1. HRCT THORAX
Dr.Nihaal Reddy
MD
India

2. HRCT … MEANING
HRCT is the use of thin section CT images (0.625 to 2 mm slice thickness) often
with a high-spatial-frequency reconstruction algorithm to detect and
Characterize disease affecting the pulmonary parenchyma and airways.
There are 2 general approaches are available for acquiring HRCT images.
The first and more traditional or “dedicated” method entails obtaining axial
HRCT images spaced at 10 to 20 mm intervals throughout the thorax, which
is an approach applicable to both single-detector and multi-detector scanners.
The second uses the ability of multi-detector row CT (MDCT) scanners to
Provide volumetric data sets allowing spaced,contiguous, and/or overlapping
HRCT images to be reconstructed.
With both methods, image data are routinely acquired at full inspiration with
patients in the supine position.
Additional options include obtaining prone images to evaluate for
basilar lung disease, and end-expiratory images to evaluate for air-trapping

3. Goals
The main objective of HRCT is to detect, characterize, and determine the
extent of diseases that involve the lung parenchyma and airways.
Indications
The indications for the use of HRCT of the lungs include, but are not limited
to, the following:
1. Evaluation of diffuse pulmonary disease discovered on chest radiographs,
conventional CT of the chest,or other CT examinations that include portions
of the chest, including selection of the appropriate site for biopsy of diffuse
lung disease.
2. Evaluation of the lungs in patients with clinically suspected pulmonary
disorders with normal or equivocal chest radiographs.
3. Evaluation of suspected small and/or large airway disease.
4. Quantification of the extent of diffuse lung disease for evaluating
effectiveness of treatment.

4. a. High-spatial-frequency reconstruction algorithm, such as a bone algorithm.
b. Slice thickness (≤2 mm for nonhelical CT, ≤1.5 mm nominal slice thickness for
helical CT).
c. Table speed for volumetric HRCT to enable single-breath-hold acquisition, when
possible.
d. Gantry rotation: ≤1 second.
e. Detector configuration selection (e.g., 2 channels on MDCT for incremental
HRCT).
f. Axial (incremental HRCT) or helical (volumetric HRCT) modes of data acquisition.
g. Field of view (FOV) for small, medium, and large patients
h. kVp and mA both per slice as well as optimized for volumetric data acquisition.
Typically this entails use of 120 kVp and approximately ≤240 mA, although use of
lower doses is encouraged, especially for younger patients or those who may need
serial imaging. In the latter case, using identical technical parameters for each study
facilitates direct comparison between studies and is of particular value when
quantitative CT measurements are employed.
i. Superior and inferior extent of the region of interest to be imaged.
j. Patient positioning (supine and/or prone).
k. State of respiration (inspiration and/or expiration).
Protocol

5. The secondary lobule is the basic anatomic unit of pulmonary structure and
function.
Interpretation of interstitial lung diseases is based on the type of
involvement of the secondary lobule.
It is the smallest lung unit that is surrounded by connective tissue septa.
It measures about 1-2 cm and is made up of 5-15 pulmonary acini, that
contain the alveoli for gas exchange.
The secondary lobule is supplied by a small bronchiole (terminal
bronchiole) in the centre, that is paralleled by the centrilobular artery.
Pulmonary veins and lymphatics run in the periphery of the lobule within
the interlobular septa.
Under normal conditions only a few of these very thin septa will be seen.
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.
Anatomy

7. Secundary lobules. The centrilobular artery (in blue: oxygen-poor blood)
and the terminal bronchiole run in the center. Lymphatics and veins (in red:
oxygen-rich blood) run within the interlobular septa

8. Perilymphatic area is the peripheral part of the secundary lobule.
It is usually the site of 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.
Centrilobular area is the central part of the secondary lobule.
It is usually the site of diseases, that enter the lung through the airways
( i.e. hypersensitivity pneumonitis, respiratory bronchiolitis, centrilobular
emphysema ).

9. There are six basic patterns:
1. Air-space or alveolar consolidation
2. Linear or septal
3. Reticular
4. Nodular
5. Reticulonodular
6. Ground-glass opacity

10. • To confirm or exclude diffuse lung disease in patients with normal or
equivocal radiographic appearances and/or functional abnormalities
• To narrow the differential diagnosis or make a histospecific diagnosis in
patients with obvious but nonspecific radiographic abnormalities
• To guide the type and site of lung biopsy
• To investigate patients presenting with haemoptysis
• To investigate patients with suspected bronchiectasis or unexplained severe
obstructive airways disease
• To assess the distribution of emphysema in patients considered for lung
volume reduction surgery
• To evaluate disease reversibility, particularly in patients with fibrosing lung
disease
Indication for HRCT

11. REVERSIBLE PATTERNS ON HRCT

12. Air-space or Alveolar Consolidation
The terms air-space consolidation and alveolar consolidation
refer to diseases associated with pathologic filling of
alveoli(i.e., replacement of alveolar air) as the predominant
abnormality.
Radiographic abnormalities indicating the presence of air-
space or alveolar disease-
( 1) confluent or homogeneous opacities obscuring vessels,
(2) air bronchograms,
(3) ill-defined or fluffy opacities
( 4) air alveolograms,
(5) acinar or air-space nodules
( 6) preserved lung volume
(7) a tendency for opacities to extend to pleural surfaces.

13. In general, the differential diagnosis of air-space consolidation is based on
a consideration of the substance that is replacing alveolar air:
1. Water (e.g., the various types of pulmonary edema)
2. Blood (e.g., pulmonary hemorrhage)
3. Pus (e.g., pneumonia)
4. Cells (e.g., bronchioloalveolar carcinoma, lymphoma,
eosinophilic pneumonia, organizing pneumonia [bronchiolitis
obliterans organizing pneumonia or BOOP],
hypersensitivity pneumonitis)
5. Other substances (e.g., lipoprotein in alveolar proteinosis,
lipid in lipoid pneumonia).
Patients with consolidation may be divided into two primary groups for the
purpose of diagnosis: those with diffuse or bilateral consolidation and those
with focal consolidation.

