Multiple Parenchymal Abnormalities on Chest CT scan: Don't Panic, Let's Be Pragmatic: The Eight Questions Rule

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1 Multiple Parenchymal Abnormalities on Chest CT scan: Don't Panic, Let's Be Pragmatic: The Eight Questions Rule Poster No.: C-1064 Congress: ECR 2013 Type: Educational Exhibit Authors: M. Baque-Juston, L. Mondot, S. Leroy, B. PADOVANI ; Nice/ FR, Nice Cedex 1/FR Keywords: Diagnostic procedure, CT-High Resolution, CT, Thorax, Cardiovascular system, Education and training DOI: /ecr2013/C-1064 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 38

2 Learning objectives LEARNING OBJECTIVE Multiple parenchymal lung abnormalities (MPLAs) can be secondary to more than 100 different conditions. They may appear on CT scans as a patchy mixture of lines, nodules, condensations, bands, ground-glass and hypo attenuations areas. These features can be the result of: Interstitium infiltration Bronchial or bronchiolar pathology Cardiovascular dysfunction Alveolar filling Some diseases can cause all of these abnormalities concurrently. Some patients suffer from several pathologies at once. These facts alone suffice to explain why only few radiologists feel comfortable suggesting an acceptable list of differential diagnoses (DD) when confronted to such findings. The aim of this work is to develop a simplified and check list based methodology to help non specialist radiologists address the following issues: a) Are the abnormalities encountered secondary to an easily diagnosable pathology which can be evaluated in a non-specialized environment? b) Or alternatively, is it a complex case to be discussed in multidisciplinary team MDT meetings? c) Does the situation require urgent treatment? In a) and c) situations, all radiologists should be able to provide a short list of differential diagnoses. In b) however, a precise description of the lesions is arguably sufficient before specialist review and MDT discussions. The strategy presented here also facilitates the recognition of multiple aetiologies of lung changes in poly-diseased patients e.g. infective pneumonia in a chronic obstructive pulmonary disease (COPD) patient with a hint of cardiac failure. In these cases, the Page 2 of 38

3 checklist format helps to ensure that less obvious pathologies are not obscured by the principal diagnosis. Background Since the beginning of HRCT in the 1990s, which provided a few millimetric highresolution slices of the lungs in selected patients, technology has rapidly evolved. Multidetector computer tomography (MDCT) of the chest nowadays generates contiguous millimetric images of the entire lung parenchyma of every patient scanned, with possibility of multiplanar reconstruction and post-processing image treatment. Furthermore the actual rapidity of CT scan acquisitions allows detailed observation of the cardio-vascular system especially when IV contrast is injected. In the meantime, histopathological characterization of lung diseases and radiologypathology correlations have also greatly evolved. These changes have been leading to the emergence of: A new classification of interstitial pneumonias (IP) in 2002 with a shift towards an integrated clinical, radiological and histo-pathological approach. Multi-disciplinary team discussions are replacing the usual histologic goldstandard [1] A new glossary of terms for thoracic imaging (2008) with consensual definitions formulated by The Fleischner Society's members [2] Iterative lengthening of differential diagnosis lists encountered with each abnormal scanographic finding, given rapid growth of available data in the literature. The method we propose to disentangle these difficulties relies on the following four key building blocks. Understanding secondary pulmonary lobule [3] (Fig 1) Page 3 of 38

4 Fig. 1 Applying post treatment techniques once the acquisition has been performed. Observing the lesions in multi-planar reformation allows a better assessment of regional distribution (interest of coronal reconstructions). Furthermore Maximum Intensity Projection reconstructions (MIP) help to characterize micronodules and to review the vascular bed while Minimum Intensity Projection reconstructions (MinIP) emphasize hypo-attenuation areas and mosaic attenuation patterns [4] (Fig 2) Page 4 of 38

5 Fig. 2 Using consensual descriptive vocabulary from the Fleischner Society's glossary of terms to describe the findings [2] (Fig 3) Page 5 of 38

6 Fig. 3 References: Radiology Interpreting images in the context of patient's history, easily collected from a specific written questionnaire (Fig 4) distributed in the waiting-room before the scan is performed Page 6 of 38

