Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

HRCT Chest - By Dr. Tinku Joseph

3,146 views

Published on

PowerPoint presentation on the topic HRCT Chest. This presentation is divided into 5 different parts. 1)Introduction to HRCT chest 2)Technichal aspects of HRCT 3) Relevant anatomy for HRCT interpretation 4)Pattern of lung disease in HRCT 5)HRCT pattern in various ILD’s

Published in: Health & Medicine
  • Hi there! Essay Help For Students | Discount 10% for your first order! - Check our website! https://vk.cc/80SakO
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Nice !! Download 100 % Free Ebooks, PPts, Study Notes, Novels, etc @ https://www.ThesisScientist.com
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

HRCT Chest - By Dr. Tinku Joseph

  1. 1. HRCT in Lung Diseases Dr.Tinku Joseph MD, DM, FCCP Consultant Pulmonologist AIMS, Kochi
  2. 2. Reference  Radiopedia.com  Lunghouse.com  Chestradiology.com  Radiologyassistant.com  Various journals & text books  Google images
  3. 3. CONTENTS 1. Introduction to HRCT chest 2. Technichal aspects of HRCT 3. Relevant anatomy for HRCT interpretation 4. Pattern of lung disease in HRCT 5. HRCT pattern in various ILD’s 3
  4. 4. HRCT -: Meaning  High resolution CT imaging  Resolution : Means ability to resolve small object that are close together ,as separate form. Actual meaning  A scan performed using high- spatial frequency algorithm to accentuate the contrast between tissue of widely differing densities, eg: - air & vessels (lung) • (Radiopedia.com) 4
  5. 5. INTRODUCTION  HRCT - Use of thin section CT images (0.25 to 2 mm slice thickness) often with a high-spatial-frequency reconstruction algorithm to detect and characterize disease affecting the pulmonary parenchyma and airways.  Superior to chest radiography  Detection of lung disease  Points a specific diagnosis  Helps in identification of reversible disease. 5
  6. 6. History  1982– The term HRCT was first used by Todo et. Al  1985 – Nakata et.al and Naidich et.al published first report on HRCT  Since then has been an important tool in pulmonary medicine  Recent development of MDCT scanner capable of volumetric high resolution scanning has improved the investigation 6
  7. 7. Technical aspects of HRCT Chest PART- 1 7
  8. 8. Technical aspect Parameters  Slice thickness  Filming  Patient position  Types of HRCT  Artifacts 8
  9. 9. Slice thickness  Thin sections 0.25 – 1.5 mm is essential for optimal spatial resolution  Thicker slices are prone for reduction in ability to resolve smaller structure  Better for delineation of bronchi, wall thickness and diameter 9
  10. 10. 10
  11. 11. Window settings Lung window  window widths of 1000 to 1500 HU are appropriate for a routine lung window. Mediastinal & Soft tissue window  Window level/width setting of 40-50/ 350-450 HU are best for evaluation of the mediastinum, hila, and pleura. 11
  12. 12. Inspiratory level : Routine HRCT is obtained in suspended full inspiration, which  optimizes contrast between normal structures, various abnormalities and normal aerated lung parenchyma; and  reduces transient atelectasis, a finding that may mimic or obscure significant abnormalities. Expiratory scan : valuable in obstructive lung disease or airway abnormality Lateral decubitus CT : Mainly in children 12
  13. 13. Patient Position and the Use of Prone Scanning  Supine adequate in most instances.  Prone for diagnosing subtle lung abnormalities.  e.g., asbestosis, suspected early lung fibrosis  Prone scan is useful in differentiating dependent lung atelectasis from early lung fibrosis 13
  14. 14. The prone images shows complete resolution of the opacity suggesting dependent atelectasis. 14
  15. 15. Persistent opacity in the posterior lung in a patient with pulmonary fibrosis. 15
  16. 16. Normal lung Attenuation  Attenuation gradient : densest at dependent region of lung as a result of regional difference in blood and gas density due to gravity  In children, lung attenuation is greater than adults.
  17. 17. Normal expiratory HRCT  Performed to detect air trapping in small airway obstruction  Attenuation increases with expiration.  60 % of normal individual shows air trapping in the superior segment of lower lobe and involving single lobule, normal variant.
