRCT. Conversely, the combination of such findings (reticulation, and honeycombing are characteristic of a UIP pattern) can be crucial in selecting the proper diagnosis. For that reason, the purpose of this review is Learning how to recognize the different signs and HRCT basic patterns that can be seen in interstitial lung disease and their hystopathologic correlation. How proper identification of those "basic ingredients" and their combination in each case can help discriminate between the different disease entities in ILD. Background 2. CT anatomy of pulmonary lobule and acinus As defined by Miller and Heitzmann, the secondary pulmonary lobule (SPL) is the smallest unit of the lung parenchyma surrounded by septa (1) (Fig. 1 on page 5). They are irregularly polyhedral and vary in sizes between central/peripheral and upper/ lower portions of the lung, ranging from 1 to 2.5 cm (1-5). Page 2 of 91

3 Fig. 1 On thin section CT the SPL have three components: interlobular septa, centrilobular region and the lobular parenchyma. It has an afferent "lobular" bronchiole, pulmonary arteriole and connective tissue accompanying in a centrilobular manner. In the periphery (within the septum) there are lymphatics, pulmonary venules and connective tissue. Contrarily, the acinus is the portion of the lung distal to a terminal bronchiole, which is the last conducting airway. Therefore, the acinus is the largest unit of the lung involved in the gas exchange. A SPL is composed of up to 12 acini, number which is highly variable in the literature. Page 3 of 91

4 Fig. 2 The primary pulmonary lobule was defined in 1947 by Miller, as the alveolar ducts, sacs and alveoli distal to the last respiratory bronchiole, associated with the correspondent pulmonary arteriole, lymphatics, nerves, veins and connective tissue (1). This term it is not used actually. 2.1 Interlobular septal anatomy Forming part of the peripheral interstitial system described by Weibel et al, the interlobular septa envelopes the lung, beneath the visceral pleura and penetrates the lung parenchyma (1) (Fig. 1 on page 5). Usually, they measure 0.1 mm, being at the lower resolution of CT. In healthy patients, few septa could be seen and usually they are inconspicuous. Also, pulmonary vein and Page 4 of 91

5 lymphatics are located in the interlobular septa, surrounded by connective tissue (Fig. 1 on page 5). 2.2 Centrilobular region Central structures include a lobular bronchiole, which is a preterminal bronchiole, preterminal pulmonary artery, lymphatics, all surrounded by connective tissue, forming the "axial fiber system" described by Weibel et al (1). The lobular bronchiole bifurcates in an irregularly dichotomous manner, arising from it subsequent preterminal bronchioles, terminal bronchioles and respiratory bronchioles. Lobular arteries and bronchioles measure up to 1 mm diameter. On thin section CT, lobular pulmonary artery are represented as a linear, branching or dot like opacity located in the center of SPL or within 1 cm of the pleural surface. Contrarily, the diameter of the lobular bronchiole is not associated with its conspicuousness but the wall thickness. In fact, in an in vitro study only bronchioles with at least 2 mm diameter or 0.1 mm of wall thickness were visible on thin section CT (1,6-8). 2.3 The lobular parenchyma Include alveoli and its pulmonary capillary bed, pulmonary artery and vein, lymphatics and a connective tissue stroma within the alveolar septa, named "septal fibers" by Weibel et al (1). Images for this section: Page 5 of 91

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8 Imaging findings OR Procedure details 3. Signs and patterns of disease 3.1 Linear pattern: Reticulation The major constituents of reticulation in HRCT include: (1) interlobular septal thickening, (2) intralobular septal thickening, (3) subpleural interstitial thickening and (4) centrilobular branching lines and (5) parenchymal bands (9). Fig. 3 Page 8 of 91