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8 Fig. 4 Only then can the systematic questioning using the FI_BRO-VA_GA_KIT mnemonic be applied: THREE CORE QUESTIONS Are they interstitial lesions producing FIbrosis and architectural distortions? (FI) Are there any BROnchial or bronchiolar abnormalities? (BRO) Are they any cardio-vascular abnormalities? (VA) TWO GAMMUT HELP (GA) Is the disease producing consolidating areas (or macro-nodules or masses)? Is the disease producing cysts? THREE ETIOLOGIES NOT TO BE MISSED: regardless of findings, could the abnormalities be secondary to Oncologic pathology? (K) Infectious agent?(i) Treatment toxicity? (T) The purpose of this work is neither to detail each aetiology which would need hundreds of pages, nor to display exhaustive lists of differential diagnoses. These matters are treated in excellent comprehensive textbooks. It is rather to gather scanographic findings belonging to each of these categories, to list the most frequent related aetiologies and to grade difficulties in diagnosing them. [MDT] will be placed adjacent to diseases most frequently requiring multidisciplinary expert opinions and additional tests such as lung biopsies. These questions will be treated both in acute and in chronic (or sub-acute situations): Imaging findings OR Procedure details PROCEDURE DETAIL 1. Are they interstitial lesions producing fibrosis? (FI) Page 8 of 38

9 Scanographic findings suggesting fibrosing lung disease The most specific elements: Segmental, lobar or lung volume loss Architectural distortion and fissural displacement (best seen on coronal reconstructions) Traction bronchiectasis or bronchiolectasis Honeycombing Reticulations created by intra-lobular septal thickening Frequently associated but less specific elements Inter-lobular septal thickening Ground-glass areas in particular when they are associated with traction bronchiectasis Fig 5 Fig. 5 Differential diagnoses for diffuse fibrosing lung disease Page 9 of 38

10 Chronic respiratory symptoms Sarcoïdosis: Upper lobe distribution, lymphatic micronodules along pleura, fissures and bronchovascular bundles, galaxy sign, mediastinal and hilar lymphadenopathy (eggshell calcifications). Relatively easy to diagnose when typical, however a range of atypical manifestations provides a challenge for radiologists [MDT] Idiopathic Pulmonary Fibrosis (IPF) also referred to as Usual Interstitial Pneumonia (UIP) by pathologists: Typically man in his 60s, apicobasal gradient, sub pleural honeycombing, reticulations, volume loss. Easy to diagnose when typical, poorest prognosis of ILD [MDT] Non specific interstitial pneumonia (NSIP): Ground glass attenuation in subpleural regions without apico-basal gradient, reticulations, no or little honeycombing [MDT] Chronic hypersensitivity pneumonitis (CHP): History of exposure, can be very similar to NSIP or UIP, reticular changes, little honeycombing. More specific findings include ground-glass micronodules (associated lesion of acute hypersensitivity), head-cheese sign (combination of hypo-attenuated lobules, ground-glass areas and normal lung), cysts, air trapping [MDT] Asbestosis:Sub pleural basal reticulations and honeycombing. Can show the same features as IPF, more specific elements are provided by pleural disease: pleural plaques, crow's feet images, parenchymatous bands and entrapped atelectasis [MDT] Interstitial fibrosing lesions secondary to drug toxicity can take a variety of appearances as described in the last chapter [MDT] Fig 6 Page 10 of 38

11 Fig. 6 Key point 1: Multiple etiologies can hide behind the UIP and NSIP radiological and histological patterns: connective tissue diseases, drug toxicity, environmental exposure, trauma or vasculitides amongst others. Key point 2: Chronic hypersensitivity, asbestosis and drug toxicity causing fibrosing lung disease can show either UIP or NSIP radiological-histological patterns, or more characteristic appearances allowing for specific diagnosis. These overlaps result in great diagnostic difficulties and except for some typical cases of IPF, sarcoidosis or asbestosis, diffuse fibrosing diseases require MDT review and additional investigations such as BAL and lung biopsies. Key point 3: Localised areas of fibrosis can also occur Following radiotherapy treatment (easily identifiable in the context) Page 11 of 38

