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APPROACH TO RETICULONODULAR PATTERN IN HRCT

APPROACH TO RETICULONODULAR PATTERN IN HRCT

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  • 1.Nodular peribronchovascular interstitial thickening in a patient with sarcoidosis. Numerous small nodules surround central bronchi and vessels.2.
  • patient with right lung carcinoma shows smooth thickening of interlobular septa (small arrows) in the right upper lobe. Thickening of the peribronchovascular interstitium results in apparent increased thickness of right-sided bronchi (large arrow). Right pleural effusion is also present. Left lung appears normal.
  • Cut surface of lung in a different patient with lymphangitic spread of neoplasm. Smooth thickening of interlobular septa (small arrows) and peribronchovascular interstitium (large arrow) are seen.
  • Intralobular interstitial thickening reflects thickening of distal peribronchovascular interstitial tissue and the intralobular interstitium.Most commonly associated with lung fibrosis, like UIP or asbestosis.
  • Parenchymal bands represents areas of peribronchovascular fibrosis, coarse scars or atelectasis associated with lung infiltration or pleural fibrosis.
  • Notice the ground glass opacity in the left lower lobe as a result of fibrous tissue replacing the air in the alveoli. There is also a lower lobe predominance and widespread traction bronchiectasis
  • Honeycombing » air filled cysts » irregular septal linesSubpleural location

Hrct ii Hrct ii Presentation Transcript

  • PRESENTED BY : DR SHAMIMGUIDED BY : DR A PATIL (MD)GMC BHOPAL
  • Interpretation of interstitial lung diseases isbased on the type of involvement of thesecondary lobule.
  •  Centrilobular area diseases, that enter the lung through the airways  ( i.e. hypersensitivity pneumonitis, respiratory bronchiolitis,). Perilymphatic area diseases, that are located in the lymphatics of in the interlobular septa  ( i.e. sarcoid, lymphangitic carcinomatosis, pulmonary edema). These diseases are usually also located in the central network of lymphatics that surround the bronchovascular bundle.
  • This exhibit was displayedat the 72nd scientificassembly and annualmeeting of theRadiological Society ofNorth America 30th Nov –5th Dec, 1986, Chicago, Illinois. Itwas recommended by thePanel and was acceptedfor publication on august3. 1987.
  • 3 steps
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES Represents thickening of interstitial fibers of lung by - fluid or - infiltration by cells or - fibrous tissue Either as a result of thickening of  peribronchovascular interstitium  interlobular septa Or as a result of fibrosis as in honeycombing.
  • SMOOTH • Pulmonary edema/ hemorrhage • Lymphoma / leukemia (Venous, lymphatic ) • Lymphangitic spread of carcinoma NODULAR • Sarcoidosis(lymphatic or infiltrative • Lymphangitic spread of carcinoma diseases) IRREGULAR • TB (Due to adjacent lung • Sarcoidosis, fibrosis ) • Silicosis, talcosis
  • NodularSmooth
  • Nodular 26
  • 27
  •  Outline secondary pulmonary lobule, Often well depicted in the apices Perpendicular to the pleura if present in periphery Most Common Causes 1. pulmonary edema 2. pulmonary hemorrhage 3. lymphangitic cancer spread
  •  Smooth  Nodular  IrreguarD/D are similar to that of PBIT.
  • Thickened SeptaPulmonaryveins SMOOOOTHHH...
  • SMOOOOTHHH...
  • Interlobular septalthickening associatedwith several septalnodules givingbeaded appearance
  • • Indicate fibrosis
  • Irregular reticular opacities(arrows) in a patient withidiopathic pulmonary fibrosisshows
  • smooth thickeningof interlobularseptaPeribronchovascularInterstitium thickening SMOOOOTHHH... Effusion
  •  Lymphangitic Carcinomatosis results from hematogenous spread to the lung, with subsequent invasion of interstitium and lymphatics. Seen in carcinoma of the lung, breast, stomach, pancreas, prostate, cervix, th yroid and metastatic adenocarcinoma from an unknown primary
  • Histologic specimen in patientwith lymphangitic spread oftumor shows secondarypulmonary lobule with nodulesof tumor (large arrows) in theinterlobular septa. Tumor (smallarrow) is also visible incentrilobularperibronchovascular region.