9 The thickening of the parenchymal interstitium that surrounds the alveoli does not cause linear opacities because of being outside the CT resolution. Contrarily it could be observed as ground glass opacities Interlobular septal thickening: Definition: Corresponds to a thickening of the interlobular septa, surrounding the SPL. They are 1-2 cm of length and roughly perpendicular to the pleura when peripheral (1,9,10). Fig. 4 The normal distribution of them is not homogeneous, being thicker and more conspicuous in healthy individuals in the anterior and lateral upper and middle lobes, and in the anterior, diaphragmatic and mediastinal regions in lower lobes. Page 9 of 91

10 Physiopathology: Because the specific anatomy of the boundaries of the SPL, pathological substrate related with interlobular septal thickening includes: Infiltration of the interstitium by cells, fluid or fibrosis Septal edema secondary to venous congestion Pathological alterations in and around the lymphatics Linear deposition of material within the periphery of SPL, mimicking a true septal thickening; the perilobular pattern. Smooth septal thickening is also seen in association with ground glass opacities (GGO) creating a differential pattern: the "crazy paving" pattern, with a specific differential diagnosis. Differential diagnosis: The interlobular septal thickening could be smooth, nodular or irregular. 1. Smooth septal thickening is usually associated with venous congestion, lymphatic congestion or infiltrative diseases. Fig. 5 Page 10 of 91

11 2. Nodular septal thickening: when present the interlobular septa appear as a beaded septum and are usually associated with involvement of the lymphatics. It is usually associated with a perilymphatic distribution. Fig In irregular septal thickening is usually associated with fibrosis. Has limited diagnostic value and is usually associated with other related findings. The presence of honeycombing and architectural distortion difficult the appropriate identification. Fig Perilobular pattern: alteration of the periphery of the secondary pulmonary lobule but also the peribronchovascular interstitium of larger bronchi and pulmonary arteries who are too large to be located at the center of the SPL Intralobular septal thickening Page 11 of 91

12 Definition: Presence branching lines separated a few millimeters conferring a netlike appearance that extends from the center of the SPL to the periphery. Usually associated with an interface sign defined as the presence of irregular interfaces between lung parenchyma, vessels, bronchi or visceral pleura (1,9). Physiopathology: Thickening of the intralobular connective tissue septa secondary to inflammatory interstitial infiltration, fibrosis or both. Also could be secondary to airspace disease with linear deposition of material in the periphery of the acini (1). Thickening of the parenchymatous connective tissue is beyond the resolution of CT and would present as a GGO. Also it could be seen in association with GGO creating a "crazy paving" pattern (10,11). When fibrosis is present, coarse appearance with traction bronchiectasis, architectural distortion and small honeycomb cysts (around 1 mm) could become visible (9). Differential diagnosis: Intralobular septal thickening with fibrosis (traction bronchiectasis, interface sign, etc.) Intralobular septal thickening without fibrosis Fig. 8 Page 12 of 91

13 3.1.3 Subpleural interstitial thickening Definition: Thickening of subpleural interstitium usually associated with interlobular septal thickening. It is sometimes difficult to recognize and, because of the involvement of lung fissures, is in those locations where is more easily depicted (10). Physiopathology: The affection can result from interstitial lung disease and, because of the presence of lymphatic vessels, also diseases affecting in and around lymphatics could present with it. Differential diagnosis: Could be smooth, irregular or nodular with the same differential diagnosis as in interlobular septal thickening, and is often associated with it. It is a common finding observed in UIP, collagen - related and drug - related lung diseases Centrilobular branching lines Definition: Are defined as Y shaped or X shaped opacities at the center of the secondary pulmonary lobule. Can be seen when the distal intralobular peribronchovascular interstitium is thickened. When fibrosis is present, bronchiolectasis develops ( Fig. 3 on page 49 ) (9). Physiopathology: This pattern is related to: Involvement of centrilobular peribronchovascular interstitium Involvement in or around the lymphatics Involvement of centrilobular bronchioles Involvement of centrilobular arterioles Page 13 of 91

14 Fig Parenchymal bands Definition: Non tapering linear or reticular opacity of 1 to 3 mm of thickness and 2 to 5 cm of length (9,10,12). Usually is peripheral, perpendicular to and in contact to the pleural surfaces. Page 14 of 91