12 In association with ankylosing spondylarthropathy (bi-apical fibrosis) Secondary to infectious episodes (suggesting a history of tuberculosis when there is apical sub pleural fibrosis associated with areas of calcifications) Acute or sub acute respiratory symptoms Acute interstitial pneumonia (AIP) observed in clinical setting of Acute Respiratory Distress Syndrome (ARDS): patchy bilateral geographical areas of ground glass attenuation rapidly progressing, dense consolidation areas in dependant lungs, distortion and reticulations, association with OP patterns. Radiological recognition of this pattern is necessary as it allows rapid management of the patient in intensive care units improving the prognosis of this severe condition. Organizing Pneumonia (OP) [MDT] Transient and migratory findings, subpleural, basal, peribronchovascular or perilobular airspace consolidations, nodules (mixed density), ground glass, reverse halo sign, large curvilinear bands, architectural distortion. Eosinophilic Pneumonia (EP) [MDT] Multiple sub pleural consolidation areas (reverse bat-wing sign), upper lobes predominance, elements of architectural distortion, findings transient and migratory Fig 7 Page 12 of 38

13 Fig. 7 Key point 1:Traction bronchiectasis can be reversible in these cases Key point 2: Since 2002 IPF, NSIP, OP and AIP are classified in the complex family of interstitial pneumonias (IP). These clinical-radiological-pathological entities can be idiopathic (IIP) or secondary to multiple aetiologies. The IPs family also includes three "non macroscopically fibrosing" diseases: Respiratory Bronchiolitis with Interstitial Lung Disease (RB-ILD), Desquamative Interstitial Pneumonia (DIP), both secondary to smoking toxicity, and Lymphoid Interstitial Pneumonia (LIP) [5, 6]. 2. Are there any bronchial or bronchiolar abnormalities? (BRO) Page 13 of 38

14 Bronchial tree abnormalities allow for different features on CT scan dependent on the proximal or the distal situation of the lesions Scanographic findings suggesting bronchial pathology Proximal bronchial abnormalities Bronchial wall thickening Cylindric, varicose or cystic bronchiectasis, not to be confused with traction bronchiectasis. Mucoid impaction, diagnosed by observing bronchial lumen's permeability when scrolling through axial views Bronchocele Key point. Diffuse thickening of bronchovascular bundles can be misleading as it can also be secondary to venous or lymphatic dilatation rather than bronchial mucosal thickening. Association with other cardio-vascular or lymphatic lesions are diagnostic clues in such cases (refer to next chapters). Distal bronchial abnormalities and small airway disease (airways with internal diameter equal to or smaller than 2 mm) Bronchiolectasis Branching micronodules and tree-in-bud pattern Acinar rosettes (coalescence of branching micronodules) Poorly defined centrilobular micronodules Mosaic attenuation pattern Air trapping on expiratory scans Emphysema (centrilobular, paraseptal or panlobular), arguably classified in this category being the end-stage of bronchiolo-alveolar and acinar destruction. Fig 8 Page 14 of 38

15 Fig. 8 Fig 9 Page 15 of 38

16 Fig. 9 Fig 10 Page 16 of 38

17 Fig. 10 Differential diagnoses for MPLAs of bronchial origin Chronic respiratory symptoms Asthma: bronchial wall thickening, small airway disease Bronchiectasis (can be secondary to multiple aetiologies including cystic fibrosis, chronic infection or inflammation, proximal airways obstruction) Chronic bronchitis (smoking related or not): non specific bronchial wall thickening Chronic bronchiolitis and small airway disease: most frequently constrictive obliterative bronchiolitis [MDT] which can be secondary to multiple conditions such as infection, auto-immune disorders, connective tissue diseases, toxic inhalation or drugs Emphysema Key point 1.Bronchial and bronchiolar abnormalities are often associated and non specific. The interest of CT scan in those cases is mostly to confirm a clinical diagnosis Page 17 of 38

18 and to evaluate the extent of the lesions. CT may also depict inflammatory or infectious complications superadded on chronic changes: consolidation areas, mucus plugging, segmental atelectasis or post-obstructive pneumonia which could prove reversible under antibiotic treatment. Key point 2. Cigarette smoking is one of the best provider of chronic bronchial disease. Tobacco toxicity can produce a wide range of lung lesions to be recognized as a group of diseases because there can be varying combinations of these lesions in the same heavy smoker Fig. 11 Fig. 11 Acute respiratory symptoms When acute respiratory symptoms are associated with localized or diffuse bronchial wall abnormalities adjacent to nodules or consolidation areas, the first diagnostic to suggest is Infection Page 18 of 38

