hrct.pptx high resolution ct patterns
- 1. HIGH RESOLUTION CT : LUNG PATTERNS DR. SABHILASH SUGATHAN Aquino SL, Gamsu G, Webb WR, Kee SL. Thoracic imaging: pattern frequency and significance on HRCT , 3rd edition 2018.
- 2. FUNDAMENTAL TECHNICAL PROTOCOLS • Slice thickness: 0.625 – 1.25mm • Scan time :0.5 – 1 sec • Kv: 120 • mAs:100-200 • Reconstruction algorithm: high spatial frequency algorithm • Window: lung window • Patient position: supine(routinely) or prone(if suspect ild) • Level of inspiration: full inspiration(routinely) expiratory hrct scans in patients with obstructive lung diseases
- 3. HRCT VS ROUTINE CT
- 4. WE WILL DISCUSS THE FOLLOWING SUBJECTS: • ANATOMY OF THE SECONDARY LOBULE • BASIC HRCT PATTERNS • DISTRIBUTION OF ABNORMALITIES • DIFFERENTIAL DIAGNOSIS OF INTERSTITIAL LUNG DISEASES
- 5. ANATOMY OF SECONDARY LOBULE
- 6. • The secondary lobule is the basic anatomic unit of pulmonary structure and function. • It is the smallest lung unit that is surrounded by connective tissue septa. • It measures about 1-2.5 cm and is made up of 5- 15 pulmonary acini, that contain the alveoli for gas exchange. • The central portion of secondary lobule referred to as CENTRILOBULAR, contains Pulmonary A and terminal bronchiole that supply the lobule. • the Pulmonary Artery can be seen in normal lung as a dot or branching structure 5-10mm from the pleural surface • The centrilobular bronchi is normally invisible
- 7. • The pulmonary veins and lymphatics run in the periphery of the lobule within the interlobular septa. • There are two lymphatic systems: a central network, that runs along the bronchovascular bundle towards the centre of the lobule and a peripheral network, that is located within the interlobular septa and along the pleural linings. • Under normal conditions only a few of these very thin septa can be seen.
- 8. Irregular polygonal in shape
- 9. The normal pulmonary vein branches are seen marginating pulmonary lobules. The centrilobular artery branches are visible as a rounded dot
- 10. • ACINUS: Portion of lung parenchyma supplied by a single respiratory bronchiole 6-10mm in diameter • PRIMARY LOBULE: Lung parenchyma associated with a single Alveolar duct 4-5 Primary Lobules Acinus 6-12 Acini Secondary Lobule
- 11. • CENTRILOBULAR AREA is the central part of the secondary lobule. • It is usually the site of diseases, that enter the airways ( i.e. Hypersensitivity pneumonitis, respiratory bronchiolitis, centrilobular emphysema • PERILYMPHATIC AREA is the peripheral part of the secondary lobule. • It is usually the site of diseases, that spread through Sarcoid, lymphangitic carcinomatosis, pulmonary These diseases are usually also located in the central lymphatics that surround the broncho vascular bundle.
- 12. LUNG INTERSTITUM Lung interstitium Peribronchovascul ar interstitium Centrilobul ar interstitium Subpleural interstitium Interlobular septa Axial fiber system Peripheral fiber system * Generally it is not visible on HRCT unless • IntraLobular
- 13. BASIC INTERPRETATION A STRUCTURED APPROACH • What is the dominant HRCT - pattern: • Reticular • Nodular • High attenuation (ground-glass, consolidation) • Low attenuation (emphysema, cystic) • Where is it located within the secondary lobule HRCT-pattern: • Centrilobular • Perilymphatic • Random • Is there an upper versus lower zone or a central versus peripheral predominance
- 14. HRCT FINDINGS IN LUNG DISEASES: •LINEAR & RETICULAR OPACITIES • NODULES & NODULAR OPACITIES • INCREASED LUNG OPACITY • DECREASED LUNG OPACITY
- 15. LINEAR AND RETICULAR OPACITIES • INTER LOBULAR SEPTAL THICKENING • INTRA LOBULAR SEPTAL THICKENING • HONEYCOMBING
- 16. INTER LOBULAR SEPTAL THICKENING abnormal widening of an inter lobular septum or septa, usually caused by edema, cellular infiltration or fibrosis may be: • smooth • Nodular / irregular Associated findings of septal thickening regardless of cause include: • Peri- bronchial interstial thickening – Peribronchial cuffing • Thickening of fissures
- 18. SMOOTH SEPTAL THICKENING Septal thickening and ground-glass opacity with a gravitational distribution in a patient with cardiogenic pulmonary edema. Thickening of the peribronchovascular interstitium, which is called peribronchial cuffing, and fissural thickening are also common. Common additional findings are an enlarged heart and pleural fluid.