15 Fig. 10 Physiopathology: Occasionally it represents several contiguous thickened interlobular septa (9). Differential diagnosis: Although being non - specific and related to a variety of procedures, was firstly described in patients with asbestos exposure (9). Subpleural lines have been defined as curvilinear opacities measuring less than 10 mm of thickness and parallel to the pleural surface. They are non -specific and usually related to atelectasis, fibrosis or inflammation. It has been associated to fibrotic lung diseases, like asbestosis (10,12). 3.2 Nodular pattern: centrilobular vs perilymphatic Page 15 of 91

16 A nodular pattern is characterized by the presence of multiple nodular opacities ranging in size from 2 mm to 3 cm. The differentiation between small and large pulmonary nodule has a threshold value of 1 cm. Nodules less than 7 mm are termed "micronodules" (10,13). In the assessment of diffuse nodular infiltrations the evaluation of the nodule characteristics (appearance pattern) and the relationship with the components of the SPL (distribution pattern) are important (9). Hystopathologically, at least four nodule distribution could be recognized (14): Bronchiolocentric: related to the centrilobular and lobular bronchi. Angiocentric: related to pulmonary arteries within the SPL Lymphatic - perilymphatic: related to lymphatic - perilymphatic vessels Random: no definable distribution Fig. 11 Page 16 of 91

17 Because bronchi and pulmonary artery are in close relationship within the SPL, in HRCT the bronchiolocentric and angiocentric distribution could not be easily differentiated and, therefore, are group in the centrilobular distribution pattern. Thus, in HRCT only three nodular pattern distributions are described: (1) centrilobular; (2) perilymphatic and (3) random (1) Centrilobular pattern Definition: Pulmonary nodules distributed in the center of the SPL. Could be well or ill defined, roughly evenly spaced and located separately from the pleural surface and the interlobular septa. They are located about 5-10 mm from the pleural surface ("subpleural sparing") (1,9,10,15). Physiopathology: The histologic correlation vary from the underneath etiology. It could be secondary to angiocentric or bronchocentric diseases ( Fig. 11 on page 53). Page 17 of 91

18 Fig. 12 Although lymphatic and perilymphatic diseases could be presented as centrilobular nodular pattern, usually are associated with involvement of other regions of the SPL (see perilymphatic distribution) (15,16). Fig. 13 Page 18 of 91

19 Fig. 14 Differential diagnosis: Angiocentric distribution: look at the pulmonary artery as a clue finding Bronchocentric distribution Page 19 of 91

20 Fig Tree in bud pattern Definition: Centrilobular branching structures resembling a budding tree. Is usually more pronounced in the periphery of the lung and usually associated with large airways disease. Although rare, it has also been described in peripheral "microangiopathic" pulmonary diseases, mainly secondary to intravascular metastasis involving the centrilobular arteries (1,17). In that case, pulmonary artery should be assessed as in those cases signs of pulmonary hypertension may be seen (1,15,17). Physiopathology: Reflects a spectrum of endo and peribronchiolar abnormalities: (1) bronchiolar dilatation and wall thickening, (2) peribronchiolar inflammation and (3) Page 20 of 91

21 bronchiolar luminal impaction by mucus, pus or fluid. Also, fibrocellular intimal hyperplasia (carcinomatous endarteritis) could be seen in tumoral emboli. Differential diagnosis: Fig Perilymphatic distribution Definition: It is characterized by the presence of well - defined nodules in or along the lymphatic vessels in the lung. Usually abuts the costal and pleural fissural surfaces and have a patchy distribution (1,9,10). Page 21 of 91

22 Fig. 17 Physiopathology: Involves (1) the subpleural, (2) the peribronchovascular bundles, (2) the interlobular and (4) centrilobular region. By definition, there are no presence of pulmonary nodules between the centrilobular structures and the interlobular septa. Differential diagnosis: Page 22 of 91