19 Fig. 12 Fig. 12 Keypoint 1: CT findings prove of little specificity for responsible germ in pulmonary infection but location of the lesions can suggest some diagnosis: abnormalities in apical segments of upper and/or lower lobes should raise the possibility of mycobacterial infection, especially if it is associated with bronchial wall thickening, acinar rosettes, branching nodules and excavating lesions. Alternatively, bronchial wall thickening and areas of consolidation in dependant areas of the lungs can be suggestive of aspiration pneumonia. Keypoint 2: Organizing pneumonia can also be associated with focal areas of bronchial thickening and consolidations areas but the diagnosis is often made retrospectively when there is no response to antibiotic treatment [MDT] 3. Are they any cardio-vascular abnormalities? (VA) Page 19 of 38

20 Observing the heart and the pulmonary vessels is mandatory, given the frequency of cardio-vascular diseases and the anatomical-physiological interdependency of pulmonary and cardio-vascular systems. Cardiovascular anatomy to be reviewed Left ventricle (LV) tranversal size (<5.7 cm), right ventricle (RV) transversal size (ratio RV/LV<1.1), left atrium and right atrium appearances. Main pulmonary artery (PA) diameter (<33mm, PA/Ascending Aorta ratio <1.1), lobar and segmental pulmonary arteries (artery/bronchus ratio <1.25) and when available enhanced pulmonary arteries have to be screened as incidental thrombi might be discovered in non-dedicated CT scans Bronchial arteries diameter (<1.5mm), interest of MIP reconstructions Pulmonary veins appearance: normal proximal smooth tapering Coronary or valvular calcifications Fig 13 Fig. 13 Page 20 of 38

21 Differential diagnoses of MPLA secondary to cardio-vascular dysfunction Left cardiac failure and interstitial pulmonary oedema Thrombo-embolic disease (acute or chronic) Pulmonary arterial hypertension Fig 14 Fig. 14 Key point 1: In all cases, pleural or fissural effusion is suggestive of interstitial oedema, unless there is an obvious inflammatory pleural process often associated with thickened enhancing pleura. Interstitial edema can be cardiogenic (hence the interest of screening cardiac elements), secondary to fluid overload or to lung injury (permeability edema) Key point 2: However minor, cardiac failure has to be depicted on CT scan, especially if it complicates underlying lung disease: not only will Furosemide treatment quickly improve Page 21 of 38

22 respiratory symptoms, but also a repeat CT scan after a few days of treatment will allow proper reassessment of lung fields without the ground glass and septal lines secondary to the cardiac pathology. Fig 15 Fig. 15 Key point 3: There is a rare condition called pulmonary veno-occlusive disease, revealed by a combination of findings from pulmonary hypertension and pulmonary interstitial edema (without evidence of left cardiac dysfunction). This condition is important to recognize as it is a contraindication to anti-pulmonary-hypertension treatment [MDT] 4. GAMMUT HELP Once the "core" origin of the lesions has been looked for, diagnostic possibilities are still vast. It is useful to know a couple of lists of differential diagnoses for potentially discriminating lesions such as areas of consolidation or parenchymal lung cysts. Page 22 of 38

23 a/ Is the disease producing consolidating areas? Unique or multiple consolidating areas reflect dense parenchymal filling which can be produced in many different conditions: context and clinical information are mandatory to narrow the list Cavitation or surrounding ground glass may also help to narrow the list and will be mentioned when commonly associated. The attenuation characteristics are described when helpful Evolution of the consolidation over time is another discriminating element hence the necessary review of previous examination when available. Consolidation and ground glass attenuation can take a confusing, sponge-like appearance when there is a background of honeycombing or emphysematous parenchymal lung destruction Fig 16 Page 23 of 38

24 Fig. 16 Patient with normal immune status Etiologies Cavitation GG Consolidation Discriminating elements Infectious pneumonia + ++ Bronchial wall thickening in the same territory Page 24 of 38

25 Incl. community acquired pneumonias and atypical germs Lung infarct rare + Pleurally based Central lucencies No air bronchogram Adenocarcinoma bronchioloalveolartype + ++ Distorted bronchi Sponge appearance like Non resolving lung changes Organizing Pneumonia ++ Migratory changes Peripheral, peribronchovascular and perilobular changes Eosinophilic pneumonia ANCA-associated granulomatous vasculatides Migratory changes ++ Migratory changes Associated nodules and masses GG secondary to alveolar hemorrhage Lung lymphoma + Dense homogeneous condensation Angiographic sign Diffuse alveolar haemorrhage +++ Rapid changes and resolution Acute interstitial pneumonia +++ Dependant areas Ground glass Page 25 of 38