14. Water (edema)
Hydrostatic (cardiogenic) pulmonary edema
Increased permeability (noncardiogenic) pulmonary edema with
diffuse alveolar damage (acute respiratory distress syndrome [ARDS])
Blood (hemorrhage)
Aspiration of blood
Bleeding diathesis
Chemotherapy
Leukemia
Low platelets
Collagen-vascular disease and
immune complexVasculitis
Goodpasture's syndrome
Idiopathic pulmonary hemosiderosis
Trauma
Vasculitis
Other substances
Alveolar proteinosis (lipoprotein)
Lipoid pneumonia (lipid)
Pus (pneumonia)
Bacterial pneumonia
Pneumonia in an immunosuppressed
patient
Tuberculosis
Nontuberculous mycobacteria
Fungal pneumonia (histoplasmosis,
aspergillosis most common)
Cells
Neoplasm
Bronchioloalveolar carcinoma
Lymphoma
Eosinophilic pneumonia
Organizing pneumonia (BOOP)
Hypersensitivity pneumonitis
Idiopathic interstitial pneumonias
DIFFUSE

15. Perihilar consolidation
Perihilar "bat-wing" consolidation shows central consolidation with
sparing of the lung periphery seen in :
• pulmonary edema (hydrostatic or permeability).
• pulmonary hemorrhage,pneumonias (including bacteria and atypical
pneumonias such as Pneumocystis jiroveci and viral pneumonia),
• inhalational lung injury.

16. Peripheral subpleural consolidation is the opposite of a bat-wing
pattern (ie., a reverse bat-wing pattern). Consolidation is seen adjacent to the
chest wall, with sparing of the perihilar regions. It is most often seen in a
patients with a chronic lung disease (also the reverse of what is true of a bat-
wing pattern). It is classically associated eosinophilic pneumonia
but may also occur with organizing pneumonia (BOOP), sarcoidosis, radiation
pneumonitis, lung contusion, or bronchioloalveolar carcinoma.

17. Diffuse patchy consolidation may be seen with any pneumonia
(bacterial, mycobacterial, fungal, viral, PCP); pulmonary edema (hydrostatic
and permeability); acute respiratory distress syndrome (ARDS); pulmonary
hemorrhage syndromes; aspiration; inhalational diseases; eosinophilic
diseases; and diffuse bronchioloalveolar carcinoma. The patchy opacities may
correspond to consolidation of lobules, subsegments, or segments

18. Diffuse air-space nodules as a prominent feature of consolidation are
typical of endobronchial spread of disease . This appearance is seen in patients
with endobronchial spread of infection such as tuberculosis (TB) or
mycobacterium avium complex (MAC), bacterial bronchopneumonia,viral
pneumonia (cytomegalovirus [CMV], measles), endobronchial spread of
bronchioloalveolar carcinoma, pulmonary hemorrhage, or sometimes
aspiration.

19. Focal Consolidation
Water (edema) (uncommon)
Edema in a patient with
Pulmonary artery obstruction
Hypoplastic pulmonary artery
Swyer-James syndrome
Decubitus position
Reexpansion edema
Pulmonary vein occlusion
Systemic to pulmonary artery shunt
Bland aspiration
Atelectasis with drowned lung
Blood (hemorrhage)
Contusion
Infarction
Aspiration of blood
vasculitis
Pus (pneumonia)
Bacterial
Tuberculosis or nontuberculous
mycobacterial
Fungal
Virus (uncommon)
Pneumocystis (uncommon)
Aspiration pneumonia
Atelectasis with post-obstructive
pneumonia
Cells
Neoplasm
Bronchioloalveolar carcinoma
Lymphoma and other lymphoproliferative
diseases
Eosinophilic pneumonia or other
eosinophilic diseases
Organizing pneumonia (BOOP)
Sarcoidosis
Other substances-lipoid pneumonia

20. Lobar consolidation is most typical of pneumonia (including S.
pneumoniae, Klebsiella , Legionella, and TB) and abnormalities associated
with bronchial obstruction

21. Round or spherical consolidation is most typical of bronchioloalveolar
carcinoma, lymphoma or lymphoproliferative disease, or pneumonia (i.e., round
pneumonia). A round or spherical pneumonia is typical of organisms that spread
via the pores of Kohn and progress to being lobar, such asS. pneumoniae, Klebsiella
or TB
Segmental (or sub segmental) consolidation may be diagnosed if a wedge-
shaped opacity of more than a few centimeters in size is visible with the apex of the
wedge pointing toward the hilum. This finding suggests an abnormality related to a
segmental (or subsegmental) bronchus or artery; such as bronchial obstruction due
to mucus or tumor, bronchopneumonia, focal aspiration, or pulmonary embolism
with infarction.