- 19. NODULAR SEPTAL THICKENING SARCOIDOSIS : right lung base shows interlobular septal thickening associated with several septal nodules giving beaded LYMPHANGITIC CARCINOMATOSIS : show diffuse smooth and nodular septal thickening.
- 20. PULMONARY LYMPHANGITIC CARCINOMATOSIS (PLC) • In 50% of patients the septal thickening is focal or unilateral (distinguishing PLC from other causes like sarcoidosis or cardiogenic pulmonary edema). • Hilar lymphadenopathy is visible in 50% and usually there is a history of malignancy.
- 21. HONEYCOMBING Honeycombing reflects extensive lung fibrosis with alveolar destruction and results in a characteristic reticular appearance. On HRCT, necessary findings for the diagnosis of Honeycombing are 1. Air-filled (Black) cysts 2. The cysts have a thick (Easily recognizable) wall 3. The cysts are usually from 3 mm to 1 cm in diameter (although they may be larger or Smaller in some cases) 4. Cysts are immediately beneath the pleural surface 5. Cysts share walls Three cysts in a row, at the pleural surface, is a minimum for the diagnosis of honeycombing
- 22. Associated findings of fibrosis include: reticular opacities, traction bronchiestasis UIP - basal and peripheral predominance
- 23. Identification of honeycombing on HRCT: 1. It indicates fibrotic lung disease, although further progression can be seen in patients with honeycombing. 2. It indicates that a lung biopsy probably will not prove diagnostic 3. In a patient without an associated disease (e.g., Collagen-vascular disease) or exposure (e.g., Asbestos, drugs, organic antigens), IPF is likely the diagnosis. 4. It points to a poor prognosis in patients with IPF Honeycombing in a patient with UIP associated with rheumatoid arthritis.
- 24. INTRALOBULAR INTERSTITIAL THICKENING (INTRALOBULAR LINES) • Results in a fine reticular pattern on HRCT, with the visible lines separated by a few millimeters • Fine lace- or netlike appearance • Causes : Pulmonary fibrosis Asbestosis Chronic eosinophilic pneumonitis.
- 25. NODULAR PATTERN
- 26. • Round opacity atleast moderately well marginated and not greater than 3cm in maximum diameter. • Small < 1cm Micro < 7mm Miliary<2mm • Smooth • Irregular • cavitating • Noncavitating • Centrilobular • Perilymphatic • random NODULAR PATTERN
- 27. PERILYMPHATIC DISTRIBUTION CENTRILOBULAR DISTRIBUTION RANDOM DISTRIBUTION
- 28. PERILYMPHATIC DISTRIBUTION Nodules are seen in relation to pleural surfaces, interlobular septa and the peribronchovascular interstitium. Nodules are almost always visible in a subpleural location, particularly in relation to the fissures. Nodules in • subpleural regions • peribronchovascular regions • in relation to interlobular septa
- 29. Notice the overlap in differential diagnosis of perilymphatic nodules and the nodular septal thickening in the reticular pattern. Sometimes the term reticulonodular is used.
- 30. SARCOIDOSIS: peribronchovascular and subpleural predominance of Nodules with more extensive abnormalities in the upper lobes and may be symmetrical or asymmetrical. SILICOSIS AND CWP subpleural and centrilobular peribronchovascular But with • symmetrical, posterior, upper lobe predominance of nodules. • exposure history usually is available.
- 31. LYMPHANGITIC SPREAD OF TUMOR which typically predominates in relation to interlobular septa and the peribronchovascular interstitium most severe at the lung bases and often is asymmetrical
- 32. CENTRILOBULAR DISTRIBUTION • Unlike perilymphatic and random nodules, centrilobular nodules spare the pleural surfaces. The most peripheral nodules are centered 5-10mm from fissures or the pleural surface. • Centrilobular nodules are seen in diseases, that enter the lung through the airways. The pathogens enter the central area of the secondary lobule via the terminal bronchiole (Although abnormalities occurring in relation to small vessels also may result in this finding.) • Hypersensitivity pneumonitis • Respiratory bronchiolitis in smokers • Infectious airways diseases (endobronchial spread of tuberculosis or nontuberculous mycobacteria, bronchopneumonia) • Uncommon in bronchioloalveolar carcinoma, pulmonary edema, vasculitis
- 35. Bacterial bronchopneumonia - patchy centrilobular Centrilobular nodules in hypersensitivity pneumonitis.