  18. 18. - • MDCT scanner are capable of rapid scanning and thin slice acquisition. Advantages : 1. Viewing of contiguous slice for better delineation of lung abnormality 2. Complete imaging of lung and thorax 3. Reconstruction of scan data in any plane using MIPs or MinIPs. Disadvantage : greater radiation dose. 19 Volumetric HRCT Technique of scan acquisition
  19. 19. Multidetector Helical HRCT  Multidetector CT is equipped with a multiple row detector array  Multiple images are acquired Advantages -  Shorter acquisition times  whole-lung HRCT can be performed in one breath-hold.  Retrospective creation of both thinner and thicker sections from the same raw data 20
  20. 20. Low dose HRCT  Low dose HRCT uses Kvp of 120- 140 and mA of 20-30 at 2 sec scan time.  Equivalent to conventional HRCT in 97 % of cases  Disadvantage : Fails to identify GGO in few cases and have more prominent streak artifact.  Not recommended for initial evaluation of patients with lung disease.  Indicated in following up patients with a known lung abnormality or in screening large populations at risk for lung ds.  Ongoing trials -: Screening tool for CA lung 21
  21. 21. Radiation dose  PA CHEST Radiograph ----- ----- ----- 0.05 mSv  Spaced axial HRCT (10mm space) ----- 0.7 mSv ( 14 X ray)  Spaced axial HRCT (20 mm space) ------ 0.35 mSv ( 7 X ray)  Low Dose Spaced axial HRCT -------- 0.02 mSV  MD-HRCT ---- ------- 4 - 7 msv ( 60-80 x ray) 22
  22. 22. HRCT artifact  Streak Artefacts :  Fine, linear, or netlike opacities  Radiate from the edges of sharply marginated , high-contrast structures such as bronchial walls, ribs, or vertebral bodies.  More evident on low mA 23
  23. 23. Streak Artifacts
  24. 24. The streak artifacts emanating from the implant
  25. 25. Motion-related artifacts  Pulsation / Star/ Doubling artifacts  Visible at lung base  Adjacent to heart due to cardiac pulsation 26
  26. 26. Patient related artifacts  Motion artifacts (Resp, Cardio or both) -: create pseudobronchiectasis, pseudo- GGO and star artifacts  Dependent atlectasis-: sub-pelural lung disease 27
  27. 27. Interpretive artifacts  Incorrect window width and level  Failure to detect bronchiectasis due to mucous plugging. 28
  28. 28. Modification of scan protocol  Scan protocol can be modified in relation to disease or patients comfort.  If a disease has basal predominance, it may be wise to begin scanning near the diaphragm and proceed cephalic . 29
  29. 29. Post processing techniques Maximum intensity projection  High attenuation films  Improves detection of pulmonary nodules.  Characterize distribution of small nodules.  Assessing the size and location of vessels. 30
  30. 30. 31
  31. 31. Post processing techniques Minimum intensity projection  Lowest attenuation films  Enables detection of low-density structures  Optimal tool for the detection, localization, and quantification of ground-glass and linear attenuation patterns. 32
  32. 32. 33
  33. 33. HRCT Technique- Summary  In all cases:  Breath hold  Full Inspiration  Expiratory images – Emphysema  Prone images  HRCT types  Artefacts  MIP/ Min MIP
  34. 34. Relevant Anatomy PART- 2 35
  35. 35. Lung anatomy  Right lung is divided by major and minor fissure into 3 lobes and 10 broncho- pulmonary segments  Left lung is divided by major fissure into 2 lobes with a lingular lobe and 8/9 bronchopulmonary segments 36
  36. 36. There are approximately 23 generation of dichotomous branching From trachea to the alveolar sac HRCT can identify upto 8th order central bronchioles 38
  37. 37. Tracheal anatomy  10-12 cm in length, from C6 level to upper border of D5.  Extrathoracic (2-4cm) and Intrathoracic(6-9 cm beyond manubrium)  In men, tracheal diameter – 25-27 mm  women – 21- 23 mm  The posterior portion of the tracheal wall is a thin fibromuscular membrane----- allows for oesophageal expansion.