  •  Thickening of fissures and peribronchovascular interstitium (bronchial cuffing). Interlobular septal thickening, Focal or unilateral abnormalities in 50% of patients. Depending on filling with fluid or with tumor cells, septal thickening is irregular or smooth. Hilar lymphadenopathy in 50% Pleural effusion due to pleuritic carcinomatosis ( > 50% of patients).
  •  Identical findings can be seen in Lymphoma and in children with HIV infection, who develop Lymphocytic interstitial pneumonitis (LIP) , a rare benign infiltrative lymphocytic disease.
  • Focal Distribution.This finding distinguishingfrom other causes ofinterlobular septalthickening like pulmonaryedema or sarcoid.There is alsolymphadenopathy
  • A central bronchogenic carcinoma (blue arrow) is producing unilateral interstitial edema (bluecircles) characteristic of lymphangitic carcinomatosis with a pleural effusion (redarrow), thickening and irregularity of the bronchovascular bundles (yellow arrow) and thickeningof the interlobular septa (light blue arrow).
  •  Bilateral septal thickening Ground-glass opacity. Perihilar and gravitational distribution predominatly in the dependent lung. Pleural fluid. Cardiomegaly
  • Thickened SeptaPulmonaryveins SMOOOOTHHH...
  • SMOOOOTHHH...
  • There is smooth septal thickening and ground glass opacity in thedependent part of the lungs.Bilateral pleural fluid.
  •  Lymphangitic carcinomatosis Interstitial pneumonia (viral, mycoplasma) ARDS Pulmonary hemorrhage
  •  Results in a fine reticular pattern, with the visible lines separated by a few mm Fine lace- or netlike appearance Causes : Pulmonary fibrosis Asbestosis Chronic Eosinophilic pneumonitis. 58
  •  Non tapering , reticular opacity usually 1 to 3 mm in thickness and from 2 to 5 cm in length. Is often peripheral and generally contracts the pleural surface D/D : 1. Tuberculosis with scar. 2. Asbestosis 3. Silicosis/ coal worker 4. Sarcoidosis 60
  •  Clustered cystic air spaces, of comparable diameters (3–10 mm) characterized by well-defined walls composed of dense fibrous tissue. Honeycombing suggests extensive lung fibrosis with alveolar destruction . Honeycombing is the typical feature of usual interstitial pneumonia (UIP).
  •  Often predominate in the peripheral and sub- pleural lung regions regardless of their cause. Typically occur in several contiguous layers.  This finding can allow honeycombing to be distinguished from paraseptal emphysema in which subpleural cysts usually occur in a single layer.
  • Typical UIP pattern with honeycombing and traction bronchiectasis ina patient with idiopathic pulmonary fibrosis
  • HONEYCOMBING Lower lobe Upper lobe predominance : predominance :• UIP • End stage • IPF sarcodosis • Connective • Radiation tissue disorders • End stage ARDS • Asbestosis• NSIP (rare)
  • LINEAR AND RETICULAR OPACITIES NODULES AND INCREASED LUNG NODULAR ATTENUATION OPACITIES PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSE MA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • Nodules can be classified according to their ,  Distribution in relation to other lung structures  Centrilobular,  Perilymphatic,  Random.  Appearance  Well-defined (likely interstitial) or  Ill -defined (likely air-space)
  •  Centrilobular Perilymphatic  Random
  • IS IT IN CONTACT WITH PLEURA NO YESCENTRILOBULAR PERILYMPHATIC RANDOM
  • IS IT IN CONTACT WITH PLEURA NO YESCENTRILOBULAR PERILYMPHATIC RANDOM
  •  Distributed primarily within the centre of the secondary pulmonary lobule Reflect the presence of either airspace or interstitialabnormalities Sub pleural lung(5-10mm from fissures or the pleural surface) is typically spared, distinguishes from diffuse random nodules. 86
  •  Infectious airways diseases  endobronchial spread of mycobacteria ( tuberculosis or nontuberculous)  bronchopneumonia Hypersensitivity pneumonitis Respiratory bronchiolitis Uncommon in  Bronchioloalveolar carcinoma,  Pulmonary edema,  Vasculitis
  •  Centrilobular nodules may be further characterized by presence or absence of ‘‘tree-in-bud.’’
