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HRCT IV
 

HRCT IV

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LOW ATTENUTION LESION IN HRCT LUNG

LOW ATTENUTION LESION IN HRCT LUNG

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  • The yellow arrows indicates the pulmonary vessels

HRCT IV HRCT IV Presentation Transcript

  • DECREASED LUNG ATTENUATION
  • 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, AN D 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
  • DECREASED LUNG ATTENUATION
  •  Lung cysts are defined as, well defined , circumscribed air containing lesions with a wall thickness of less than 4mm. They are lined by usually fibrous or cellular epithelium. Cavitiesare defined as radiolucent areas with a wall thickness of more than 4mm and are seen in infection (TB, Staph, fungal, hydatid), septic emboli, squamous cell carcinoma and Wegeners disease.
  •  Common cause are : 1. Langerhans Histiocytosis 2. Lymphangiomyomatosis 3. Lymphoid interstitial pneumonia
  • Multiple bizarre shaped cysts.There was an upper lobepredominance.The patient had a long history of smoking.
  • Multiple bizarre shaped cysts.There was an upper lobepredominance.The patient had a long history of smoking.
  • 40 year old female with no history of smoking . Multiple cysts that areevenly distributed througout the lung ( in contrast to LCH).Notice thepneumothorax.
  • Ehler Danlos Tuberous Sclerosis Pneumocystis
  •  Histopathological Considerations: Pulmonary Langerhans‟ cell histiocytosis (LCH) is a granulomatous disorder which is strongly linked to cigarette smoking. The earliest histologic abnormality is a proliferation of Langerhan‟s cells, around the small airways; cellular nodules develop and become increasingly fibrotic as the disease progresses. Nodules usually cavitate (often at different times) and eventually give rise to cysts (often with unusual outlines). HRCT Appearances: The HRCT appearances depend on the stage of the disease. Not surprisingly, in early disease, nodules will predominate. However, as some nodules begin to cavitate there is evidence of a temporal heterogeneity. The cysts of pulmonary LCH tend to be small (typically less than 1cm in diameter) and may initially be thick-walled. The bizarre outline of and distribution (mid and upper zonal with relative sparing of the lung bases and the tip of the middle lobe/lingula) of cysts is a useful diagnostic feature
  • Langerhans’ Cell Histiocytsosis: the early phaseis characterised by a nodular infiltrate.
  • This photomicrograph shows multiple cysts, thelargest of which has a bizarre shapecharacteristic of late stage disease.
  •  Langerhans cell histiocytosis is also known as pulmonary histiocytosis X or eosinophilic granuloma. LCH is probably an allergic reaction to cigarette smoke since more than 90% of patients are active smokers. In the early nodular stage it is characterized by a centrilobular granulomatous reaction by Langerhans histiocytes. In the cystic stage bronchiolar obliteration causes alveolar wall fibrosis and cyst formation.
  •  Early stage:  Small irregular or stellate nodules in centrilobular location. Late stage (more commonly seen)  Cystic airspaces Cysts have bizarre shapes, they may coalesce and than become larger.  Upper and mid lobe predominance.  Recurrent pneumothorax.
  • Multiple small nodules and cysts in a patient withpulmonary Langerhans‟ cell histiocytosis. Note thatthere is relative sparing of the middle lobe andlingula.
  • “Honeycomb” lung in pulmonary Langerhans‟ cellhistiocytosis. Multiple thin-walled cysts of variablesize and some with bizarre outlines. Few nodulesare seen at this stage. stage.
  • On the left early stage Langerhans cellhistiocytosis with small nodules.There are no cysts visible
  • ate stage Langerhans cell histiocytosis. Cysts progress to typical bizarre shaped cysts.In a later stage the nodules start to cavitate and becomecysts.These cysts start as round structures but finally coalesce tobecome the typical bizarre shaped cysts of LCH.In patients with LCH 95% have a smoking history.