- 36. TREE-IN-BUD • Irregular and often nodular branching structure, most easily identified in the lung periphery. It represents dilated and impacted (mucus or pus- filled) centrilobular bronchioles. • It almost always indicate presence of infection
- 37. tree-in-bud (arrows) in patient with airway infection.
- 39. RANDOM DISTRIBUTION • Nodules are randomly distributed relative to structures of the lung and secondary lobule. Nodules can usually be seen to involve the pleural surfaces and fissures, but lack the subpleural predominance often seen in patients with a perilymphatic distribution. • Small random nodules are seen in: • Hematogenous metastases • Miliary tuberculosis • Miliary fungal infections • Sarcoidosis • Langerhans cell histiocytosis (early nodular stage)
- 40. Nodules may involve the pleural surfaces, peribronchovascular interstitium, and interlobular septa but do not show a predominance in relation to these structures as is present with a perilymphatic pattern. The overall distribution appears diffuse and uniform.
- 41. Random nodules in a patient with miliary tuberculosis. The nodules are small, sharply defined, and diffuse and uniform in distribution. Some nodules are seen at the pleural surface.
- 45. • GROUND GLASS OPACITIES • CONSOLIDATION • Increased lung attenuation is called ground-glass-opacity (GGO) if there is a hazy increase in lung opacity without obscuration of underlying vessels and is called consolidation if the increase in lung opacity obscures the vessels. • In both ground glass and consolidation the increase in lung density is the result of replacement of air in the alveoli by fluid, cells or fibrosis. • In ggo the density of the intrabronchial air appears darker as the air in the surrounding alveoli - dark bronchus sign. • In consolidation, there is exclusively air left in the bronchi. This is called the air bronchogram.
- 47. CONSOLIDATION • Consolidation is synonymous with airspace disease. When you think of the causes of consolidation, think of 'what is replacing the air in the alveoli'? Is it pus, edema, blood or tumor cells • Even fibrosis as in UIP, NSIP and long standing sarcoidosis can replace the air in the alveoli and cause consolidation. Patchy areas of consolidation with air bronchogram in a patient with organizing pneumonia (OP).
- 49. GROUND-GLASS OPACITY • Ground-glass opacity (GGO) represents: GGO is a nonspecific term referring to a hazy increase in lung opacity that is not associated with obscuration of underlying vessels The location of the abnormalities in ground glass pattern can be helpful: • Upper zone predominance: respiratory bronchiolitis, pneumocystis pneumonia. • Lower zone predominance: UIP, NSIP, DIP. • Centrilobular distribution: hypersensitivity pneumonitis, respiratory bronchiolitis
- 51. A peripheral increase in lung attenuation represents ground-glass opacity. Vessels remain visible in the dense lung regions. This patient had acute dyspnea due to pulmonary edema.. B: Patchy ground-glass opacity is visible in the upper lobes. This immunosuppressed patient had symptoms of acute fever and cough. Bronchoscopy revealed cytomegalovirus pneumonia
- 52. TREATABLE OR NOT TREATABLE • Ground-glass opacity is nonspecific, but a highly significant finding since 60-80% of patients with ground-glass opacity on HRCT have an active and potentially treatable lung disease. • In the other 20-40% of the cases the lung disease is not treatable and the ground-glass pattern is the result of fibrosis. • In those cases there are usually associated HRCT findings of fibrosis, such as traction bronchiectasis and honeycombing. • The images show two cases with GGO, one without fibrosis and potentially treatable and the other with traction bronchiectasis indicating fibrosis. LEFT: No fibrosis, so potentially treatable lung disease. RIGHT: Fibrosis, so no treatable lung disease.
- 53. CRAZY PAVING • Crazy paving is a combination of ground glass opacity with superimposed septal thickening It was first thought to be specific for alveolar proteinosis, but later was also seen in other diseases. • Crazy paving can also be seen in: • Alveolar proteinosis • Sarcoid • NSIP • Organizing pneumonia (COP/BOOP) • Infection (PCP, viral, mycoplasma, bacterial) • Neoplasm (bronchoalveolar ca (BAC) • Pulmonary haemorrhage • Oedema (heart failure, ARDS, AIP)
- 54. CRAZY PAVING IN A PATIENT WITH ALVEOLAR PROTEINOSIS.