  38. 38. Bronchial Anatomy  Approximately 23 generations of branches from the trachea to the alveoli.  Bronchi with a wall thickness of less than 300 um is not visible on CT or HRCT.  As a consequence, normal bronchi less than 2 mm in diameter or closer than 2 cm from pleural surfaces equivalent to seventh to ninth order airways are generally below the resolution even of high-resolution CT
  39. 39. Bronchus BLOOD SUPPLY Bronchial Arteries— 2 on left side i.e. superior and inferior 1 on right side Left arises from thoracic aorta Right from either thoracic aorta, sup. left bronchial or right 3rd intercostal artery VENOUS DRAINAGE on right- azygous vein on left- left superior intercostal or accessory hemiazygous vein • NERVE SUPPLY Pulmonary plexus at hilum (vagus and sympathetic)
  40. 40. Broncho-arterial ratio (B/A)  Internal diameter of both bronchus and accompanying arterial diameter calculated and ratio measured.  Normal ratio is 1:1  B/A ratio >1.5 indicates bronchiectasis. NB:: B/A ratio increases with age and may exceed 1 in normal patients > 40 years. 42
  41. 41. Increased broncho-arterial ratio  Ageing  High altitude Pathological conditions -  Bronchiectasis  Chronic asthma Conditions that can reduce pulmonary arterial calibres  Chronic embolism Decreased broncho-arterial ratio  < 0.65 conditions that cause bronchoconstriction
  42. 42. Secondary pulmonary lobule  Smallest lung unit that is surrounded by connective tissue septa.  The basic anatomic unit  Irregular polyhedral in shape.  Measures 1 to 2.5 cm 45
  43. 43. Anatomy of the Secondary Lobule and Its Components 1. Interlobular septa and contiguous subpleural interstitium, 2. Centrilobular structures, and 3. Lobular parenchyma and acini.
  44. 44. Interlobular septa and contiguous subpleural interstitium  The secondary pulmonary lobule is marginated by septa which extends from the pleural surface.  They measure 0.1 mm in thickness.  They are less well defined in central lung Lobular core  The secondary lobule is supplied by arteries and bronchioles that measures approximately 1 mm in diameter.  It consists of functioning lung parenchyma namely the alveoli, alveolar duct and vessels. The parenchyma is supported by network of central and peripheral fibers of interstitium.
  45. 45. Pulmonary acinus  Portion of lung parenchyma supplied by a single respiratory Bronchiole.  Size is 7 to 8 mm in adults  3 to 24 acini = Sec Pul. Lobule 49
  46. 46. A group of terminal bronchioles
  47. 47. Accompanying pulmonary arterioles
  48. 48. Surrounded by lymph vessels
  49. 49. Pulmonary veins
  50. 50. Pulmonary lymphatics
  51. 51. 56 Connective Tissue Stroma
  52. 52. Lung interstitum Lung interstitium Axial fiber system Peribronchovascular interstitium Centrilobular interstitium Peripheral fiber system Subpleural interstitium Interlobular septa
  53. 53.  The peribronchovascular interstitum invests the bronchi and pulmonary artery in the perihilar region.  The centrilobular interstitium are associated with small centrilobular bronchioles and arteries  The subpleural interstitium is located beneath the visceral pleura; envelops the lung into fibrous sac and sends connective tissue septa into lung parenchyma.  Interlobular septa constitute the septas arising from the subpleural interstitium.