  • On the left radiological pathological correlation of Langerhans cell histiocytosis in respectively nodular stage and early and late cystic stagepecimen of Langerhans cell histiocytosisin three different stage
  •  On the left a chest film of a 19 year old patient with Langerhans cell histiocytosis. The dominant findig on the chest film is a reticular patern and thats about as far as you can go. There is also hyperinflation. No way you would have recognized that this pattern was caused by multiple cysts. This is late stage Langerhans cell histiocytosis. The most challenging differential diagnosis in this patient is centrilobular emphysema. Emphysema however is defined as airspaces without definable walls. Usually we can identify the central dot sign. The upper lobe predominance is not helpfull in the differential as we can appreciate this in many inhalational diseases and also in emphysema.
  • On the left another case of Langerhans cell histiocytosis. It started as small noduli, which progressed over time to cavitating nodules. In the end this will progress to bizarre shaped cysts, that replace normal lung tissue.Langerhans cell histiosytosis: early phase and late phase
  •  Nodular LCH:  Sarcoidosis: perilymphatic distribution.  Metastases: random distribution. Cystic LCH:  LAM: round cysts, evenly distribution in women in the child-bearing age  Cystic bronchiectasis: signet ring sign.  Centrilobular emphysema: no walls, central dot.  LIP
  •  Emphysema, when it is severe, can mimick Langerhans cell histiosytosis. When it extends beyond the centrilobular area to the edge of the secondary lobule, it may look as if it is cystic with walls. In patients with LCH, the pathologist may find LCH, but also areas of emphysema, respiratory bronchiolitis and even fibrosis. So these smoking-related diseases do not represent discrete entities.
  • Histopathological Considerations: Lymphangioleiomyomatosis (LAM) is a rare, idiopathic disorder occurring exclusively in females of child-bearing age. The cardinal histopathologic findingis the abnormal proliferation of „immature‟ smooth muscle cells (so-called LAM cells) around the small airways, pulmonary vessels, lymphatics and alveolar septa and account for the typical clinical features (recurrent pneumothoraces, chylous effusions and airflow obstruction). Interestingly, the pulmonary abnormalities of LAM are similar to those seen in patients with tuberose sclerosis. HRCT Appearances: The striking finding on HRCT is of multiple thin-walled cysts of roughly uniform size. Unlike LCH, the cysts in LAM tend to be rounded and uniformly distributed throughout the parenchyma with no regional sparing. Furthermore, there is a conspicuous absence (except in a few rare reported cases) of nodules. Important ancillary diagnostic features include recurrent (chylous) pleural fluid and pneumothoraces.
  • Lymphangioleiomyomatosis characterised byareas of smooth muscle proliferation (LAM cells)which contribute to the wall of a typical cyst.
  • Rare disease, that occurs only in premenopausal womenCharacterized by progressive proliferation of atypical muscle cells along the bronchioles leading to air trapping and the development of thin-walled cysts, that replace normal lung parenchyma. Identical pulmonary changes seen in 1% of patients with tuberous sclerosis (predominant involvement of young men). Clinical findings: Majority of patients present with dyspnea. Chylous pleural effusions (40%), Pneumothorax (40%), hemoptysis (40%). Patients die within 10 years of the onset of symptoms. Pregnancy may exacerbate disease.
  • Numerous thin-walled cysts, surrounded by normal parenchyma. Cysts range from 2mm to 5cm in diameter, are round in shape and more or less uniform.Cysts are distributed diffusely throughout the lungs and upper and lower lobes are involved to a similar degree. Wall thickness of the cysts ranges from barely perceptible to 4 mm. Mediastinal or hilar adenopathy and pleural effusions (40%). Recurrent pneumothorax (40%)
  • On the left a typical case of LAM with multiple evenlyspread thin walled cysts complicated by apneumothorax.
  • HRCT in a patient with lymphangioleiomyomatosis. Multiple thin-walledcysts, of reasonably uniform size, are seen in both lungs; importantly, incontrast to Langerhans‟ cell histiocytosis, there are no nodules.
  • Langerhans cell histiocytosis: > 90% are smokers, cysts have irregular shapes and the basal costophrenic angles are spared. Centrilobular emphysema: characterized by airspaces that have no perceptible wall, centrilobular artery seen as dot in the centre. Lymphoid interstitial pneumonitis: seen in patients with HIV and Sj?gren syndrome.