22. Acute
• Pulmonary edema- hydrostatic ( central ), interstitial ( patchy)
• Pneumonia – lobar,segmental or diffuse
• Hemorrhage – focal or diffuse
• Aspiration
Chronic
• Cryptogenic organizing pneumonia
• Chronic eosinophilic pneumonia – peripheral and upper lobes
• Neoplsam-post obstructive or non segmental ( BAC ,
Lymphoma)
• Alveolar proteinosis- crazy paving

23. Linear or Septal Pattern
A linear pattern is defined by the presence of Kerley's A ,B or C lines.
Kerleys A and B lines result from thickening of interlobular
septa this pattern also may be referred to as septal.
Kerley A lines are seen less often. They are oblique in orientation,
several centimetres in length. and are located within the central or
parahilar lung.
Kerley B lines are most common. They are horizontal lines, 1 to 2 cm. in
length. They are seen in contact with the pleural surface and are best seen
laterally at the costophrenic angles
Kerley C lines are seen at the lung bases and represent interlobular septa
en face. They result in a nonspecific, reticular pattern and are unimportant
in diagnosis, because B lines invariably are visible as well

24. • Causes
• Pulmonary edema - most common cause , lower lung
distribution, smooth interlobular thickening
• Lymphangitic carcinomatosis – usually focal and nodular
with lymph node enlargemnt seen initially ( 30% cases)
• Sarcoidosis – thickening maybe smooth or nodular associated
with bilateral hilar and mediastinal lymphadenopathy
• UIP – irregular septal thickening with other changes of fibrosis
• Asbestosis- irregular septal thickening with associated findings
of fibrosis and pleural plaques or thickening
• Chronic or recurrent pulmonary hemorrhage and
hemosiderosis

25. Lymphangitic ca
Pulmonary edema

26. Reticular Pattern
• Usual interstitial pneumonia
• Alveolar proteinosis
• Collagen-vascular disease
• Drug-related fibrosis
• Asbestosis
• End-stage HP
• End-stage sarcoidosis
• Nonspecific interstitial pneumonia
• Radiation
• End-stage adult respiratory distress
syndrome
• Cystic lung disease
• Langerhans' cell histiocytosis
• Lymphangiomyomatosis
• Tuberous sclerosis
• Sjogren's syndrome with UP
• LIP
• Cystic bronchiectasis
• Papillomatosis
• Pneumonia with
• pneumatoceles

27. Reticular means netlike, which is an excellent description of the appearance
of this pattern. A reticular pattern is characterized by multiple intersecting
lines, often irregular in appearance, outlining round or irregular spaces .
The reticular pattern has been subdivided into three sub-patterns, based on
the size of the spaces surrounded by lines:
Fine pattern (spaces smaller than 3 mm )- Some cystic lung diseases
(e.g., Langerhans cell histiocytosis, lymphangiomyomatosis [LAM]) result
in a reticular pattern because of superimposition of the walls of cysts

28. Medium pattern (spaces 3 to 10 mm. ) - A medium pattern is typical of
patients with pulmonary fibrosis and honeycombing ; the reticulation often
appears to have a peripheral, posterior, and lower lobe predominance
Coarse pattern (spaces larger than 10 mm.)- it is seen in cystic disease
UIP

29. MIMICS
Perilobular distribution may give the spurious impression of thickening of
the interlobular septa. The disposition of the pathologic process, such that it is
‘smeared’ around the internal lobular surface, creates the appearance of a
thickened lobular margin The perilobular sign is encountered in cases of
organizing pneumonia

30. Another situation in which there may be apparent, rather than real,
interlobular septal thickening in patients with emphysema; the residual
peripheral alveoli collapse against the lobule margins, and in so doing
spuriously thicken the interlobular septa. Furthermore, in cigarette smokers
there may also be accompanying interstitial fibrosis,which is partly
responsible for conspicuous thickening of the ‘Remnant’ interlobular
septa

31. Crazy paving pattern ( septal thickening with underlying ground glass
opacification)
• Alveolar proteinosis
• Sarcoid
• NSIP
• Organizing pneumonia
• (COP/BOOP)
• Infection(PCP, viral,
• Mycoplasma, bacterial)
• Neoplasm
• (Bronchoalveolar ca (BAC)
• Pulmonary hemorrhage
• Edema ( ARDS, AIP)

32. Perilymphatic distribution
Seen in pleural surfaces, interlobular septa and the peribronchovascular
interstitium.
Nodules are almost always visible in a subpleural location, particularly in
relation to the fissures.
Centrilobular distribution
Nodules are limited to the centrilobular region.
Centrilobular nodules spare the pleural surfaces.
The most peripheral nodules are centered 5-10mm from fissures or the
pleural surface.
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.
Nodular Pattern
A nodular pattern is characterized on chest radiographs by the presence of
innumerable small rounded opacities that are discrete and range in
diameter from 2 to 10 mm

34. Sarcoidosis

35. HP

36. Metastatic lung ca

37. Miliary TB

38. Centrilobular tree-in-bud Pattern
When a centrilobular distribution of nodules is present, the tree-in-bud pattern
should be sought.This finding nearly always represents the presence of dilated
and fluid-fillied (with mucus or pus) centrilobular bronchioles
Nodular branching opacities are visible in the lung periphery, and these are
considerably larger than normal branching vessels. Tree’s-in-bud, which are
centrilobular, tend to be centered 5 to 10 mm from the pleural surface when
they are seen in the peripheral lung. Centrilobular nodules or clusters of
nodules (rosettes) also may be seen.
Differential diagnosis
• Endobronchial spread of infection (bacteria, tuberculosis,mycobacteria,
fungus)
• Airways diseases with infection (e.g., ~c fibrosis,bronchiectasis)
• Mucous plugging (asthma, allergic bronchopulmonary aspergillosis)
• Aspiration
• Bronchioloalveolar carcinoma (rare)

39. A.Tree-in-bud in a patient with Pseudomonas bronchopneumonia.
B. CentrilobuJar nodules and tree-in-bud in a patient with
Haemophilus influenzae bronchopneumonia

40. RETICULONODULAR PATTERN
The term reticulonodular, indicating a perceived combination of lines
and dots, is used commonly by radiologists but is of limited value in
diagnosis. Reticulonodular opacities observed on plain radiographs
often are artifactual, resulting from the superimposition of mostly lines
or mostly nodules. Thus, it is generally a good idea, if a reticulonodular
pattern is detected on plain radiographs, to decide whether a reticular
or nodular pattern predominates and use that finding for differential
diagnosis.
Sarcoidosis, lymphangitic spread of tumor, and diffuse amyloidosis.