  54. 54. Lymphangitic carcinomatosis : show diffuse smooth and nodular septal thickening. • Focal septal thickening in lymphangitic carcinomatosis Sarcoidosis : right lung base shows interlobular septal thickening associated with several septal nodules giving beaded appearance
  55. 55. The normal pulmonary vein branches are seen marginating pulmonary lobules. The centrilobular artery branches are visible as a rounded dot
  56. 56. Anatomy of pleural surfaces and chest wall. 63
  57. 57. Pattern of lung disease in HRCT PART - 3
  58. 58. Q.1. What is the dominant HR-pattern ? Q.2. Where is it located within the secondary lobule (centrilobular, Perilymphatic or random) ? Q.3. Is there an upper versus lower zone or a central versus peripheral predominance ? Q.4. Are there additional findings (pleural fluid, lymphadenopathy) ? Structured approach
  59. 59. HRCT PATTERN INCREASED LUNG ATTENUATION LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR OPACITIES PARENCHYMAL OPACIFICATION consolidation Ground glass DECREASED LUNG ATTENUATION CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION AIR TRAPPING ON EXPIRATORY SCANS
  60. 60. Linear and reticular opacities  Represents thickening of interstitial fibers of lung by - fluid or - fibrous tissue or - infiltration by cells 67
  61. 61. Interface sign Irregular interfaces between the aerated lung parenchyma and bronchi, vessels, or visceral pleural surfaces. Represent thickened interlobular septa, intralobular lines, or irregular scars. Nonspecific. Common in patients with an interstitial abnormality, fibrotic lung disease. Described by Zerhouni et al
  62. 62. Peribronchovascular Interstitial Thickening PBIT Smooth Pulmonary edema/ hemorrhage Lymphoma / leukemia Lymphangitic spread of carcinoma Nodular Sarcoidosis Lymphangitic spread of carcinoma Irregular Due to adjacent lung fibrosis Sarcoidosis, silicosis, TB and talcosis Venous, lymphatic or infiltrative disease lymphatic or infiltrative diseases
  63. 63. sarcoidosis Unilateral lymphangitic spread of carcinoma
  64. 64. Interlobular septal thickening  Normally, only a few septa seen  On HRCT, if numerous interlobular septas are seen, it almost always indicate abnormality.  Septal thickening d/t -interstitial fluid, cellular infiltration or fibrosis.  The thickened interstitium outline the secondary pulmonary lobules and are perpendicular to the pleura.  D/D are similar to that of PBIT.
  65. 65. Smooth Septal thickening Septal thickening and ground-glass opacity with a gravitational distribution in a patient with cardiogenic pulmonary edema.
  66. 66. Nodular Septal thickening Focal septal thickening in lymphangitic carcinomatosis Lymphangitic carcinomatosis : show diffuse smooth and nodular septal thickening. Sarcoidosis : right lung base shows interlobular septal thickening associated with several septal nodules giving beaded appearance
  67. 67. Intralobular interstitial thickening (Intralobular lines)  Results in a fine reticular pattern on HRCT, with the visible lines separated by a few millimeters  Fine lace/ netlike appearance  Causes :  Pulmonary fibrosis  Asbestosis 74
  68. 68. Parenchymal Bands  Non tapering , reticular opacity usually 1 to 3 mm in thickness and from 2 to 5 cm in length.  Is often peripheral and generally contacts the pleural surface  D/D :  1. Asbestosis  2. Sarcoidosis  3. Silicosis/ coal worker pneumoconiosis  4. Tuberculosis with associated scarring. 75
  69. 69. Subpleural Interstitial Thickening  Mimic thickening of fissure.  DD similar to that of interlobular septal thickening.
  70. 70. Honeycombing  Small cystic spaces with irregularly thickened bronchiolar walls composed of fibrous tissue.  Predominate in the peripheral and subpleural lung regions  Indicates the presence of “END stage” disease regardless of the cause. The Fleischner Society definition is clustered cystic air spaces (between 3-10 mm in diameter but occasionally as large as 2.5 cm) which are usually subpleural and basal in distribution. The walls of the cysts are well-defined and often thick (1-3 mm)
  71. 71. Causes Lower lobe predominance : 1. UIP or interstitial fibrosis 2. Connective tissue disorders 3. Hypersensitivity pneumonitis 4. Asbestosis 5. NSIP (rare) Upper lobe predominance : 1. End stage sarcodosis 2. Radiation 3. Hypersensitivity Pneumonitis 4. End stage ARDS 78
  72. 72. Size, Distribution, Appearance Nodules and Nodular Opacities Size Small Nodules: <10 mm Miliary - <3 mm Large Nodules: >10 mm Masses - >3 cms Appearance Interstitial opacity:  Well-defined, homogenous, Soft-tissue density Obscures the edges of vessels or adjacent structure Air space: Ill-defined, inhomogeneous. Less dense than adjacent vessel – GGO small nodule is difficult to identify 79
  73. 73. Interstitial nodules Air space opacity Miliary tuberculosis sarcoidosis in a lung transplant patient with bronchopneumonia
  74. 74. RANDOM: no consistent relationship to any structures PERILYMPHATIC: corresponds to distribution of lymphatics CENTRILOBULAR: related to centrilobular structuresDistribution 81
  75. 75. Perilymphatic distribution Nodules in relation to pulmonary lymphatics at  Perihilar peribronchovascular interstitium,  Interlobular septa,  Sub-pleural regions, and  Centrilobular interstitium. 82
  76. 76. Perilymphatic nodules: D/D  Sarcoidosis  Lymphangitic carcinomatosis  Lymphocytic interstitial pneumonia (LIP)  Lymphoproliferative disorders  Amyloidosis, Silicosis 83
  77. 77. Centrilobular nodules  Distributed primarily within the centre of the secondary pulmonary lobule  Reflect the presence of either interstitial or airspace abnormalities  Dense or ground-glass opacity  Subpleural lung is typically spared- distinguishes from diffuse random nodules.