  • black holes with no walls
  •  Permanent dilatation of the air spaces distal to terminal bronchiole, accompanied by destruction of their alveolar walls without obvious fibrosis Emphysema typically presents as areas of low attenuation without visible walls as a result of parenchymal destruction.
  •  Most common type Strongly associated with smoking. Often the centrilobular artery is visible within the centre of these lucencies. Most commonly in the upper lobes 48
  • Centrilobular emphysema due to smoking. Theperiphery of the lung is spared (blue arrows).Centrilobular artery (yellow arrows) is seen in thecenter of the hypodense area
  • Centrilobular artery (arrows) in many of the low-attenuatingareas.
  • Histologic specimen shows areas of lung destruction surrounding asmall centrilobular artery (arrow)
  •  Affects the peripheral parts of the secondary pulmonary lobule adjacent to the pleura and interlobar fissures Produces subpleural lucencies. Can be isolated phenomenon in young adults, or in older patients with centrilobular emphysema 52
  •  Paraseptal emphysema is localized near fissures and pleura and is frequently associated with bullae formation (area of emphysema larger than 1 cm in diameter). Apical bullae may lead to spontaneous pneumothorax
  • Paraseptal emphysema with small bullae
  • Paraseptal emphysema Honeycomb cystsOccur in a single layer at the May occur in several layers in thepleural surface subpleural lungPredominate in the upper lobes Predominate at the lung basesUnassociated with significant Asso with other findings offibrosis fibrosis.Associated with other findings of -emphysema 57
  •  Affects the entire secondary pulmonary lobule with complete destruction of the entire pulmonary lobule. Results in an overall decrease in lung attenuation Reduction in size of pulmonary vessels  Lower lobe predominance In alpha-1-antitrypsin deficiency, but also seen in smokers with advanced emphysema 58
  • Alpha-1-antitrypsin deficiency
  • • Does not represent a specific histological abnormality• Emphysema characterized by large bullae• Often associated with centrilobular and paraseptal emphysema
  • Previously known as irregular or cicatricial emphysema  can be seen in association with fibrosis  with silicosis and progressive massive fibrosis or  sarcoidosis 63
  • Centrilobular Panlobular Paraseptal emphysema emphysema emphysema• Most common type • Affects the whole • Adjacent to the• Irreversible secondary lobule pleura and destruction of • Lower lobe interlobar fissures alveolar walls in predominance • Can be isolated the centrilobular • In alpha-1- phenomenon in portion of the antitrypsin young adults, or in lobule deficiency, but older patients with• Upper lobe also seen in centrilobular predominance and smokers with emphysema uneven advanced • In young adults distribution emphysema often associated• Strongly with spontaneous associated with pneumothorax smoking.
  •  A sharply demarcated area of emphysema ≥ 1 cm in diameter A thin epithelialized wall ≤ 1 mm. Uncommon as isolated findings, except in the lung apices Usually associated with evidence of extensive centrilobular or paraseptal emphysema When emphysema is associated with predominant bullae, it may be termed bullous emphysema 67
  • A thin-walled, gas-filled space within the lung, Associated with acute pneumonia or hydrocarbon aspiration.• Often transient.• believed to arise from lung necrosis and bronchiolar obstruction.• Mimics a lung cyst or bulla on HRCT and cannot be distinguished on the basis of HRCT findings. 68
  •  Thicker and more irregular walls than lung cysts .• In diffuse lung diseases - LCH, TB, fungal infections, and sarcoidosis. Also seen in rheumatoid lung disease, septic embolism, pneumonia, metastatic tumor, tracheobronchial papillomatosis, and Wegener granulomatosis 70
  • Fungal Pneumonia
  • Is the abnormal dilatation of the medium-sizedbronchi (>2 mm in diameter) caused by destruction ofthe muscular and elastic components of bronchialwalls. The proximal bronchi are less affected becausethey have more cartilage and are more resistant todilation. 75
  •  Bronchial dilatation # The broncho-arterial ratio (internal diameter of the bronchus /pulmonary artery) exceeds 1. # In cross section it appears as “signet ring appearance” Lack of bronchial tapering # the earliest sign of cylindrical bronchiectasis # One indication is lack of change in the size of an airway over 2 cm after branching. Visualization of peripheral airways # Visualization of an airway within 1 cm of the costal pleura is abnormal and indicates potential bronchiectasis 76
  • Gross pathologic lung specimen from a patient with bronchiectasis. Notice the smallpulmonary artery abutting the much larger dilated bronchus (arrow), both of whichare seen on a cross-sectional view.