- 55. MOSAIC ATTENUATION • A patchwork of regions of varied attenuation interpreted as secondary to regional differences in perfusion • There are patchy areas of black and white lung. • Differential Diagnosis
- 56. MOSAIC PERFUSION: In homogenous lung opacity resulting from regional differences in lung perfusion MOSAIC PERFUSION GROUND GLASS OPACITY relatively smaller Pulmonary vessels pulmonary vessels are equal throughout in lucent areas Airway abnormality may be enlarged pulmonary arteries may be appreciated seen in lucent areas Accentuated on expiratory scans remains the same on expiratory scans
- 57. It can be difficult to distinguish these entities. There are two diagnostic hints for further differentiation: Look at the vessels • If the vessels are difficult to see in the 'black' lung as compared to the 'white' lung, than it is likely that the 'black' lung is abnormal. Look at expiratory scans for air trapping • Accentuation of attenuation differences in airway diseases • Uniform increase in attenuation in infiltrative and vascular disorders
- 60. • It includes abnormalities that result in decreased lung attenuation or air-filled lesions. These include: • Emphysema • Lung cysts (LAM, LIP, langerhans cell histiocytosis) • Bronchiectasis • Honeycombing • Most diseases with a low attenuation pattern can be readily distinguished on the basis of HRCT findings.
- 61. EMPHYSEMA Emphysema : focal region / regions of low attenuation usually without visible walls resulting from actual or perceived enlarged air spaces & destroyed alveolar walls. May be associated with air trapping. •CENTRILOBULAR EMPHYSEMA • Most common type • Irreversible destruction of alveolar walls in the centrilobular portion of the lobule • Upper lobe predominance and uneven distribution • Strongly associated with smoking. Centrilobular emphysema due to smoking. The periphery of the lung is spared (blue arrows). Centrilobular artery (yellow arrows) is seen in the center of the hypodense area
- 62. • Pulmonary vessels in the affected lung appear fewer and smaller than normal. • Panlobular emphysema is diffuse and is most severe in the lower lobes. • In severe panlobular emphysema, the characteristic appearance of extensive lung destruction and the associated paucity of vascular markings are easily distinguishable from normal lung parenchyma. • Affects the whole secondary lobule(large area of low attenuation) • Usually Diffuse and associated with decreased vessel size • Lower lobe predominance • In alpha-1-antitrypsin deficiency, but also seen in smokers with advanced emphysema PANLOBULAR EMPHYSEMA
- 63. • Adjacent to the pleura and interlobar fissures(subpleural lucencies marginated interlobular septa) • Can be isolated phenomenon in young adults, or in older patients with centrilobular emphysema • In young adults often associated with spontaneous pneumothorax • frequently associated with bullae formation (area of emphysema larger than 1 cm in diameter). PARASEPTAL EMPHYSEMA
- 64. CYSTIC LUNG DISEASE • Lung cysts are defined as radiolucent areas with a wall thickness of less than 4mm.
- 65. lymphangiomyomatosis (LAM). Langerhans cell histiocytosis (LCH) • related to tuberous sclerosis genes 1 and 2 • women, usually of childbearing age • uniformly distributed cysts, round, and similar in size and shape • a neoplastic proliferation of perivascular epithelioid cells • small percentage of patients with tuberous sclerosis have LAM. • irregularly or bizarrely shaped cysts • upper-lobe predominance, • associated with nodules and cavitary nodules in early stages of the disease • spare the costophrenic angles. • smokers.
- 66. BRONCHIECTASIS Bronchiectasis is defined as localized, irreversible bronchial dilatation. The diagnosis of bronchiectasis is usually based on a combination of the following findings: •bronchial dilatation (signet-ring sign) •bronchial wall thickening •lack of normal tapering with visibility of airways in the peripheral lung •mucus retention in the bronchial lumen •associated atelectasis and sometimes air trapping A signet-ring sign represents an axial cut of a dilated bronchus (ring) with its accompanying small artery (signet). The most common cause of bronchiectasis is prior infection, usually viral, at an early age. It also occurs in patients with chronic bronchitis, COPD and cystic fibrosis.
- 68. CONED AXIAL HRCT IMAGE SHOWS BRONCHIAL DILATION WITH LACK OF TAPERING . BRONCHIAL MORPHOLOGY IS CONSISTENT WITH VARICOSE BRONCHIECTASIS. 75
- 70. DISTRIBUTION WITHIN THE LUNG
- 73. PLEURAL EFFUSION
- 74. LYMPHADENOPATHY • 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 This is commonly seen in lymph nodes in patients with silicosis and coal-worker's pneumoconiosis and is sometimes seen in sarcoidosis, post irradiation Hodgkin disease, blastomycosis and scleroderma.