  78. 78. • Ill defined centrilobular nodules of ground glass density in a patient with hypersensitivity pneumonitis
  79. 79. Tree-in-bud  Centrilobular nodules m/b further characterized by presence or absence of ‘‘tree-in-bud.’’  Tree-in-bud - 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  This finding is almost always seen with pulmonary infections.
  80. 80. Centrilobular nodules with or without tree-in-bud opacity: D/D : With tree-in-bud opacity  Bacterial pneumonia  Typical and atypical mycobacteria infections  Bronchiolitis  Diffuse panbronchiolitis  Aspiration  Allergic bronchopulmonary aspergillosis  Cystic fibrosis  Endobronchial neoplasms (particularly Broncho alveolar cell carcinoma) Without tree-in-bud opacity  All causes of centrilobular nodules with tree-in-bud opacity  Hypersensitivity pneumonitis  Respiratory bronchiolitis  Cryptogenic organizing pneumonia  Pneumoconioses  Langerhans’ cell histiocytosis  Pulmonary edema  Vasculitis  Pulmonary hypertension
  81. 81. Random nodules  Random nodules – No definable distribution  Are usually distributed uniformly throughout the lung parenchyma in a bilaterally symmetric distribution. Random nodules: Miliary tuberculosis.
  82. 82. Random nodules: D/D 1. Haematogenous metastases 2. Miliary tuberculosis 3. Miliary fungal infection 4. Disseminated viral infection 5. Silicosis or coal-worker’s pneumoconiosis 6. Sarcoidosis ( extensive) 7. Langerhans’ cell histiocytosis (early nodular stage)
  83. 83. Parenchymal Opacification Ground-glass opacity Consolidation Lung calcification & high attenuation opacities.
  84. 84. Ground glass opacities  Hazy increased attenuation of lung, with preservation of bronchial and vascular margins  Pathology : it is caused by # partial filling of air spaces, # interstitial/ alveolar wall thickening, # partial collapse of alveoli, # normal expiration, or # increased capillary blood volume 93
  85. 85. Importance of GGO  Can represent - microscopic interstitial/ alveolar disease  In the absence of fibrosis, mostly indicates the presence of an ongoing, active, potentially treatable process  NB :: Ground Glass opacity should be diagnosed only on scans obtained with thin sections : with thicker sections volume averaging is more - leading to spurious GGO, regardless of the nature of abnormality
  86. 86. Differential diagnosis : GGO
  87. 87.  The location of the abnormalities in ground glass pattern can be helpful:  Upper zone predominance: Respiratory bronchiolitis PCP.  Lower zone predominance: UIP, NSIP, DIP.  Centrilobular distribution: Hypersensitivity pneumonitis, Respiratory bronchiolitis
  88. 88. GGO with few cystic and reticular lesion in HIV + ve patient -- PCP Combination of GGO with fibrosis and tractional bronchiectasis-- NSIP
  89. 89. Persistent chest abnormality, weight loss • Broncho-alveolar cell carcinoma with ground-glass opacity & consolidation
  90. 90. Crazy paving pattern  It is scattered or diffuse ground-glass attenuation with superimposed interlobular septal thickening and intralobular lines.  Causes:
  91. 91. Combination of ground glass opacity and septal thickening : Alveolar proteinosis.