23 Fig. 18 Examples: Fig. 19 on page 61, Fig. 20 on page 62, Fig. 21 on page Random distribution Definition: Uniformly widespread nodular pattern with no definable distribution related to the SPL estructures. Nodules may be located in the center of the lobule, in the interlobular septa, subpleural regions and in the lung parenchyma in between. Usually the nodules are distributed in a bilateral and symmetric fashion (9,10). Page 23 of 91

24 Fig. 22 Physiopathology: Results from a vascular spread in which the agent passes the centrilobular structures and distributes along the small vessels and capillaries. Differential diagnosis: Page 24 of 91

25 Fig. 23 Algorythm of Nodular pattern: Page 25 of 91

26 Fig Ground glass opacities (GGO) and "crazy paving" pattern Definition: Ground glass opacity is defined as hazy increase opacity of the lung with preservation of bronchial and vascular margins (10). Is a non-specific finding that reflect volume averaging of abnormalities that could not be completely addressed by HRCT. Page 26 of 91

27 Fig. 25 It should be interpreted as active and potentially reversible disease when there is absence of fibrotic associated changes in the lung. If there is associated lung fibrosis, biopsy should be directed towards GGO areas. When there are interlobular and intralobular thickening superimposed on GGO, this is defined as a "crazy paving" pattern (10,11,18). It usually has a geographic outline. Page 27 of 91

28 Fig. 26 Physiopathology: It is caused by partial filling of airspaces, interstitial thickening secondary to fluid, cells or fibrosis, partial collapse, increased capillary blood volume or a combination (18,19). Differential diagnosis: The importance of GGO and "crazy paving" patterns depends on the clinical scenario and distribution of the disease (9). But also, in the case of GGO, ancillary findings should be taken into consideration. 1. GGO: Page 28 of 91

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30 Fig "Crazy paving" pattern: Page 30 of 91

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32 Fig Mosaic pattern and air trapping Definition: The mosaic attenuation corresponds to a patchwork of regions of different attenuation ("inhomogeneous lung opacity"), usually outlining secondary pulmonary lobules, that may represent (1) patchy interstitial lung disease, (2) obliterative small airways disease or (3) occlusive vascular disease (1,10,20). Fig. 31 Air trapping is defined as the retention of air in the lung distal to an obstruction, usually partial (1,10,20). When areas of low, normal and high attenuation patterns are seen, sharply demarcated from each other, with abrupt density transitions, these findings constitutes a headcheese sign (21). Page 32 of 91

33 Physiopathology: Pulmonary density is related to blood volume within the lung. Therefore, any alteration of the lung blood volume may alter it attenuation. This phenomenon produces areas of relatively increased lung attenuation (hyperperfused lung) and other areas of lower attenuation (hypoperfused lung). Mosaic hypoperfusion could be differentiated from GGO by identification of small vessels within relatively hypodense lung regions, reflecting the diminished lung perfusion (22). Contrarily, in GGO the caliper of the vessels seen in hyper and hypoattenuated areas did not differ. These could be secondary to: Airways obstruction: including large airways diseases and bronchiolitis. Vascular occlusion: from embolic origin, vascular remodeling or capillaritis. Expiratory imaging helps to differentiate mosaic pattern secondary to vascular occlusion from those related to bronchial obstruction. When the mosaic pattern remains roughly similar in inspiratory and expiratory images, a vascular etiology is suspected. Contrarily, when hypodense areas are accentuated on hypoperfusion imaging, reflecting air locked into the SPL, this is consistent with air trapping and a bronchial obstruction should be considered. Occasionally air trapping on expiratory images could be seen in otherwise normal inspiratory explorations. This could be a normal finding, when mild, in healthy individuals but also could be presented in small airways disease (23). The headcheese sign is indicative of a mixed infiltrative and obstructive process, usually accompanied with bronchiolitis. While the GGO represent the infiltrative component, mosaic attenuation and air trapping are related to small airways disease with related hypoxic vasoconstriction (21). Differential diagnosis: 1. Mosaic Pattern: Page 33 of 91