  • # Bronchial wall thickening : normally wall of bronchus should be less than half the width of the accompanying pulmonary artery branch.# Mucoid impaction# Air trapping and mosaic perfusion 84
  • mild to severe signs of bronchiectasis (curved arrows) and mild tomoderate signs of bronchial wall thickening. In addition, CT scan showsmucous plugging (straight arrows) and mosaic perfusion (∗).
  • Extensive, bilateral mucoid impaction. Mosaic perfusion caused bylarge and small airway obstruction. Small centrilobular nodules arevisible in the right lower lobe
  •  Cylindrical Bronchiectasis  Varicose Bronchiectasis  Cystic Bronchiectasis  Traction Bronchiectasis
  • # mildest form of this disease,# thick-walled bronchi that extend into the lung periphery and fail to show normal tapering 88
  • # beaded appearance of bronchial walls - dilated bronchi with areas of relative narrowing# string of pearls.# Traction bronchiectasis often appears varicose.
  • # Group or cluster of air- filled cysts,# cysts can also be fluid filled, giving the appearance of a cluster of grapes.
  • # Defined as dilatation of intralobular bronchioles because of surrounding fibrosis# due to fibrotic lung diseases 92
  • 1. Infective : childhood pneumonia,pertusis, measles, tuberculosis2. Non- infective causes : Bronchopulmonary aspergillosis, inhalation of toxic fumes3. Connective tissue disorder : Ehlers-Danlos Synd, Marfan synd , tracheobronchomeglay4. Ciliary diskinesia : Cystic fibrosis, Kartangener synd, agammaglobulinemia .5. Tractional bronchiectasis in interstitial fibrosis.6. Bronchial obstruction: with endobronchial tumors, broncholithiasis, and foreign body aspiration. 95
  • • Emphysema: areas without walls• Cyst: discrete, thin walls• Honeycombing: multiple subpleural cysts arranged in rows
  • 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
  • MOSAIC ATTENUATION AND PERFUSION• Definition: Heterogeneous lung density with areas of“groundglass attenuation” alternating with areas of“decreased” lung density usually having a zonal orgeographic pattern of distribution
  •  Mosaic perfusion refers to areas of decreased attenuation which results from regional differences in lung perfusion secondary to airway disease or pulmonary vascular disease. The pulmonary arteries will be reduced in size in the lucent lung fields thus allowing mosaic perfusion to be distinguished from ground-glass opacities.
  •  Lungdensity and attenuation depends partially on amount of blood in lung tissue. May be due to  vascular obstruction,  abnormal ventilation or  airway disease 105
  •  Patchy ground glass infiltrates resulting from airspace/interstitial disease: eg PCP Air-trapping resulting from large and small airway obstruction: eg constrictive bronchiolitis Vascular disease: eg. chronic embolic PHT
  •  Parenchymal disease: high attenuation regions are abnormal and represent ground-glass opacity Obstructive small airways disease: low attenuation regions are abnormal and reflect decreased perfusion of the poorly ventilated regions, e.g. Bronchiectasis, cystic fibrosis,constrictive bronchiolitis Occlusive vascular disease: low attenuation regions are abnormal and reflect relative oligaemia e.g. Chronic pulmonary embolism
  •  Peripheral Vessels : if vessels in hypoattenuated regions of the lung are smaller than in the other regions, the pattern is due to mosaic perfusion (i.e. airways or vascular disease rather than ground-glass) Central Vessels : pulmonary hypertension, reflected as dilatation of the central pulmonary arteries, suggests a vascular cause Small Airways : the presence of abnormally dilated or thick walled airways in the relatively lucent lung confirms underlying airway disease