41. Ground-glass Opacity
Ground-glass opacity represents an increase in lung density without the
presence of frank consolidation.
ground-glass opacity on HRCT does not obscure the pulmonary vasculature
At a microscopic level, the changes responsible for ground-glass opacity are
partial filling of the airspaces, considerable thickening of the interstitium, or a
combination of the two, Nevertheless, the basic mechanism behind the
generation of the HRCT pattern of ground-glass opacification of the lungs is
nothing more or less than the displacement of air. Thickening of the
intralobular interstitium by fluid or a cellular infiltrate is below the limits of
resolution of HRCT and volume averaging results in an amorphous increase in
lung density.
In cases in which the presence of ground-glass opacity is equivocal, it may be
helpful to compare the attenuation of the lung parenchyma with air in the
bronchi: in normal individuals the difference in density is marginal,
whereas ground-glass opacity makes the airways more obvious (the ‘black
bronchus’ sign).

42. In the normal state, most of the volume of the voxels is taken up by air.
In situations in which there is gross thickening of the interstitium and/or
partial filling of the airspaces with cells or fluid (causing displacement of
air) there is an increase in density, seen as ground-glass opacification on
HRCT

43. • Subacute hypersensitivity pneumonitis
• Acute respiratory distress syndrome and acute interstitial pneumonia
• Desquamative interstitial pneumonia
• Respiratory bronchiolitis–interstitial lung disease
• Pneumocystis jirovecii pneumonia, cytomegalovirus pneumonia,
severe acute respiratory syndrome (SARS)
• Sarcoidosis
• Nonspecific interstitial pneumonia
• Pulmonary edema
• Idiopathic pulmonary hemorrhage and diffuse pulmonary vasculitis
• Bronchioloalveolar cell carcinoma
• Eosinophilic pneumonias
• Lymphoid interstitial pneumonia
• Idiopathic pulmonary fibrosis (atypical)
• Radiation pneumonitis
• Drug toxicity
• Alveolar proteinosis
• Sickle cell disease
• (Normal lung at near residual volume, particularly in children)
Differentials

44. • Distribution (e.g. subpleural location in nonspecific interstitial
pneumonia)
• Texture (e.g. fine granularity may reflect intralobular fibrosis)
• Superimposed nodularity (e.g. poorly defined centrilobular
nodules in RB-ILD)
• Background mosaic attenuation pattern (e.g. subacute
hypersensitivity pneumonitis)
• Overlay of interlobular septal thickening (e.g. in alveolar proteinosis
– ‘crazy-paving’ sign)
• Thin-walled cysts (e.g. in lymphoid interstitial pneumonia)
• Dilatation and distortion of bronchi (implies retractile fibrosis)
• Mediastinal lymphadenopathy (e.g. sarcoidosis)
Additional useful features in conditions characterized by
ground-glass opacity

45. The pulmonary vasculature is not obscured by this degree of opacification and the
air-filled
bronchi are more conspicuous than usual (black bronchus sign) but not unduly
dilated

47. MOSAIC ATTENUATION PATTERN
Patchy areas of decreased lung attenuation in patients with
abnormal lung perfusion and reduced regional pulmonary blood
volume.

48. Air Trapping on Expiratory Computed Tomography
In patients with mosaic perfusion resulting from airway disease, air trapping
often is visible on expiratory scans in lucent lung regions. Although mosaic
perfusion and air trapping look the same, and often are related, they are
distinct findings. Mosaic perfusion is an inspiratory scan finding, and air
trapping is an expiratory scan finding. A variety of techniques can be used to
obtain expiratory scans.
Dynamic expiratory scans are most sensitive.
These are obtained with a spiral scanner by continuing to rotate the gantry as
the patient exhales, obtaining a series of five or six scans at a single level.
Normally, lung increases homogeneously in attenuation on expiratory scans
(usually by more than 100 HU), although dependent lung increases more than
nondependent lung .
In the presence of air trapping. the lung remains lucent on expiration, with
little increase in measured attenuation, and shows little change in volume.
Patchy air trapping is characteristic of small airway diseases. Larger areas of
air trapping (e.g., an entire lobe) suggest a large airway abnormality. Air
trapping on HRCT is associated principally with bronchiolitis

49. Mosaic perfusion due to bronchiolitis
obliterans. Minimum intensity projection
Maximum intensity projection

50. B: Expiratory scan shows a normal increase in
attenuation of the dense regions shown in
{A). The relatively lucent regions in {A) show little
change in attenuation on the expiratory
scan due to air trapping.
Mosaic perfusion and air trapping in a patient with
bronchiolitis obliterans A: Inspiration scan shows
inhomogeneous lung attenuation
due to mosaic perfusion. Several regions (arrows)
appear relatively dense and
contain larger vessels. Other lung regions appear
relatively lucent and contain small vessels.

51. CYSTIC AIRSPACES
A cyst is an air filled lesion that has a smooth and uniform wall 3 mm or less
in thickness.
Several lung diseases are characterized by cysts as their primary
abnormality.
• Langerhans cell histiocytosis (LCH),
• Lymphangiomyomatosis (LAM),
• Lymphoid interstitial pneumonia(LIP)
• Tuberous sclerosis (TS)
• Neurofibromatosis,
• Pneumatoceles
• Hypersensitivity pneumonitis (subacute)
• Sjorgren's syndrome
• Tracheal papillomatosis
• Traumatic cysts

52. Langerhans cell histiocytosis (LCH),
• Lung involvement in 40%; 90% of adult patients are smokers
• Granulomas in early stages ( predominantly peribronchiolar )
• Lung cysts late in course ( usually less than 1 cm )
• Cysts irregular in shape
• Upper lobe predominance
• Spare costophrenic angles
• Nodules or cavitary nodules in some