34 Fig Headcheese pattern: Fig Halo sign/reversed halo sign Page 34 of 91

35 Definition: The halo sign is a ground-glass opacity surrounding a pulmonary nodule or mass with central soft tissue attenuation. It is non-specific (12,24). Fig. 34 The reversed halo sign (atoll sign or fairy ring sign) is defined by de presence of ground-glass opacity with a surrounding halo or crescent consolidation (12,25,26). It should be differentiated from cavitation (defined gas-filled space seen within a pulmonary consolidation, nodule or mass) or pseudocavitation (internal bronchiolectasis seen in subtypes of lung adenocarcinoma). Page 35 of 91

36 Fig. 35 Physiopathology: The halo sign is usually associated to hemorrhage associated with other types of nodules, but also corresponds to non-hemorrhagic pathological substrates such as pulmonary infiltration by neoplasm or non-hemorrhagic lesions (24). The reversed halo sign corresponds to central alveolar inflammation associated with peripheral airspace granulomatous tissue or dense intraalveolar infiltrates (25,26). Differential diagnosis: 1.Halo sign Page 36 of 91

37 Fig Reverse halo sign (atoll sign) Page 37 of 91

38 Fig Lung cysts and honeycombing (HC) Definition: HC is defined as clustered cystic airspaces, of comparable diameter, ranging from 3 to 10 mm and as large as 2.5 cm. They are subpleural in location and characterized by well-defined cystic lesions with sharing walls. Page 38 of 91

39 Fig. 38 Frequently are accompanied with other signs of fibrosis, such as, coarse reticulation, architectural distortion, traction bronchiectasis and irregular septal pattern (9,23). This sign is of great importance as, in association with other HRCT criteria, could be diagnostic of usual interstitial pneumonia (UIP) pattern, obviating the need of lung biopsy. Fig. 39 Cysts are defined as a round parenchymal lucency with a well-defined interface with normal lung (10). Cysts have variable thickness but usually are thin-walled. Usually contain air but can contain fluid or solid material (10,27). Page 39 of 91

40 Fig. 40 Physiopathology: HC represents destroyed and fibrotic lung tissue, containing numerous cystic airspaces with thick fibrous wall and loss of acinar architecture (10). Cysts may have various appearances and are lined by metaplastic bronchiolar epithelium (27). Represent the end stage of several lung diseases. Pathologically, cysts are a round and circumscribe space surrounded by epithelial or fibrous wall of variable thickness (27). Page 40 of 91

41 Fig. 41 Differential diagnosis: Page 41 of 91

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43 Fig. 43 Diagnostic algorithm: 1. Honeycombing: Page 43 of 91

44 Fig Cysts: Page 44 of 91

45 Fig. 45 Examples: Fig. 46 on page 79, Fig. 47 on page 80, Fig. 48 on page Bronchiectasis Definition: Is defined as irreversible localized or difuse bronchial dilatation. Bronchiolectiasis is defined as dilatation of the bronchioles (12). There are several signs describing bronchiectasis, which include: 1. Increased bronchoarterial ratio: ratio of internal diameter of the bronchus to its adjacent pulmonary artery > 1. It is the most specific finding. By using this parameter, the normal value is less than one (0.62 ± 0.13) (12). Ascending order of severity include cylindrical, varicose and cystic. Increased bronchoarterial ratios could be seen in asthmatic patients and patients living at high altitudes (28). The signet ring sign refers to this altered bronchoarterial ratio seen in cross sectional imaging. Is composed by a ring Page 45 of 91