  • WITH TREE-IN-BUD OPACITY WITHOUT TREE-IN-BUD OPACITY  All causes of tree-in-bud Typical and atypical opacity mycobacteria infections  Hypersensitivity Bacterial pneumonia pneumonitis Diffuse panbronchiolitis  COP Bronchiolitis  Pneumoconioses Aspiration  Langerhans’ cell ABPA histiocytosis Cystic fibrosis  Pulmonary edema Endobronchial-neoplasms  Vasculitis (particularly broncho  Pulmonary hypertension alveolar carcinoma) 90
  •  Impaction of centrilobular bronchus with mucous, pus, or fluid, resulting in dilation of the bronchus, with associated peribronchiolar inflammation . Dilated, impacted bronchi produce Y- or V-shaped structures Centrilobular dots and linear branching opacities This finding is almost always seen with pulmonary infections
  • Tree-in-budopacities,consisting ofbranchingstructures (blackarrows) and buds(white arrows).
  •  Endobronchial spread of infection (TB, MAC, any bacterial bronchopneumonia) Airway disease (cystic fibrosis, bronchiectasis) Less often, an airway disease associated primarily with mucus retention (allergic bronchopulmonary aspergillosis, asthma).
  •  Infections  Aspiration or inhalation of  Bacterial foreign substances  Fungal  Immunologic disorders  Viral  Connective tissue disorders Congenital disorders  Rheumatoid arthritis  Cystic fibrosis  Sjögren syndrome  Kartagener syndrome  Peripheral pulmonary ABPA vascular disease Obliterative bronchiolitis  Idiopathic disorders Diffuse panbronchiolitis
  • Typical Tree-in-bud appearance in a patient with active TB
  • Impacted mucus- and pus-filled bronchioles (arrows)are visible throughout thelung; this is the pathologicexamination equivalent ofthe tree-in-bud sign.
  • WITH TREE-IN-BUD OPACITY WITHOUT TREE-IN-BUD OPACITY  All causes of tree-in-bud Typical and atypical opacity mycobacteria infections  Hypersensitivity Bacterial pneumonia pneumonitis Diffuse panbronchiolitis  COP Bronchiolitis  Pneumoconioses Aspiration  Langerhans’ cell ABPA histiocytosis Cystic fibrosis  Pulmonary edema Endobronchial-neoplasms  Vasculitis (particularly broncho  Pulmonary hypertension alveolar carcinoma) 109
  •  In many cases centrilobular nodules are of ground glass density and ill defined They are called acinar nodules.
  • •The nodules are poorly definedand have ground-glassattenuation.•Measure 3-5 mm in diameter•Typically appear as clusters.•Centered a few millimetersaway from the pleuralsurfaces, interlobar fissures, andinterlobular septa .
  • Hypersensitivity pneumonitis.
  • Small arrows - Interlobular septa .Large arrows- Ill-defined peribronchiolar and alveolar infiltrates that predominate in center of a secondary lobule
  • Follicular Bronchiolitis
  • Diffuse panbronchiolitisSmall arrows outline a secondary lobule. Peribronchiolar infiltrates (large arrow)predominate in centers of several secondary lobules. Centrilobular bronchioles aredilated.
  • Ill defined centrilobular nodules of ground glass density in a patient withhypersensitivity pneumonitis
  • 25-year-old man with severe dyspnea after attic renovation. Chestradiographs (not shown) were normal. Thin-section CT (1.0-mmcollimation), initially interpreted as normal, shows, inretrospect, subtle centrilobular nodules (arrowhead).
  •  Also known as extrinsic allergic alveolitis (EAA). Allergic lung disease caused by the inhalation of a variety of antigens (farmers lung, bird fanciers lung, hot tub lung, humidifier lung). Classified into acute, subacute, and chronic stages. Mostly HRCT is performed in the subacute stage of HP, weeks to months following the first exposure to the antigen or in the chronic phase.