53. • Lymphangiomyomatosis (LAM),
• Proliferation of immature-appearing smooth muscle cells
• Women of childbearing age
• Identical to the lung disease seen in tuberous sclerosis
• Cystic lung destruction
• Chylous effusions
• Renal angiomyolipomas are present in 15%
• Lung cysts
• Round in shape
• Diffuse distribution
• Involve the costophrenic angles
• Nodules occasionally seen

54. • Tuberous sclerosis (TS)
TS is an autosomal-dominant genetic disease of mesoderm associated with
the classic triad of seizures, mental retardation. and adenoma sebaceum. It
also is associated with abnormalities such as angiomyolipomas of the
kidneys, cardiac rhabdomyomas, and retinal phacomas.
Maybe be individually indistinguishable from LAM, however renal
anamolies affect TS more than LAM

55. NEUROFIBROMATOSIS
Lung disease is present in 10% to 20% of adult patients with
neurofibromatosis. It is characterized histologically by bullae in the upper
lobes and interstitial fibrosis at the lung bases. Patients typically present
with dyspnea.
Radiographs usually show upper lobe lucency or bullae, which usually are
symmetrical. A reticular pattern. Which sometimes is characterized by
Kerley's B lines, is seen at the lung bases in 50% of cases . Lung volumes
typically are increased, with flattening of the diaphragms.
Neurofibromatosis.
HRCT shows cysts and bullae
indistinguishable from emphysema

56. PNEUMATOCELES
Pneumatoceles are thin-walled, air filled cysts that typically occur in
association with acute pneumonia, trauma, or aspiration of hydrocarbon
fluid and is usually transient.
They may increase in size due to air trapping. Pneumatoceles are commonly
seen in patients with P. jiroveci (P. carinii) pneumonia in association with
AIDS, S. aureus pneumonia and other bacterial infections.
In distinction to lung abscess or pulmonary gangrene, the wall of an airfilled
pneumatocele tends to be thin and of uniform thickness
HRCT in a patient with AIDS
shows ground-glass opacity
consistent with P. Jiroveci
pneumonia. Thin-walled
pneumatoceles are
visible bilaterally.

57. Tracheal Papillomatosis
Papillomas may be visible radiographically as nodular mass lesions within
the lung, and they often cavitates.
Eventually, cavitary lesions may progress to large thick- or thin-walled
cysts. Nodules representing papillomas may be seen within cysts

58. EMPHYSEMA
As defined by the American Thoracic Society, emphysema is a condition of
the lung characterized by permanent abnormal enlargement of air spaces
distal to the terminal bronchiole accompanied by the destruction of their
walls, but without obvious fibrosis.
CLASSIFICATION
1) Centrilobular
• Affects the respiratory bronchioles in the central portions of lobules
• Cigarette smoking
• Upper lobe predominance
• Small round areas of low attenuation
• Walls usually invisible
• Several mm to 1 cm in diameter
• May be associated with bullae
• May become confluent

60. 2) Panlobular
• Affects the entire lobule
• Alpha-1-antitrypsin deficiency or cigarette smoking
• Diffuse or lower lobe predominance
• Diffuse decrease in lung attenuation
• Focal areas of destruction or bullae usually absent
• Reduction in vessel size
• May be subtle in its early stages

61. 3)Paraseptal
• Affects subpleural lobules
• Cigarette smoking or idiopathic
• Upper lower predominance
• May be associated with centrilobular emphysema
• Focal subpleural lucencies marginated by interlobular septae
• Bullae common

62. Bullous Emphysema
• Emphysema associated with bullae ( > 1 cm in dimaeter)
• May be seen with paraseptal or centrilobular emphysema
• Cigarette smoking or idiopathic
• "Vanishing lung syndrome"
• Large bullae
• Often upper lobe
• Often asymmetric
• Compression of normal lung
• Bullae increase or sometimes resolve

63. Irregular Air-space Enlargement
It is an additional type of emphysema that occurs in patients with
pulmonary fibrosis;
This form of emphysema also is referred to as paracicatricial or irregular
emphysema. It commonly is found adjacent to localized parenchymal scars,
diffuse pulmonary fibrosis, and in pneumoconiosis associated with
progressive massive fibrosis.

65. BRONCHIECTASIS
Bronchiectasis is defined as localized, irreversible dilatation of the bronchial
tree. Usually, this term is used to refer only to cartilage-containing airways,
larger than 2 to 3 mm in diameter.
CAUSES
• Infection
• Bacteria
• Mycobacteria
• Virus
• Mycoplasma
• Immune deficiency states
• Congenital
(e.g.,hypogammaglobulinemia)
• Acquired (e.g., AIDS)
• Cystic fibrosis (abnormal mucus)
• Dyskinetic cilia syndrome
• Young's syndrome
• Congenital bronchial atresia
• Endobronchial tumor
• Bronchial wall abnormalities
• Tracheobronchomegaly
• Immune reactions
• ABPA
• Asthma
• Lung transplant rejection
• Graft-versus-host disease
• Proteinase-antiproteinase imbalance
• Alpha-1-antitrypsin deficiency
• Systemic Diseases
• Collagen vascular disease
• Inflammatory bowel disease

66. CT Differentiation of causes of Bronchiectasis
1.Lower lobe bronchiectasis is most typical of childhood infections and
syndromes associated with impaired mucociliary clearance or
immunodeficiency .
2. Bilateral upper lobe bronchiectasis is seen most commonly in patients with
CF and ABPA.
3. Unilateral upper lobe bronchiectasis is most common in patients with
tuberculosis.
4. Central bronchiectasis is more common in patients with ABPA and CP.
5. Severe and extensive bronchiectasis is most common in patients with
ABPA and CP.
6. Lobar bronchiectasis suggests infection or bronchial obstruction.
7. Middle lobe and lingular bronchiectasis suggests MAC infection.