46 shaped opacity (dilated bronchi) and a smaller adjacent opacity representing the pulmonary artery. Lack of bronchial tapering: Earliest sign in cylindrical bronchiectasis. Could be assessed as lack of change in size of an airway over 2 cm after branching (9). Visualization of small airways in periphery (within 1 cm to the pleura): the presence of dilatation of small airways with signs of fibrosis is defined as traction bronchiolectasis. Mucous impaction: fluid or mucus filled bronchi. When they fill bronchioles could be presented as centrilobular or tree in bud pattern. Mosaic perfusion and air trapping. Fig. 49 Physiopathology: Bronchiectasis and bronchiolectasis may result from obstruction, abnormal mucus production, infection and/or congenital abnormalities of the bronchial wall. Page 46 of 91

47 Bronchiolectasis may be caused by inflammatory airways disease, which is potentially reversible, or fibrosis (traction bronchiectasis). For the differential diagnosis is of great importance the distribution of the bronchiectasis. Fig. 50 Differential diagnosis: Page 47 of 91

48 Fig Spatial and temporal distribution There are several histological hallmarks defining usual interstitial pneumonia (UIP) which are (29-32): Heterogeneous appearance at low magnification with areas of normal lung interspersed with zones of stablished fibrosis and honeycombing and, between them regions of active inflammation (fibroblastic foci). This has been defined as "spatial and temporal heterogeneity" and "patchwork pattern". Page 48 of 91

49 Fig. 52 The alterations are predominantly located at the periphery of the secondary pulmonary lobule, with fibrosis located near and in the interlobular septa, subpleural region and near the veins, but also near large bronchovascular bundles as they are pass between pulmonary lobules up to the level of terminal bronchioles: periobular pattern. Honeycombing, as the end-stage landmark (collapse of fibrotic alveoli and dilation of alveolar ducts). By means of asymmetric distribution and lobular heterogeneity we could assess both temporal and spatial heterogeneity by HRCT (32). Images for this section: Page 49 of 91

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86 Conclusion Accurate identification and understanding of HRCT basic signs and patterns underlying ILD is essential, particularly for radiology residents. Review of some of these patterns and their associations can enhance proper diagnosis. References Bibliography 1. Webb WR (2006) Thin-section CT of the secondary pulmonary lobule: anatomy and the image--the 2004 Fleischner lecture. Radiology 239: doi: / radiol Heitzman ER, Markarian B, Berger I, Dailey E (1969) The secondary pulmonary lobule: a practical concept for interpretation of chest radiographs. II. Application of the anatomic concept to an understanding of roentgen pattern in disease states. Radiology 93: doi: / Weibel ER (1979) Fleischner Lecture. Looking into the lung: what can it tell us? AJR Am J Roentgenol 133: doi: /ajr Raskin SP (1982) The pulmonary acinus: historical notes. Radiology 144:31-4. doi: /radiology Osborne DR, Effmann EL, Hedlund LW (1983) Postnatal growth and size of the pulmonary acinus and secondary lobule in man. AJR Am J Roentgenol 140: doi: /ajr Webb WR (1989) High-resolution CT of the lung parenchyma. Radiol Clin North Am 27: Webb WR, Stein MG, Finkbeiner WE, et al. (1988) Normal and diseased isolated lungs: high-resolution CT. Radiology 166:81-7. doi: /radiology Murata K, Itoh H, Todo G, et al. (1986) Centrilobular lesions of the lung: demonstration by high-resolution CT and pathologic correlation. Radiology 161: doi: / radiology Gotway MB, Reddy GP, Webb WR, et al. (2005) High-resolution CT of the lung: patterns of disease and differential diagnoses. Radiol Clin North Am 43:513-42, viii. doi: /j.rcl Page 86 of 91