26 Radiation pneumonitis ++ Sarcoidosis Lipoid pneumonia Medical history Alveolar form of the disease ++ Decreased attenuation of condensation with negative fatty HU values (pathognomonic) Crazy paving Amiodarone toxicity Increased attenuation condensation possible calcifications of and Fig 17 Page 26 of 38

27 Fig. 17 Immuno-suppressed patient in addition to all of the above Invasive aspergillosis (neutropenic patients): nodules surrounded by ground glass (halo sign) Infection: CMV, HSV, candida Kaposi sarcoma Key point 1: Angio invasive aspergillosis is an emergency in immuno-compromised patients. In this context, the presence of consolidation areas or nodules surrounded by GG should be considered angio-invasive aspergillosis until proven otherwise. Key point 2: Multiple lung nodules or masses share a close list of differential diagnoses with multiple consolidation areas. In addition to all of the above aetiologies, they can also be caused by metastases, septic emboli and lung abscesses, Langerhans cell Histiocytosis and rheumatoid nodules, which can all cavitate b/ Is the disease producing cysts? Page 27 of 38

28 Cysts are round parenchymal thin-walled lucencies with no central artery (the differentiation with centrilobular emphysema can be difficult). One or two elements can be physiological in elderly patients (>75 years old) but when more numerous, most frequent diagnoses are Langerhans cell histiocytosis Lymphangiomyomatosis Sub-acute or chronic hypersensitivity pneumonitis Desquamative interstitial pneumonia (smoker) Lymphoid interstitial pneumonia (connective tissue background or HIV status) Pneumocystis Jiroveci pneumonia (immuno-compromised patient) in a sub acute form Fig 18 Fig. 18 Page 28 of 38

29 Key point: This list is exclusive of the characteristic honeycombing sub-pleural cysts seen most frequently in IPF. 5. ETIOLOGIES NOT TO BE MISSED At the end of the check list and no matter what conclusions have been drawn so far, three "not-to-be missed" aetiologies have to be reviewed: Could the abnormalities be due to oncologic or infectious lesions? In these two cases, complementary examinations and treatment have to be urged. And eventually, could the changes encountered be of iatrogenic origin and then simply stopping the treatment could improve the situation. These 3 aetiological groups can show polymorphic and often non specific findings. They are unavoidable overlaps with the above sections. Cancer (K) Oncologic findings: "ring an onco-bell" signs A few signs must alert on the possibility of underlying malignancy Sub-pleural or scissural micronodules (DD: sarcoidosis) Micro nodular thickening of interlobular septae or beaded septum sign (DD: sarcoidosis). Irregular thickening of bronchovascular bundles (DD: sarcoidosis) Micronodular miliary: can be of metastatic or infectious in origin (TB, viral) Multiples round lung nodules of different sizes in random distribution (main differential diagnosis: septic emboli) Persisting consolidation areas or lung changes despite antibiotic treatment: raises possibility of adenocarcinoma Solitary nodule over one centimetre in size of mixed attenuation (combination of consolidation and ground glass areas), ground-glass attenuation or spiculated shape Golden S sign: area of atelectasis adjacent to a fissure with a convex bulge (S shaped fissure) suggesting possible underlying mass Circumferential pleural thickening reaching mediastinal pleural surface: adenocarcinoma, mesothelioma. Mediastinal lymphadenopathies suspicious in size or number Bone destruction (in particular when adjacent to pulmonary lesion) Hepatic or adrenal lesions Page 29 of 38

30 Fig 19 Fig. 19 Keypoint: Sub-pleural or fissural micronodules, micro nodular thickening of interlobular septae (beaded septum sign) and irregular thickening of bronchovascular bundles are secondary to lymphatic spread of micronodules and raise two differencial diagnoses: Sarcoidosis and lymphangitis carcinomatosa. In the latter case, abnormalities are frequently asymmetrical and associated with pleural effusion. Etiologies of MPLAs of carcinologic origin Classical broncho-pulmonary carcinoma is usually revealed on CT-scan by a lung mass and diagnosed on lung biopsy. However, confusing multiple parenchymal lung abnormalities can reveal three forms of lung malignancies : Adenocarcinoma of bronchioloalveolar-type Lymphangitis carcinomatosa Lung lymphoproliferative disorders. Page 30 of 38