67. Specific findings of bronchial dilatation
• Increased bronchoarterial ratio.
• Internal bronchial diameter> adjacent pulmonary artery (Signet-ring)
• Lack of tapering
• Contour abnormalities
• Cylindrical bronchiectasis-"tram tracks"
• Varicose bronchiectasis-"string of pearls"
• Cystic bronchiectasis-"cluster of grapes"
• Visibility of airways in peripheral 1 cm of lung
Normal Elderly
High altitude
True bronchiectasis
Normal

68. Major and ancillary HRCT signs of
bronchiectasis:
(1)Nontapering or flaring of bronchi
with wall thickening and Identification
of bronchi within 1 cm of pleura (not
adjacent to mediastinum)
(2) Signet ring sign;
(3) Mucus-filled dilated bronchi
(‘flame and blob’ sign)
(4) Plugged thickened centrilobular
bronchioles (‘tree-in-bud’ sign)
(5) Crowding of bronchi with
associated volume loss
(6) Areas of decreased attenuation
reflecting small airways obliteration

69. Reid Classification of Bronchiectasis
Cylindrical bronchiectasis. Bronchial dilatation is mild, and the
bronchi retain their regular and relatively straight outline.
• Varicose bronchiectasis. Bronchial dilatation is greater than in
cylindrical bronchiectasis and is accompanied by local constrictions
that give the airway an irregular outline. Obstruction and
obliteration of small airways is more pronounced.
• Cystic (saccular) bronchiectasis. This is the most severe form of
bronchiectasis. The airway takes on a ballooned appearance and
the number of bronchial divisions is greatly reduced.

70. Cylindrical and cystic bronchiectasis

71. Bronchial wall thickening
Mucous plugging

72. Cystic fibrosis (CF)
HRCT findings
• Central bronchi and upper lobes involved in all cases
• Typically severe (varicose and cystic) and widespread
• Bronchial wall thickening
• Central and upper lobe distribution
• Right upper lobe first involved
• Mucous plugging
• Tree-in-bud
• Large lung volumes
• Atelectasis
• Mosaic perfusion
• Air trapping on expiration
• Autosomal-recessive genetic defect in CF transmembrane conductance
regulator
• Abnormal chloride transport resulting in abnormal mucus
• Bronchiectasis and infection universal
• Pseudomonas (90%)
• Aspergillus (50%

73. Cystic fibrosis with upper lobe involvement

74. Allergic Bronchopulmonary Aspergillosis
• Hypersensitivity reaction to Aspergillus
• History of asthma or atopy, cystic fibrosis
• Type I (lgE-mediated) hypersensitivity results in wheezing
• Type Ill (lgG-mediated antigen-antibody complex) reaction
• results in bronchiectasis
HRCT findings
• Central bronchiectasis, widespread
• Upper lobe predominance common
• Mucous plugging; mucus plugs
appear high-density
• Tree-in-bud
• Atelectasis
• Peripheral consolidation or diffuse
ground-glass opacity
• Mosaic perfusion
• Air trapping on expiration

75. ABPA showing branching mucous plugs within dilated
central bronchi.

76. BRONCHIOLITIS
Bronchiolitis includes a spectrum of inflammatory and fibrosing
disorders that predominantly affect the small airways (terminal and
respiratory bronchioles)
Myers and Colby classification:
1. Constrictive bronchiolitis (obliterative bronchiolitis, bronchiolitis
obliterans)
2. Cryptogenic organizing pneumonia (bronchiolitis obliterans
organizing pneumonia [BOOP], proliferative bronchiolitis)
3. Acute bronchiolitis (infectious / cellular bronchiolitis)
4. Small airways disease (adult bronchiolitis)
5. Respiratory bronchiolitis (smoker’s bronchiolitis, respiratory
bronchiolitis-associated interstitial lung disease)
6. Mineral dust airways disease (early pneumoconiosis)
7. Follicular bronchiolitis
8. Diffuse panbronchiolitis

77. Constrictive bronchiolitis
It is a condition characterized by bronchiolar and peribronchiolar
inflammation and fibrosis that ultimately leads to luminal obliteration.
The early change is a cellular inflammation that is intraluminal, mural, and
peribronchial, affecting membranous and respiratory bronchioles.
Inflammatory cells are a mixture of neutrophils, lymphocytes, and plasma
cells. The mature lesion is a peribronchiolar fibrosis, encroaching on the
lumen with eventual occlusion of the airway.

78. Causes
• Infection (viral, bacterial, mycoplasma)
• Toxic fume inhalation
• Drug treatment
• Collagen-vascular disease, particularly rheumatoid arthritis
• Chronic lung transplant rejection
• Bone marrow transplantation with chronic graft-versus-host disease
• HRCT Findings
• Areas of decreased attenuation (black lung)
• Reduction in calibre of the macroscopic pulmonary vessels within
• black lung
• Patchy involvement (mosaic attenuation pattern) unless advanced
• and end stage
• Abnormalities of the large airways – may be bronchiectasis or
• wall thickening
• Air-trapping seen as enhancement of the mosaic pattern and lack of
change of cross-sectional area of affected parts of the lung on scans
obtained at end-expiration

79. Constrictive bronchiolitis . A, Patchy attenuation differences and mild
bronchial abnormalities on CT obtained at near total lung capacity. B, End-
expiratory CT accentuating the mosaic attenuation pattern and showing
relative lack of change
in the area of the decreased attenuation of the lung.

80. Diffuse Panbronchiolitis
Diffuse panbronchiolitis is the exudative small airways disease par
excellence and is characterized by a tree-in-bud pattern at HRCT.
It is associated with infection (H. influenzae, P. aeruginosa, type 1 human
T-lymphotropic virus) and genetic susceptibility (including two HLA
haplotypes unique to Asians).
HRCT findings
• Profuse tree-in-bud pattern (most obvious peripherally, more lower
zone initially)
• Cylindrical bronchiectasis (mild)
• Mosaic attenuation pattern (inconspicuous or absent)
DPB typically affects middle-aged patients, and men are involved twice as
often as women. DPB is characterized by symptoms of chronic co~ sputum
production, and dyspnea.