  • Centrilobular nodules in hypersensitivity pneumonitis.Histologic specimen shows ill-defined peribronchiolar and alveolar infiltrates(large arrows) that predominate in center of a secondary lobule. Interlobular septa (small arrows) outline parts of three lobules.
  • Subacute hypersensitivity pneumonitis with ill-defined centrilobular nodules
  • The key findings are: Ill-defined centrilobularground-glass nodules (80% of cases) Mosaic pattern : combination of patchy ground- glass opacity due to lung infiltration and patchy lucency due to bronchiolitis with air trapping
  • Subtle opacity in the centre of the secondary lobules (arrows)with sparing of the subpleural region.
  • Subtle ill-defined centrilobular opacity in a patient with subacute HP.
  • Sometimes the centrilobular opacities are more nodular in appearance
  • Mosaic Pattern.Some secondary lobules demonstrate ground-glass opacity due to lunginfiltration, while others are more lucent due to bronchiolitis with airtrapping
  • Patient who presented with acute dyspnoe and a normal chest film (not shown).The HRCT at presentation (left) shows lobular areas of ground glass attenuation.A control HRCT ten days later demonstrated, that the findings had resolved without anytreatment. The findings were thought to be due to hypersensitivity pneumonitis
  • The key findings in chronic hypersensitivity pneumonitis are: Mosaic pattern with areas of ground-glass atenuation and areas of low attenuation. Fibrosis and parenchymal distortion in a mid zone distribution.
  • The HRCT shows a mosaic pattern with hyperaerated secondarylobule and secondry lobule of increased attenuation.Additionally there is septal and intralobular reticularthickening, indicating already existing irreversible fibrosis
  •  Inspiratory and expiratory scan: the mosaic pattern with areas of ground-glass attenuation and areas of low attenuation, that become more evident on the expiratory scan, indicating air trapping. Signs of fibrosis such as distorted vessels and bronchi as well as septal thickening are more pronounced in the mid and lower lung zones, but not limited to the subpleural area. The images on the left suggest the diagnosis hypersensitivity pneumonitis. Based on the imaging findigs alone, alveolar proteinosis and other diseases with a mozaic pattern should be included in the differential diagnosis.
  •  Subacute stage:  RB-ILD: seen in smokers, upper lobe predilection, usually associated with centrilobular emphysema.  Alveolar proteinosis. Chronic stage:  UIP: may show very similar HRCT findings. UIP has a strong lower zone distribution. In chronic HP fibrotic changes are typically seen throughout the whole lung parenchyma from the periphery towards the centrum.
  • IS IT IN CONTACT WITH PLEURA NO YESCENTRILOBULAR PERILYMPHATIC RANDOM
  • IS IT IN CONTACT WITH PLEURA NO YESCENTRILOBULAR PERILYMPHATIC RANDOM
  • Centrilobular area in bluePerilymphatic area in yellow
  • Nodules in relation to pulmonary lymphatics at # perihilar peribronchovascular interstitium, # interlobular septa, # subpleural regions, and # centrilobular interstitium. 140
  •  Perilymphatic nodules are most commonly seen in sarcoidosis. They also occur in  Silicosis,  Coal-workers pneumoconiosis and  Lymphangitic spread of carcinoma. Notice the overlap in differential diagnosis of perilymphatic nodules and the nodular septal thickening .
  • Nodules along bronchi & septum + nodes
  • In addition to the perilymphatic nodules, there are multipleenlarged lymph nodes, which is also typical for sarcoidosis
  •  Sarcoidosis is a multi-organ granulomatous disease of unknown origin. It is characterized by non-caseating granulomas that may resolve spontaneously or progress to fibrosis Systemic symptoms : fatigue, night sweats and weight loss. Pulmonary manifestations are present in 90%.
  • Two photomicrographs demonstrating characteristic non-caseating granulomata (arrows):(A) centred on the bronchovascular bundle and (B) along an interlobular septum.
  • Detailed view with nodules along bronchovascular bundle (redarrow) and fissures (yellow arrow).This is the typical perilymphatic distribution of the nodules.