  92. 92.  Consolidation is defined as increased attenuation, which results in obscuration of the underlying vasculature, usually producing air bronchogram.  The presence of consolidation implies that the air within affected alveoli has been replaced by another substance, such as blood, pus, oedema, or cells.  When consolidation is evident on a chest radiograph, HRCT does not usually provide additional diagnostically useful information. Consolidation
  93. 93. D/D on the basis of presentation Acute consolidation is seen in: - Pneumonias (bacterial, mycoplasma , PCP) - Pulmonary edema due to heart failure or ARDS - Hemorrhage - Acute eosinophilic pneumonia Chronic consolidation is seen in: - Organizing Pneumonia - Chronic eosinophilic pneumonia - Fibrosis in UIP and NSIP - Bronchoalveolar carcinoma or lymphoma
  94. 94. Patchy ground-glass opacity, consolidation, and nodule mainly with peribronchovascular distribution with reversed halo signs (central ground-glass opacity and surrounding air-space consolidation) Peripheral consolidations with upper lobe predominance (photo negative of pulmonary edema)
  95. 95. Lung calcification & high attenuation opacities Multifocal lung calcification  Infectious diseases - TB, histoplasmosis, and varicella, pneumonia  Sarcoidosis , silicosis, Amyloidosis  Fat embolism associated with ARDS Diffuse & dense lung calcification  Metastatic calcification,  Disseminated pulmonary ossification, or  Alveolar microlithiasis
  96. 96. High attenuation opacity  Talcosis asso with fibrotic mass,  Inhalation of metals (tin/barium) Small focal areas of increased attenuation  Injection and embolized radiodense materials such as mercury or acrylic cement Diffuse, increased lung attn in absence of calcification  Amiodarone lung toxicity or  Embolization of iodinated oil after chemoembolization 107
  97. 97. 108
  98. 98. HRCT findings manifesting as decreased lung opacity Lung Cysts Emphysema Bronchiectasis 109
  99. 99. Lung cysts  Thin walled (less than 3mm) , well defined and circumscribed air containing lesions  They are lined by cellular epithelium, usually fibrous or epithelial in nature.  Common cause are : 1. Lymphangiomyomatosis 2. Langerhans Histiocytosis 3. Lymphoid interstitial pneumonia  They need to be differentiated from emphysematous bullae, blebs and pneumatocele.
  100. 100. Axial HRCT image through the upper lobes shows multiple bilateral bizarre- shaped cysts and small centrilobular nodules in a smoker with Langerhans’ cell histiocytosis. Axial HRCT image through the upper lobes shows multiple bilateral uniform, thin-walled cysts.
  101. 101. Bronchiectasis  Bronchiectasis is defined as localized, irreversible dilation of the bronchial tree.  HRCT findings of the bronchiectasis include # Bronchial dilatation # Lack of bronchial tapering # Visualization of peripheral airways.
  102. 102.  Bronchial dilatation  The broncho-arterial ratio (internal diameter of the bronchus /pulmonary artery) exceeds 1 , >1.5  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
  103. 103. Coned axial HRCT image shows bronchial dilation with lack of tapering . Bronchial morphology is consistent with varicose bronchiectasis.
  104. 104. A number of ancillary findings are also recognized:  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 Extensive, bilateral mucoid impaction Mosaic perfusion caused by large and small airway obstruction. Small centrilobular nodules are visible in the right lower lobe 115
  105. 105. Types 1. 1) Cylindrical bronchiectasis  Mildest form of this disease,  Thick-walled bronchi that extend into the lung periphery and fail to show normal tapering 2. 2) Varicose bronchiectasis  Beaded appearance of bronchial walls - dilated bronchi with areas of relative narrowing  String of pearls.  Traction bronchiectasis often appears varicose. 116
  106. 106. 3) Cystic bronchiectasis :  Group or cluster of air-filled cysts,  cysts can also be fluid filled, giving the appearance of a cluster of grapes. 4) Traction bronchiectasis :  Defined as dilatation of intralobular bronchioles because of surrounding fibrosis  due to fibrotic lung diseases 117
  107. 107. Differential diagnosis 1. Infective causes : specially childhood pneumonia, pertusis, measles, tuberculosis 2. Non- infective causes : Bronchopulmonary aspergillosis, inhalation of toxic fumes 3. Connective tissue disorder : Ehlers-Danlos Synd, Marfan synd , tracheobronchomegaly 4. Ciliary diskinesia : Cystic fibrosis, Kartangener synd, agammaglobulinemia . 5. Tractional bronchiectasis in interstitial fibrosis.