31 Fig 20 Fig. 20 Keypoint: Bronchioloalveolar carcinoma is arguably one of the most difficult diagnosis to suggest given the multiple forms it can take. Therefore it has to come first in the list of DD in front of non resolving lung changes. Pulmonary infection (I) Depending on the septicemic or bronchogenic nature of the contamination, and given the size and the behaviour of the pathologic agent, pulmonary infection can take multiple clinical and radiological appearances Page 31 of 38

32 Hematogeneous dissemination Septic emboli: one or numerous peripheral nodules potentially cavitating and transforming into pulmonary abscesses (can be secondary to endocarditis or IV drug injections) Miliary: diffuse randomly distributed micronodules, classically secondary to lymphohematogenous spread of tuberculosis. Can also be a feature of disseminated viral or fungal infection, or metastatic disease Bronchogenous dissemination Non specific infectious bronchitis: diffuse bronchial wall thickening Broncho-pneumonia: localized bronchial wall thickening adjacent to areas of consolidation Disseminated infectious bronchiolitis: diffuse branching micronodules Localized infectious bronchiolitis: bronchial wall thickening, discrete foci of branching micronodules, acinar rosettes resulting from micronodular coalescence, patchy areas or nodular consolidation. Atypical infection Mixed anomalies consisting of blurred nodules, non systematized ground glass areas, interlobular septal thickening and/or pleural effusion are in keeping with atypical pneumonia (viruses, Mycoplasma, Chlamydia, Legionnella). Immuno-compromised host Immunocompromised patients are at risk no only for developing all of the above infections, sometimes in an atypical manner, but also for opportunistic infections, never encountered in patients with normal immunity. Awareness of the type and severity of the immunologic status can be helpful in predicting the most likely organisms responsible for the infection. However immune status of the patient or VIH serology are not always known and a few weeks of steroid treatment can rapidly trigger immuno-suppression. Opportunistic infections have to be recognised in all centres whether they are used to deal with such patients or not. The two commonest pulmonary infections in immuno-compromised patients are Page 32 of 38

33 PCP: Extensive bilateral ground-glass opacities more marked in the upper lobes and sparing the sub-pleural regions, crazy-paving (the same findings can be seen in cytomegalovirus infections), superadded thin-walled cysts in the subacute form of the disease. Angio-invasive aspergillosis: nodules larger than one centimetre surrounded by a halo of ground glass attenuation with possible cavitation. Fig 21 Fig. 21 Keypoint: In front of large ground-glass areas predominant in upper lobes and respecting sub-pleural areas, Pneumocystosis infection has to be suggested and immune and HIV status of the patient are to be verified. Treatments, drug toxicity and iatrogenic lung disease (T) Page 33 of 38

34 Iatrogenic lung lesions can be secondary to oral treatment (short course or long term treatments) including over-the-counter medication, illicit drug use, herbal remedies, radiotherapy or nasal drop inhalation. Symptoms vary from cough and insidious progressive dyspnea to acute respiratory failure. Pulmonary drug toxicity can take the appearance of virtually every MPLA (IPF, NSIP, AIP, OP, CHS, Sarcoïdosis, interstitial oedema, intra-alveolar haemorrhage, small airway disease) hence the necessity of gathering information regarding patient's treatment. Nowadays, medical websites can prove very helpful in this matter: lists all drugs implicated in lunginjury and provides an estimate of the frequency of toxicity. HRCT is rarely specific for a drug aetiology, but a few situations are easily identified Post irradiation pneumonitis: In the acute phase, ground-glass opacities and consolidation areas appear typically 6 to 8 weeks after starting the treatment, and progress towards fibrosing lung changes within the field of radiations. Secondary organizing pneumonia can also be the consequence of radiation injury, not necessarily in the field of radiation and possibly months or years after treatment. Lipoid pneumonia appears after chronic aspiration of mineral oils, (laxative per os or oily nose drops). Low density and fatty attenuation areas of consolidation in dependant areas of the lungs are pathognomonic. They can be seen in association with crazy paving and areas of reticulation Amiodarone toxicity can be triggered by multiple different mechanisms and take different patterns. Classical findings consist of diffuse reticular opacities without any volume loss, multifocal consolidation areas, high attenuation parenchymal or pleural opacities and increased liver and spleen attenuation. Key point: Check website every time. What has not been covered? Bad news: Even when mastering all of the above knowledge, a large number of diseases are still not covered by this method (alveolar proteinosis, different types of granulomatous vasculitides, specific forms of lung diseases in collagen disorders, alveolar micro-lithiasis, broncho-pulmonary amyloïdosis, hemangiopericytosis, follicular bronchiolitis ) Good news: These diseases are rare Some of them have characteristic appearances and a pictorial atlas could help non specialists to suggest the right diagnosis Page 34 of 38