81. Diffuse panbronchiolitis. Examples from two patients: A, HRCT section
through the right middle and lower lobes showing a myriad of small nodules
and branching structures (tree-in-bud pattern) and accompanying
cylindrical bronchiectasis; and B, similar combination of findings in another
case of diffuse panbronchiolitis

82. Bronchiolitis Obliterans
Concentric fibrosis involving terminal and respiratory bronchioles
resulting in bronchiolar obstruction
HRCT findings
• Mosaic perfusion, usually patchy in distribution
• (85%-90%)
• Bronchiectasis
• Air trapping on expiration, usually patchy in distribution
• Air trapping on expiration with normal inspiratory scans
Most commonly results from infection,toxic fume inhalation (e.g .• nitrogen
dioxide , sulfur dioxide, ammonia, chlorine, phosgene, smoke, drug
treatment (e.g., penicillamine or gold, collagen-vascular disease,
particularly RA, chronic lung transplant rejection and bone marrow
transplantation with chronic GVHD

83. Mosaic perfusion and air trapping in a patient with bronchiolitis
obliterans resulting from smoke inhalation. A: inspiratory HRCT shows
mosaic perfusion. B: Dynamic expiratory scan shows air trapping
indicative of bronchiolitis obliterans

84. Follicular Bronchiolitis
Follicular bronchiolitis is characterized by a proliferation of lymphoid
follicles in the walls of bronchioles and the peribronchiolar interstitium,
associated with bronchiolar
narrowing.
Primary Follicular Bronchiolitis
Follicular bronchiolitis may in patients with collagen-vascular disease such
as RA and Sjogrens syndrome, immunodeficiency disorders including AIDS,
and hypersensitivity reactions.
Secondary Follicular Bronchiolitis
Seen incidentally in patients with chronic airways disease (e.g.,
bronchiectasis or bronchiolectasis) associated with in inflammation or
infection.

85. HRCT findings
Tree-in-bud or small nodular opacities in a centrilobular and
peribronchovascular distribution . In most cases, these measure 1 to 3 mm in
diameter. Larger ill-dened centrilobular or peribronchial nodules of ground-
glass opacity may also be seen.

86. Acute /Infectious Bronchiolitis
It is caused by infection, most often by respiratory syncytial virus or
adenovirus, Mycoplasma pneumoniae, or Chlamydia species, atypical
mycobacteria such as MAC, tuberculosis, and fungi. Infectious bronchiolitis
also occurs in association with chronic airway disease such as bronchiectasis,
chronic bronchitis
and COPD (i.e., chronic bronchiolitis), CF, immunodeficiency syndromes
including AIDS, or bronchopneumonia.
Pathologic examination shows necrosis of the bronchiolar epithelium with a
bronchiolar and peribronchiolar inflammatory cell infiltrate and bronchiolar
edema.
HRCT findings
• Patchy areas of consolidation or atelectasis.
• Streaky perihilar opacities or tram tracks due to bronchial wall or
interstitial thickening, and reticular or reticulonodular opacities.
• Mosaic perfusion or Air trapping
• Tree in bud ( adults )

87. Detail view of the right left lower lobe in a patient with Pseudomonas
infection. Many examples of tree-in-bud are visible.
B: In another patient with bacterial bronchiolitis, ill-defined
centrilobular nodules are visible in both lower lobes.

88. The idiopathic interstitial pneumonias (DPs) are a heterogeneous group
of diffuse lung diseases occuring without known cause and associated
with
varying degrees of interstitial lung inflammation and fibrosis.
They have been classified by a consensus committee of the American
Thoracic Society and the European Respiratory Society into seven
types, based on their histologic pattern, clinical features, and
radiographic appearances
1. Usual interstitial pneumonia (un>) and idiopathic pulmonary fibrosis
(IPF)
2. Nonspecific interstitial pneumonia (NSIP)
3. Cryptogenic organizing pneumonia (COP)
4. Acute interstitial pneumonia (AlP)
5. Respiratory bronchiolitis-interstitial lung disease (RB-ILD)
6. Desquamative interstitial pneumonia (DIP)
7. Lymphoid interstitial pneumonia (LIP)
The Idiopathic Interstitial Pneumonias

89. USUAL INTERSTITIAL PNEUMONIA AND IDIOPATHIC
PULMONARY FIBROSIS
Histology
• Fibroblastic foci
• Dense fibrosis
• Honeycombing
• Paucity of inflammatory cells
• Temporal and spatial non uniformity
• Causes
• Idiopathic pulmonary fibrosis
• Collagen vascular disease
• Hypersensitivity pneumonitis
• Asbestosis
• Familial
• Drugs (very rare)

90. HRCT findings highly accurate in diagnosis
• Honeycombing (usually range from 2 mm to 2 cm in diameter
but may be larger).
• Reticulation
• Subpleural and apicobasal predominance
• Ground-glass opacity
• Mediastinal lymph node enlargement is visible on CT in more than 70%
of cases. The enlarged nodes typically measure less than 15 mm.
Acute exacerbation of fibrotic lung disease
• May occur in any fibrotic lung disease, but most common in UIP
• Precipitants may include surgery, drugs, infection
• Imaging shows ground-glass abnormality or consolidation on background
of fibrosis
• High mortality

91. Complications of UIP
• Infection
– Pneumocystis jirovecii
– Nontuberculous mycobacteria
– Aspergillus
• Lung cancer
– Any cell type
• Acute exacerbation/accelerated deterioration
– AIP histology superimposed on background UIP
Characteristics of lung cancer in UIP
• Occurs in areas of lung fibrosis
• Often multifocal
• Usually in patients with moderate or advanced lung fibrosis
The cancers may appear as areas of poorly defined consolidation but are
more commonly lobulated nodules.
The preferential occurrence of these lung cancers within areas of fibrosis
may make them difficult to detect

92. Distribution (a), CT image (b), and CT pattern (c) of UIP. The distribution is
subpleural with an apicobasal gradient (red area in a). CT shows honeycombing
(green areas in c), reticular opacities (blue areas in c), traction bronchiectasis (red
area in c), and focal ground-glass opacity (gray area in c).