  108. 108. Emphysema  Permanent, abnormal enlargement of air spaces distal to the terminal bronchiole and accompanied by the destruction of the walls of the involved air spaces.
  109. 109. Centrilobular (proximal or centriacinar) emphysema  Found most commonly in the upper lobes  Manifests as multiple small areas of low attenuation without a perceptible wall, producing a punched-out appearance.  Often the centrilobular artery is visible within the centre of these lucencies. 120
  110. 110. Panlobular emphysema  Affects the entire secondary pulmonary lobule and is more pronounced in the lower zones  Complete destruction of the entire pulmonary lobule.  Results in an overall decrease in lung attenuation and a reduction in size of pulmonary vessels 121
  111. 111. Paraseptal (distal acinar) emphysema  Affects the peripheral parts of the secondary pulmonary lobule  Produces subpleural lucencies. 122
  112. 112. Cicatricial Emphysema/ irregular air space enlargement  previously known as irregular or cicatricial emphysema  can be seen in association with fibrosis with silicosis and progressive massive fibrosis/ sarcoidosis Bullous emphysema :  Does not represent a specific histological abnormality  Emphysema characterized by large bullae  Often associated with centrilobular and paraseptal emphysema
  113. 113. Paraseptal Emphysema vs Honeycombing Paraseptal emphysema Honeycomb cysts occur in a single layer at the pleural surface may occur in several layers in the subpleural lung predominate in the upper lobes predominate at the lung bases unassociated with significant fibrosis Asso with other findings of fibrosis. Associated with other findings of emphysema Absent
  114. 114. Pneumatocele  Defined as a thin-walled, air-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.
  115. 115. Cavitary nodule  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 Cavitary nodules or cysts in tracheobronchial papillomatosis. Fungal pneumonia
  116. 116. Mosaic attenuation & perfusion  Lung density and attenuation depends partially on amount of blood in lung tissue.  The term 'mosaic attenuation' is used to describe density differences between affected and non-affected lung areas.  It is seen as inhomogeneous attenuation of lung parenchyma with focal region of lucency which show smaller size of vessels  May be due to vascular obstruction, abnormal ventilation or airway disease/
  117. 117. Mosaic attenuation due to small airway disease  Air trapping and bronchial dilatation commonly seen.  Areas of increased attenuation have relatively large vessels, while areas of decreased attenuation have small vessels.  Causes include: Bronchiectasis, cystic fibrosis and bronchiolitis obliterans. Mosaic attenuation due to vascular disease  Common in patients with acute or chronic pulmonary embolism (CPE), and  Decreased vessel size in less opaque regions is often visible
  118. 118. MOSIAC PATTERN DEPENDENT LUNG ONLY PRONE POSITION RESOLVE PLATE ATELECTASIS NOT RESOLVE GROUND GLASS NONDEPENDENT LUNG EXPIRATION NO AIR TRAPPING VESSEL SIZE DECREASED VASCULAR NORMAL GROUND GLASS AIR TRAPPING AIRWAYS DISEASE
  119. 119. Inhomogeneous lung opacity: mosaic perfusion in a patient with bronchiectasis. central bronchiectasis with multifocal, bilateral inhomogeneous lung opacity. The vessels within the areas of abnormally low attenuation are smaller than their counterparts in areas of normal lung attenuation.
  120. 120. Air trapping on expiration  Most patients with air trapping seen on expiratory scans have inspiratory scan abnormalities, such as bronchiectasis, mosaic perfusion, airway thickening, or nodules suggest the proper differential diagnosis.  Occasionally, air trapping may be the sole abnormal finding on an HRCT study.  The differential diagnosis include ---  bronchiolitis obliterans; asthma; chronic bronchitis; and hypersensitivity pneumonitis
  121. 121. Air trapping on expiratory imaging in the absence of inspiratory scan findings in a patient with bronchiolitis obliterans. (A) Axial inspiratory image through the lower lobes shows no clear evidence of inhomogeneous lung opacity. (B) Axial expiratory image shows abnormal low attenuation (arrows) caused by air trapping, representing failure of the expected increase in lung attenuation that should normally occur with expiratory imaging.