35 They are usually diagnosed at MDT meetings following additional tests and expert discussions. Conclusion Remember FI_BRO_VA_GA_KIT, it takes more time to say it than to check it. Fig 22 Fig. 22 Patient medical history is needed in order to narrow the differential diagnosis lists when confronted to MPLAs. Smoking habits and medication are particularly relevant. Page 35 of 38

36 "Frequent things are frequent": infection (treatable), left cardiac failure (treatable), thrombo-embolic diseases (treatable), COPD, cancer and classical form of UIP. They can be diagnosed by every radiologist with special mention to characteristic findings in tuberculosis, PCP and angioinvasive aspergillosis. They may also be combined with other diseases. Fibrosing chronic lung diseases are challenging and final diagnosis usually relies on MDT discussions and additional diagnostic tools. However, the acute form of interstitial lung disease (acute interstitial pneumonia) should be recognised as early treatment in intensive care units improves the prognosis. Smoking related lung diseases include multiple pathologies potentially overlapping in the same patient: chronic bronchitis, emphysema, UIP, BR-ILD, DIP, LCH and lung cancer. Adenocarcinoma of bronchioloalveolar type should be considered when persisting consolidating lung changes are observed. Exploring possible drug toxicity may also help to explain abnormal CT findings ( Systematically answering these questions keeps the most frequent diagnoses in mind, allows a methodological approach in the presence of overlapping thoracic pathologies and facilitates identification of situations in need of urgent treatment. Although not comprehensive, this mnemonic can be used as a base to deepen knowledge in each category of disease. References 1: American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumo- nias (2002) This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Executive Committee, June Am J Respir Crit Care Med 165: : Hansell DM, Bankier AA, MacMahon H, McLoud TC, Müller NL, Remy J. Fleischner Society: glossary of terms for thoracic imaging. Radiology 2008 Mar;246(3): : Webb WR. Thin-section CT of the secondary pulmonary lobule: anatomy and the image: 2004 Fleischner lecture. Radiology 2006 May;239(2): Page 36 of 38

37 4:Beigelman-Aubry C, Hill C, Guibal A, Savatovsky J, Grenier PA. Multi-detector row CT and postprocessing techniques in the assessment of diffuse lung disease. Radiographics 2005 Nov-Dec;25(6): : Mueller-Mang C, Grosse C, Schmid K, Stiebellehner L, Bankier AA. What every radiologist should know about idiopathic interstitial pneumonias Radiographics May-Jun;27(3): Review. 6: Walsh SL., Hansell DM. Diffuse interstitial lung diseases: overlaps and uncertainties, Eur Radiol : : Attili AK, Kazerooni EA, Gross BH, Flaherty KR, Myers JL, Martinez FJ. Smoking-related interstitial lung disease: radiologic-clinical-pathologic correlation Radiographics Sep-Oct;28(5): : Hansell DM, Lynch DA, McAdams HP, Bankier AA. Imaging diseases of the chest, Mosby Elsevier : Muller NL, Silva CI. Imaging of the chest, Saunders Elsevier : Remi-Jardin M, Remy J. Integrated cardiothoracic imaging with MDCT, Springer, : Webb WR, Muller NL, Naidich DP. High resolution CT of the lungs, Philadelphia, Lippincott Williams and Wilkins, 2008 Personal Information Dr Marie Baque-Juston, MD, FRCR Service de Radiologie Hopital Pasteur 30 avenue de la Voie Romaine Page 37 of 38

38 Nice Cedex 1 France Contact: mariejuston@sfr.fr baque-juston.mc@chu-nice.fr Page 38 of 38