  •  Parenchymal Changes : ground glass opacity is the likely cause for mosaic attenuation if other features of infiltrative disease are present, such as reticular opacities (i.e. crazy paving pattern) or nodules Air Trapping : refers to regions of lung which following expiration do not show the normal increase in attenuation, or show little change in cross-sectional area (i.e., this is an expiratory HRCT finding). The presence of air trapping suggests airway disease
  • # Areas of increased attenuation have relatively large vessels, while areas of decreased attenuation have small vessels.# Air trapping and bronchial dilatation commonly seen.# Causes include: Bronchiectasis, cystic fibrosis and bronchiolitis obliterans. 110
  • # decreased vessel size in less opaque regions is oftenvisible# common in patients with acute or chronic pulmonary embolism (CPE),
  • MOSIAC PATTERN DEPENDENT LUNG ONLY NONDEPENDENT LUNG EXPIRATION PRONE POSITION NO AIR TRAPPING AIR TRAPPING RESOLVE NOT RESOLVE VESSEL SIZE PLATE GROUNDATELECTASIS GLASS AIRWAYS DECREASED NORMAL DISEASE GROUND VASCULAR GLASS 112
  •  Air-space Disease  Pcp, Edema Interstitial Disease  Fibrosis/Microscopic  Honeycombing Combined Air-space / Interstitial Disease
  •  Large airway disease  Bronchiectasis Small airway disease  Constrictive bronchiolitis Asthma
  • Air trapping on expiratory imaging in the absence of inspiratoryscan findings in a patient with bronchiolitis obliterans.
  •  Chronic pulmonary embolism Pulmonary hypertension 2° increased pulmonary pressure
  • Mosaic perfusion pattern with marked regional variations in attenuation ofthe lung parenchyma and disparity in the size of the segmental vessels,with larger-diameter vessels in regions of increased attenuation (arrows). Aperipheral parenchymal band or scar (arrowhead) from infarction also isdepicted.
  • mosaic lung attenuation, with segmental and subsegmentalperfusion defects. A small pleura-based opacity (arrowhead)caused by previous infarction is seen in the apical segmentof the right lower lobe.
  • Mosaic Algorithm Air trapping Small SmallAirways Vessel
  • Inspiratory
  • Expiratory
  •  It refers to mixed densities which includes # consolidation # ground glass opacities # normal lung # Mosaic perfusion• Signifies mixed infiltrative and obstructive disease
  • Common cause are : 1. Hypersensitive pneumonitis 2. Sarcoidosis 3. DIP 144
  • Headcheese sign inhypersensitivitypneumonitis.HRCT scan showslung with ageographicappearance, whichrepresents acombination ofpatchy or lobularground-glassopacity (smallarrows) and mosaic
  • Upper lung zone preference is seen in:1.Inhaled particles: pneumoconiosis (silica or coal)2.Smoking related diseases (centrilobular emphysema3. Respiratory bronchiolitis (RB-ILD)4.Langerhans cell histiocytosis5.Hypersensitivity pneumonitis6.Sarcoidosis 149
  • Lower zone preference is seen in:1. UIP2. Aspiration3. Pulmonary edema 150
  • Central Zone VS. Peripheral zone1. Sarcoidosis 1. COP2. Bronchitis 2. Ch Eosinophilic3. Cardiogenic pulmonary Pneumonia edema 3. UIP 4. Hematogenous mets 152
  • # In sarcoidosis the common pattern is right paratracheal and bilateral hilar adenopathy (1-2-3-sign). 154
  • # In sarcoidosis the common pattern is right paratracheal and bilateral hilar adenopathy (1-2-3-sign).# In lung carcinoma and lymphangitic carcinomatosis adenopathy is usually unilateral.#Eggshell calcification in lymph nodes occurs in: Silicosis and coal-workers pneumoconiosis and is sometimes seen in sarcoidosis, post irradiation Hodgkin disease, blastomycosis and scleroderma . 156
  •  Pulmonary edema Lymphangitic spread of carcinoma - often unilateral Tuberculosis Lymphangiomyomatosis (LAM) Asbestosis 159