  •  The HRCT appearance of pulmonary sarcoidosis varies greatly and depend on disease stage and is known to mimic many other diffuse infiltrative lung diseases. 60 to 70% - have characteristic radiologic findings. 25 to 30% - findings are atypical. 5 to 10% - are normal.
  •  Lymphadenopathy in left hilus, right hilus and paratracheal (1-2-3 sign). Often with calcifications. Parenchymal involvement : Small nodules in a perilymphatic distribution (i.e. along subpleural surface ; fissures ; interlobular septa and the peribronchovascular bundle) Upper and midlle zone predominence With progression : bronchocentric scarring, more pronounced in the upper zones
  • Uncommon findings: Conglomerate masses in a perihilar location. Larger nodules (> 1cm in diameter) in Grouped nodules or coalescent nodlues surrounded by multiple satellite nodules (Galaxy sign) Nodules so small and dense that they appear as ground glass or even as consolidations (alveolar sarcoidosis)
  • Nodules along fissures(red arrows)- perilymphatic distributionNodules located along the bronchovascular bundle (yellowarrow).Nodules in the subpleural region and along the fissures, is veryspecific for sarcoidosis.
  • Chest films in sarcoidosis have been classified into four stages:1. Bilateral hilar lymphadenopathy2. Bilateral hilar lymphadenopath + pulmonary disease3. Only pulmonary disease4. Irreversible fibrosis These stages do not indicate disease chronicity or correlate with changes in pulmonary function.
  • Sarcoidosis stage I: left and right hilar There is hilar and paratrachealand paratracheal adenopathy (1-2-3 adenopathy and no sign of pulmonarysign) involvement.
  • Typical presentation of sarcoidosis with hilar and small nodules alongbronchovascular bundles (yellow arrow) and along fissures (red arrows)
  • Typical presentation of sarcoidosis .Always look for small nodules along the fissures, because this is a very specificand typical sign of sarcoidosis
  •  Progressive fibrosis in sarcoidosis may lead to peribronchovascular (perihilar) conglomerate masses of fibrous tissue. The typical location is posteriorly in the upper lobes, leading to volume loss of the upper lobes with displacement of the interlobar fissure. Other diseases that result in this appearance are:  Tuberculosis  Silicosis  Talcosis
  • Typical chest film of long standing sarcoidosis with fibrosis in theupper zones and volume loss of the upper lobes resulting in hilarelevation.
  • Notice the distribution of the conglomerate masses of fibrosis in the posterior partof the lungs. In addition there are multiple small well-defined nodules. Some ofthese nodules have the typical subpleural distribution.
  • Sarcoidosis with conglomerate masses of fibrous tissue
  • Nodules so small and dense that they appearas ground glass or even as consolidations
  • In this case the appearance resembles a ground glass attenuation, but with a close look you mayappreciate that the increased attenuation is the result of many tiny grouped nodules.Also notice the hilar lymphadenopathy
  •  Nodular pattern:  Silicosis / Pneumoconiosis: predominantly centrilobular and subpleural nodules.  Miliary TB: random nodules. Fibrotic pattern:  Usual Interstitial Pneumonia (UIP): basal and peripheral fibrosis, honeycombing.  Chronic Hypersensitivity Pneumonitis: mid zone fibrosis with mosaic pattern.  Tuberculosis (more unilateral) Lymphadenopathy:  Primary TB: asymmetrical adenopathy  Histoplasmosis  Lymphoma  Small cell lung cancer with nodal metastases
  •  Pathologically distinct entities  differing histology,  resulting from the inhalation of different inorganic dusts. The radiographic and HRCT appearances  may not be distinguishable from each other  may be similar to sarcoidosis. These diseases are rare compared to sarcoidosis and occur in a specific patient group (construction workers, mining workers, workers exposed to sandblasting, glass blowing and pottery).
  •  Small well-defined nodules 2 to 5mm in both lungs. Nodules may be calcified Upper lobe predominance Centrilobular and subpleural distribution Sometimes random distribution Irregular conglomerate masses, known as progressive massive fibrosis Masses may cavitate due to ischemic necrosis. Often hilar and mediastinal lymphnodes.