- 75. EXAMPLES OF RETICULAR PATTERN: 1.Lymphangitic carcinomatosis: irregular septal thickening, usually focal or unilateral 50% adenopathy', known carcinoma. 2.Cardiogenic pulmonary edema : incidental finding in HRCT, smooth septal thickening with basal predominance (Kerley B lines), ground-glass opacity with a gravitational and perihilar distribution, thickening of the peribronchovascular interstitium (peribronchial cuffing) 3.Lymphangitic carcinomatosis 4.Lymphangitic carcinomatosis with hilar adenopathy. 5.Alveolar proteinosis: ground glass attenuation with septal thickening (crazy paving). 6.Cardiogenic pulmonary edema.
- 76. EXAMPLES OF NODULAR PATTERN 1.Hypersensitivity pneumonitis: ill defined centrilobular nodules. 2.Miliary TB: random nodules 3.Sarcoidosis: nodules with perilymphatic distribution, along fissures, adenopathy. 4.Hypersensitivity pneumonitis: centrilobular nodules, notice sparing of the area next to pleura and fissure.
- 77. MORE NODULAR PATTERN 1.Sarcoidosis: nodules with perilymphatic distribution, along fissures, adenopathy. 2.TB: Tree-in-bud appearance in a patient with active TB. 3.Langerhans cell histiocytosis: early nodular stage before the typical cysts appear. 4.Respiratory bronchiolitis in infection.
- 78. EXAMPLES OF HIGH ATTENUATION PATTERN 1.Chronic eosinophilic pneumonia with peripheral areas of ground glass opacity. 2.Sarcoid end-stage with massive fibrosis in upper lobes presenting as areas of consolidation. Notice lymphadenopathy. 3.Chronic eosinophilic pneumonia with peripheral areas of consolidation. 4.Broncho-alveolar cell carcinoma with both areas of ground glass opacity and consolidation
- 79. HIGH ATTENUATION PATTERN (2) 1.Non specific interstitial pneumonitis (NSIP): ground glass with traction bronchiectasis, no honeycombing. 2.Cryptogenic organizing pneumonia (COP). 3.Sarcoidosis end-stage: consolidation as a result of massive fibrosis perihilar and in upper lobes. 4.COP.
- 80. LOW ATTENUATION PATTERN 1.Lymphangiomyomatosis (LAM): uniform cysts in woman of child-bearing age; no history of smoking; adenopathy and pleural effusion; sometimes pneumothorax. 2.LCH: multiple round and bizarre shaped cysts; smoking history. 3.Honeycombing 4.Centrilobular emphysema: low attenuation areas without walls.
- 81. LOW ATTENUATION PATTERN (2) 1.Centrilobular emphysema: low attenuation areas without walls. Notice the centrilobular artery in the center. 2.Langerhans cell histiocytosis (LCH): multiple thick walled cysts; smoking history. 3.Honeycombing. 4.Lymphangiomyomatosis (LAM): regular cysts in woman of child-bearing age.
- 82. THANK YOU!
- 83. DIFFERENTIAL DIAGNOSIS OF INTERSTITIAL LUNG DISEASES
- 85. CHRONIC INTERSTITIAL PNEUMONITIS: Do not represent “diseases” per se; rather represent fundamental responses of lungs to injury/pathological conditions Histologically 5 types (Liebow): • usual interstitial pneumonia (UIP) • desquamative interstitial pneumonia (DIP) • lymphocytic interstitial pneumonia (LIP) • giant-cell interstitial pneumonia (GIP) • bronchiolitis with interstitial pneumonia(BIP) – BOOP/COP
- 86. COLLAGEN VASCULAR DISEASES: All collagen vascular diseases can cause pulmonary disease frequency & tendency to involve vary among them Pulmonary involvement is most common in – Rheumatoid arthritis Scleroderma (PSS) radiological features are indistinguishable from IPF HRCT: interstitial pneumonia & findings of fibrosis ground glass opacity irregular interlobular septal thickening * Peripheral & subpleural * Lower zone & posterior zone RA - pleural thickening & effusion necrobiotic nodules BOOP PSS – esophageal dilatation
- 87. IDIOPATHIC INTERSTITIAL FIBROSIS – IPF : 40-60 yrs, breathlessness & dry cough, finger clubbing late inspiratory crackles(velcro rales) Restrictive pattern on PFT Pathologically – UIP and/or DIP HRCT: fibrosis-intralobular interstitial thickening visible intralobular bronchioles honey combing traction bronchiectasis ground glass opacity irregular interlobular septal thickening * Patchy distribution * Peripheral & subpleural * Lower zone & posterior zone