  •  Ground glass •Lobular areas of lower attenuation •Normal lung parenchyma •Normal lung volumes •No architectural distortion •No nodules •No reticulation
  •  Main differential diagnosis on imaging –Subacute Hypersensitivity Pneumonitis –Atypical Infection with associated bronchiolitis –Nonspecific Interstitial Pneumonia (NSIP) –Sarcoidosis
  •  Minor subpleural lung reticulation •Minimal architectural distortion with fine honeycomb lung (Right Upper Lobe for example)+/-traction bronchiectasis bronchiolectasis •No significant ground glass remote from areas of involvement
  •  Upper, mid and lower zonal distribution •Mild heterogeneity of lung parenchyma •Pattern of reticulation extends to the pleura with no subpleural lung sparing •No nodules •No consolidation •Difficult to comment on lung volumes on study provided scout suggest slight loss of volume
  •  Main differential diagnosis on imaging: –Early Idiopathic Pulmonary Fibrosis of a UIP pattern –Chronic Hypersensitivity Pneumonitis –Pulmonary manifestation of collagen vascular disease in a Fibrotic pattern of NSIP –Pulmonary manifestation of drug reaction –Sarcoidosis
  •  Idiopathic Pulmonary Fibrosis /Usual Interstitial Pneumonia (IPF/UIP) •Nonspecific Interstitial Pneumonia (NSIP) •Hypersensitivity Pneumonitis –Acute –Subacute –Chronic •Drug reaction
  •  Specific form of chronic fibrosing interstitial pneumonia limited to the lung and associated with the histologic appearance of Usual Interstitial Pneumonia (UIP) •Temporal and geographic heterogeneity •UIP can also be seen in –Asbestosis –Chronic Hypersensitivity Pneumonitis –Drug induced disease –Familial IPF
  •  Usually symmetric •Basal predominant but may be diffuse •Irregular •Linear •May progress to reticulonodular pattern •Progress to volume loss •In smokers volumes can be normal
  •  Subpleural distribution •Lower lung zone predominant •Architectural distortion •Irregular intralobular lines •Traction bronchiectasis •Honey comb lung cysts •Air filled cysts
  •  •5% can be upper lung predominant •Ground glass is mild •Associated with fibrosis •Fewer ground glass opacities remote from fibrosis •Disease activity vs. fibrosis
  •  Emphysema in 30% •Pulmonary ossification •Lymph node enlargement •No centrilobular or peribronchovascular nodules •No extensive consolidation •No extensive ground glass opacities
  •  Idiopathic Pulmonary Fibrosis IPF •Main differential diagnosis –Fibrotic NSIP +/-relation to connective tissue disease –Asbestosis –Chronic Hypersensitivity
  •  •Hazy opacities mainly middle and lower lung zones •+/-reticular opacities •Can be normal
  • •Bilateral symmetric ground glass opacities•Fine reticular opacities•When only ground glass opacities cellular form most likely
  • •Subpleural lung sparing may be distinguishing feature compared to UIP•Honeycomb lung much less common than UIP
  •  •Subpleural lung sparing may be distinguishing feature compared to UIP •Honeycomb lung much less common than UIP
  • •Differential Diagnosis–Hypersensitivity pneumonitis–Cryptogenic organising pneumonia–IPF
  •  Chronic eosinophilic pneumonia with peripheral areas of ground glass opacity. Sarcoid end-stage with massive fibrosis in upper lobes presenting as areas of consolidation. Notice lymphadenopathy. Chronic eosinophilic pneumonia with peripheral areas of consolidation. Broncho-alveolar cell carcinoma with both areas of ground glass opacity and consolidation
  •  Lymphangiomyomatosis (LAM): uniform cysts in woman of child-bearing age; no history of smoking; adenopathy and pleural effusion; sometimes pneumothorax. LCH: multiple round and bizarre shaped cysts; smoking history. Honeycombing Centrilobular emphysema: low attenuation areas without walls.