  122. 122. Head cheese sign  It refers to mixed densities which includes presence of- # consolidation # ground glass opacities # normal lung # Mosaic perfusion  Signifies mixed infiltrative and obstructive disease  Common cause are : Hypersensitive pneumonitis Sarcoidosis DIP
  123. 123. Axial HRCT image in a patient with hypersensitivity pneumonitis shows a combination of ground-glass opacity, normal lung, and mosaic perfusion (arrow) on the same inspiratory image. 134
  124. 124. Distribution within the lung Upper lung zone preference is seen in: 1.Inhaled particles: pneumoconiosis (silica or coal) 2.Smoking related diseases (centrilobular emphysema 3. Respiratory bronchiolitis (RB-ILD) 4.Langerhans cell histiocytosis 5.Hypersensitivity pneumonitis 6.Sarcoidosis Lower zone preference is seen in: 1. UIP 2. Aspiration 3. Pulmonary edema
  125. 125. Central vs peripheral zone • Central Zone Peripheral zone 1. Sarcoidosis 1. COP 2. Cardiogenic pulmonary 2. Ch Eosinophilic Pneumonia edema 3. UIP 3. Bronchitis 4. Hematogenous mets
  126. 126. Additional findings Pleural effusion is seen in:  Pulmonary edema  Lymphangitic spread of carcinoma - often unilateral  Tuberculosis  Lymphangiomyomatosis (LAM)  Asbestosis
  127. 127. Hilar and mediastinal 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' in lymph nodes occurs in ----Silicosis and coal-worker's pneumoconiosis and is sometimes seen in sarcoidosis, post irradiation Hodgkin disease, blastomycosis and scleroderma .
  128. 128. Common Interstitial lung diseases PART 4
  129. 129. NSIP pattern
  130. 130. COP 1) Patchy consolidation with a predominantly sub-pleural and/or peribronchial distribution 2)small, ill-defined peribronchial or peribronchiolar nodules large nodules or masses 3) Bronchial wall thickening or dilatation in the abnormal lung regions 4) Perilobular pattern with ill-defined linear opacities that are thicker than the thicked interlobular septa and have an arcade or polygonal appearance 5) GGO or crazy paving 6) The reverse halo or Atoll sign is considered to be highly specific, although only seen in <20% of patients with COP 5.
  131. 131. AIP  GGO- B/L  Air space consolidation  Traction bronchiectasis >80%  Lung parenchymal architectural distortion  Resemblance to ARDS
  132. 132. RB-ILD  GGO – upper zone  Centrilobular nodules – poorly defined  Smoking related changes: centrilobular emphysema, bronchial wall thickening  Advanced-: fibrosis
  133. 133. DIP  Extensive GGO  Linear opacities, cysts  Fibrotic changes <50%  Smoking related changes  Confused with RB-ILD
  134. 134. LIP  Mid to lower zone predominance  Thickening of bronchovascular bundles  Interstitial thickening  Pulmonary nodules  GGO  Thin walled cysts  Mediastinal lymphadenopathy
  135. 135. Idiopathic Pleuro-parenchymal fibroelastosis  Marked apical pleural thickening  Architectural distortion  Reticular abnormality  Pneumothorax  Lymphadenopathy – Mediastinal/ axillary
  136. 136. Combined pulmonary fibrosis and emphysema  Centrilobular/ paraseptal emphysema – often upper zone predominant  Pulmonary fibrosis –lower lobes
  137. 137. Golden rules for HRCT interpretation 1. Honeycombing with a basal and sub-pleural predominance is highly suggestive of UIP. Lung biopsy is rarely performed when HRCT shows these findings. 2. Concentric lower lobe GGO without honeycombing suggests NSIP. In a patient with collagen vascular disease ,biopsy is uncommoly performed. 3. Patchy or noular sub-pleural or peribronchial consolidation is typical of COP. 4. Cystic air spaces or GGO may represent LIP. LIP is usually associated with other diseases. 5. Diffuse or centrilobular GGO in a smoker is typical of DIP or RB-ILD
  138. 138. Conclusion  A thorough knowledge of the basic anatomy is of utmost importance.  Overall distribution  Differential diagnosis  Correlation of history, clinical findings and radiological pattern to clinch the diagnosis.

×