87 10. Hansell DM, Bankier AA, MacMahon H, et al. (2008) Fleischner Society: glossary of terms for thoracic imaging. Radiology 246: doi: /radiol Rossi SE, Erasmus JJ, Volpacchio M, et al. (2003) "Crazy-paving" pattern at thinsection CT of the lungs: radiologic-pathologic overview. Radiographics 23: doi: /rg Hansell DM (2010) Thin-section CT of the lungs: the Hinterland of normal. Radiology 256: doi: /radiol Grenier P, Valeyre D, Cluzel P, et al. (1991) Chronic diffuse interstitial lung disease: diagnostic value of chest radiography and high-resolution CT. Radiology 179: doi: /radiology Colby T V, Swensen SJ (1996) Anatomic distribution and histopathologic patterns in diffuse lung disease: correlation with HRCT. J Thorac Imaging 11: Rossi SE, Franquet T, Volpacchio M, et al. (2005) Tree-in-bud pattern at thin-section CT of the lungs: radiologic-pathologic overview. Radiographics 25: doi: / rg Akira M, Kitatani F, Lee YS, et al. (1988) Diffuse panbronchiolitis: evaluation with high-resolution CT. Radiology 168: doi: /radiology Franquet T, Giménez A, Prats R, et al. (2002) Thrombotic microangiopathy of pulmonary tumors: a vascular cause of tree-in-bud pattern on CT. AJR Am J Roentgenol 179: doi: /ajr Franquet T, Giménez A, Bordes R, et al. (1998) The crazy-paving pattern in exogenous lipoid pneumonia: CT-pathologic correlation. AJR Am J Roentgenol 170: doi: /ajr Remy-Jardin M, Giraud F, Remy J, et al. (1993) Importance of ground-glass attenuation in chronic diffuse infiltrative lung disease: pathologic-ct correlation. Radiology 189: doi: /radiology Arakawa H, Webb WR (1998) Air trapping on expiratory high-resolution CT scans in the absence of inspiratory scan abnormalities: correlation with pulmonary function tests and differential diagnosis. AJR Am J Roentgenol 170: doi: / ajr Chong BJ, Kanne JP, Chung JH (2014) Headcheese sign. J Thorac Imaging 29:W13. doi: /RTI Im JG, Kim SH, Chung MJ, et al. Lobular low attenuation of the lung parenchyma on CT: evaluation of forty-eight patients. J Comput Assist Tomogr 20: Page 87 of 91

88 23. Arakawa H, Honma K (2011) Honeycomb lung: history and current concepts. AJR Am J Roentgenol 196: doi: /AJR Parrón M, Torres I, Pardo M, et al. (2008) [The halo sign in computed tomography images: differential diagnosis and correlation with pathology findings]. Arch Bronconeumol 44: Marchiori E, Zanetti G, Meirelles GSP, et al. (2011) The reversed halo sign on highresolution CT in infectious and noninfectious pulmonary diseases. AJR Am J Roentgenol 197:W doi: /AJR Walker CM, Mohammed T-L, Chung JH (2011) "Reversed halo sign". J Thorac Imaging 26:W80. doi: /RTI.0b013e318224cfbc 27. Genereux GP (1975) The end-stage lung: pathogenesis, pathology, and radiology. Radiology 116: doi: / Lynch DA, Newell J, Hale V, et al. (1999) Correlation of CT findings with clinical evaluations in 261 patients with symptomatic bronchiectasis. AJR Am J Roentgenol 173:53-8. doi: /ajr Travis WD, Costabel U, Hansell DM, et al. (2013) An official American Thoracic Society/European Respiratory Society statement: Update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med 188: doi: /rccm ST 30. Travis WD, King TE, Bateman ED, et al. (2002) American thoracic society/ European respiratory society international multidisciplinary consensus classification of the idiopathic interstitial pneumonias. Am. J. Respir. Crit. Care Med. pp Raghu G, Collard HR, Egan JJ, et al. (2011) An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management. Am J Respir Crit Care Med 183: doi: /rccm GL 32. Johkoh T, Sumikawa H, Fukuoka J, et al. (2014) Do you really know precise radiologic-pathologic correlation of usual interstitial pneumonia? Eur J Radiol 83:20-6. doi: /j.ejrad Personal Information Page 88 of 91

89 Fig. 53 I hope you have enjoy the exhibit. See you next ESTI. Enjoy!!! JORDI BRONCANO MD j.broncano.c@htime.org Images for this section: Page 89 of 91

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