  •  Centrilobular emphysema: low attenuation areas without walls. Notice the centrilobular artery in the center. Langerhans cell histiocytosis (LCH): multiple thick walled cysts; smoking history. Honeycombing. Lymphangiomyomatosis (LAM): regular cysts in woman of child-bearing ag
  • 35 yr old smoker with progressivedyspnea. What is the most likely dx?1. Infectiousbronchiolitis2. LAM3. Thyroid cancer4. Sarcoid5. LCH
  •  There are multiple areas of consolidation. Ancillary findings are hilar and mediastinal lymphadenopathy. The differental diagnosis of the CT-images is basically the same as of the chest film. Histology revealed alveolar sarcoid. There is only one clue to the diagnosis and that is the presence of small nodules that can be identified in image 3, but these are difficult to see. This case nicely demonstrates that sarcoidosis truely is the great mimicker. Sarcoidosis should be therefore in our differential diagnostic list!.

  • Chronic EAA: there is a mosaic attenuation pattern. Within areas of ground-glass opacification there is traction bronchiectasis and parenchymaldistortion. The areas of apparently spared “black” lung show a diminution inthe number/calibre of pulmonary vessels (indicating small airways disease)
  • Key FeaturesIdiopathic Pulmonary Fibrosis Basal and subpleural reticular pattern with honeycombing ± traction bronchiectasisSarcoidosis Acute Well-defined bronchocentric and subpleural micronodules. Symmetrical enlarged hilar/mediastinal lymph nodes (with or without calcification) Chronic Coarse bronchocentric upper lobe fibrosisHypersensitivity Pneumonitis Subacute Ill-defined centrilobular nodules, ground-glass opacification and (lobular) foci of decreased attenuation (with air-trapping on expiratory CT) Chronic Diffuse ground-glass opacification, traction bronchiectasis and parenchymal distortion. Lobular areas of air-trappingLangerhans’ Cell Histiocytosis Nodules ± cavitation bizarre-shaped, thin-walled cysts. Sparing of extreme lung bases and tip of middle lobe/lingulaLymphangioleiomyomatosis Uniform thin-walled cysts; no zonal sparing/no nodulesLymphocytic Interstitial Pneumonia Ground-glass opacification, nodules, thin-walled cystsAlveolar Proteinosis Patchy (geographical) ground-glass opacification and thickened interlobular septa (“crazy-paving” pattern)
  •  Major Criteria– Exclusion of otherknown etiologies – Abnormal PFT’S – Abn HRCT > 6 mos – TBBX/BAL excluding other etiologies Minor Criteria – Age > 50 yrs – Insidious onset DOE – Diagnosis > 3 mos duration – Bibasilar rales In absence of OLB: Dx requires all 4 major - 3/4minor criteria
  •  Lymphocytic interstitial pneumonitis or LIP is uncommon, being seen mainly in patients with autoimmune disease, particularly Sj?grens syndrome, and in patients with AIDS. Symptoms are nonspecific and often those of the patients underlying disease HRCT findings are usually nonspecific.
  •  Histopathological Considerations: Lymphocytic interstitial pneumonia (LIP) is a clinicopathological term for a pulmonary lymphoproliferative abnormality associated with several disease entities including dysproteinaemic states, connective tissue disorders and HIV infection. Is is noteworthy that idiopathic LIP is exceedingly rare. On histologic examination there is a interstitial cellular infiltrate comprising small, mature lymphocytes and plasma cells. HRCT Appearances: Admittedly, the HRCT appearances of LIP, may be wholly non-specific: in individual patients, variable combinations of ground-glass opacification, nodules (ill-defined centrilobular or subpleural) and thickening of the interlobular septa, are typical. However, in some patients with LIP, the above features may be associated with thin- walled cysts. Furthermore, in some patients with Sjögren‟s syndrome, there may be (calcified) deposits of amyloid in addition to thin-walled cysts.
  • Lymphocytic interstitial pneumonia: there is adiffuse interstitial infiltrate of lymphocytes, mostmarked around the bronchovascular bundlesand thickening of alveolar walls.
  • On the left a patient with Sjogrens syndrome with LIP
  • Lymphocytic interstitial pneumonia in Sjögren‟s syndrome. In addition tothe diffuse ground-glass opacification there are multiple thin-walled cysts inboth lungs. At least two irregular nodules (arrows), representing amyloiddeposition, are noted in the right lower lobe
  • On the left three different patients with lung cysts.From left to right: Lymphangiomyomatosis, LIP and Langerhans cellhistiocytosis.