  • Nodules of varying sizes with a random and subpleural distribution. One nodulecontains calcification (arrow). Note the absence of a lymphatic distributionpattern (peribronchovascular and along fissures), which would be suggestive ofsarcoidosis.
  • Conglomerate mass in a perihilar location in the right upper lobe.The left lobe shows multiple nodules of varying size
  •  Sarcoidosis : can be difficult to distinguish (look for distribution of nodules along fissures). Infection: miliairy TB, fungus. Hematogenous metastases: silicotic nodules in subpleural and peribronchiolar location up to the level of the secundary pulmonary lobule, may have a seemingly random distribution and simulate metastases and miliary infections. Langerhans cell histiocytosis: can be difficult to distinguish from silicosis in the early stage, when LCH is solely characterized by the presence of small nodules. Look for nodules with cavitation
  • IS IT IN CONTACT WITH PLEURA NO YESCENTRILOBULAR PERILYMPHATIC RANDOM
  • IS IT IN CONTACT WITH PLEURA NO YESCENTRILOBULAR PERILYMPHATIC RANDOM
  •  Nodules are randomly distributed relative to structures of the lung and secondary lobule. Random nodules are usually well-defined and appear diffuse, but uniform in distribution Nodules can involve the pleural surfaces and fissures, but lack the subpleural predominance The random distribution is a result of the hematogenous spread of the infection.
  •  Hematogenous metastases Miliary tuberculosis Miliary fungal infections Langerhans cell histiocytosis (early nodular stage) Wegener granulomatosis Sarcoidosis (when very extensive)
  • Miliary TB
  • Metastases
  • LEFT: miliary TB RIGHT: metastases
  •  An uncommon disease characterised by multiple cysts in patients with nicotine abuse. Very early stage, show only nodules, Later , cavitate and become cysts . Upper lobe predominance,as in all smoking related diseases,
  • early nodular stage before the typical cysts appear
  • Early nodular stage before the typical cysts appear
  • • Random – touch pleura – scattered in lung• Centrilobular –away from pleura• Perilymphatic – around vessels, bronchi – touch pleura or fissure
  • Miliary : <3 mm Small Nodules: <10 mmSize Large Nodules: >10 mm Masses : >3 cms 193
  • Interstitial opacity:  Well-defined, homogenous, Soft-tissue density Obscures the edges of vessels or adjacent structureAppearance Air space: Ill-defined, inhomogeneous. Less dense than adjacent vessel – GGO small nodule is difficult to identify 194
  • Miliary tuberculosis
  • Miliary tuberculosis
  • Sarcoidosis
  • Bronchopneumonia
  •  Hypersensitivity pneumonitis: ill defined centrilobular nodules. Miliary TB: random nodules of the same size. Sarcoidosis: nodules with perilymphatic distribution, along fissures, adenopathy. Hypersensitivity pneumonitis: centrilobular nodules, notice sparing of the subpleural area.
  •  Lymphangitic carcinomatosis: irregular septal thickening, usually focal or unilateral, 50% adenopathy, known carcinoma. Cardiogenic pulmonary edema: smooth septal thickening with basal predominance ,ground-glass opacity with a gravitational and perihilar distribution, thickening of the peribronchovascular interstitium (peribronchial cuffing) Lymphangitic carcinomatosis. Lymphangitic carcinomatosis with hilar adenopathy. Alveolar proteinosis: ground glass attenuation with septal thickening (crazy paving). Cardiogenic pulmonary edema
  •  Sarcoidosis: nodules with perilymphatic distribution, along fissures, adenopathy. TB: Tree-in-bud appearance in a patient with active TB. Langerhans cell histiocytosis: early nodular stage before the typical cysts appear. Respiratory bronchiolitis: ill defined centrilobular nodules of ground-glass opacity.
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS
  • LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR INCREASED LUNG OPACITIES ATTENUATION PARENCHYMAL Consolidation OPACIFICATION Ground glassHRCT PATTERN CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION DECREASED LUNG ATTENUATION AIR TRAPPING ON EXPIRATORY SCANS