94. NONSPECIFIC INTERSTITIAL PNEUMONIA
Histology pattern
• Spatially and temporally homogeneous
• Cellular pattern
• Mild to moderate chronic interstitial inflammation
• Type II pneumocyte hyperplasia
• Dense fibrosis absent
• Fibrotic pattern
• Mild to moderate chronic interstitial inflammation
• Fibrosis lacking the temporal heterogeneity and/or patchy
• distribution of usual interstitial pneumonia (UIP)
• Fibroblastic foci absent or inconspicuous
Causes
• Collagen vascular disease and other autoimmune
diseases
• Hypersensitivity pneumonitis
• Drugs
• Inhalational exposures

95. HRCT findings
• Ground-glass opacity
• Irregular reticulation
• Patchy consolidation
• Honeycombing absent, inconspicuous, or minimal
• Concentric subpleural and basal predominance
• Subpleural sparing may be present
Types
On the basis of the varying proportions of inflammation and fibrosis,
NSIP is divided into cellular and fibrosing subtypes .
In Cellular NSIP, the thickening of alveolar septa is primarily caused by
inflammatory cells
In Fibrosing NSIP, interstitial fibrosis is seen in addition to mild
inflammation.
MacDonald et al suggested that there was substantial overlap between
the CT findings of these subtypes, although cellular NSIP was less likely
to be subpleural in distribution, and had a higher proportion of ground-
glass
type abnormality.

96. Distribution (a), CT image (b), and CT pattern (c) of NSIP. The distribution is subpleural with
no obvious gradient (red area in a). CT shows ground-glass opacity (gray areas in c), irregular
linear and reticular opacities (blue areas in c), micronodules (red areas in c), and microcystic
honeycombing (green areas in c))

97. Cryptogenic Organizing Pneumonia
Previously known as BOOP because of the tendency of plugs of organizing
pneumonia to occlude the smaller bronchioles. For this reason, it was often
misleadingly classified as a small airways disease.
However, its clinical, imaging, and pathologic features are distinct from
those of small airways disease. There is some controversy about its inclusion
as an IIP, because the areas of organizing pneumonia involve the pulmonary
airspaces rather than the interstitium,
Its clinical presentation is more subacute than UIP, DIP or NSIP, and its
imaging features are those of airspace disease.
However, it is included in the ATS/ERS classification of IIPs, because of its
idiopathic nature, its association with collagen vascular diseases, and its
tendency to overlap with the other interstitial pneumonias, particularly
NSIP.
Patients with COP typically present with a several-month history of
nonproductive cough, low-grade fever, malaise, and shortness of breath.
Mean age is 55

98. HRCT findings
1. Patchy consolidation (80% of cases) or ground-glass opacity (60%), often
with a subpleural and/or peribronchial distribution.
2. Small, ill-defined nodules (30% to 50% of cases) which may be peribronchial
or peribronchiolar (i.e., centrilobular)
3. Large nodules or masses, which may be irregular in shape
4. Focal or lobar consolidation
5. The "atoll sign" or "reversed halo sign," in which ring shaped or crescentic
opacities are seen, with ground-glass opacity in the center of the ring (thus
resembling a coral atoll or the reverse of the halo sign.
6. Lower lung predominance

99. . Distribution (a), CT image (b), and CT pattern (c) of COP. The distribution
is peripheral or peribronchial with a basal predominance (red areas in a). CT
shows consolidation with air bronchograms (dark gray areas in c), ground-
glass opacities (light gray areas in c), linear opacities (blue areas in c), and
mild bronchial dilatation (red areas in c).

100. (COP) through the lower zones shows
multifocal consolidation – the commonest
sign of COP. The consolidation has a
strongly
peribronchovascular distribution.

101. 4. ACUTE INTERSTITIAL PNEUMONIA (ALP)
The pathology is that of organizing diffuse alveolar damage (DAD) and the
condition resembles ARDS in all respects save for the lack of an identifiable
precipitating event.
Synonyms include Hamman–Rich syndrome, accelerated interstitial
pneumonitis, and idiopathic ARDS. Key features of the condition are:
fulminant respiratory failure in a previously healthy individual, without an
identifiable precipitating event,
AIP may be differentiated histologically into acute, organizing, and fibrotic
phases.
In the acute exudative phase, there is diffuse alveolar interstitial
thickening due to edema, and associated hyaline membranes.
The histologic lung changes of organizing DAD consist of fibroblast
proliferation in the alveolar interstitium. Collagen production is also usually
mild Hyaline membranes are usually more sparse. Changes are diffuse and
temporally uniform.
Other findings include hyaline membranes, intraalveolar organization, type II
pneumocyte proliferation, and thrombi in small vessels.
In the fibrotic phase, alveolar wall collapse and apposition occurs

102. Causes
• Infection
• Immunocompromise/transplant
• Acute exacerbation of fibrotic lung disease
• Collagen vascular disease
• Drug toxicity
• Toxic inhalation
• Sepsis
• Transfusion-related acute lung injury
• Shock
• Trauma

103. HRCT findings
In the early phase of AIP, ground-glass opacities are the dominant CT pattern
and reflect the presence of alveolar septal edema and hyaline membranes .
Septal thickening is found in areas of ground-glass opacity, perhaps
corresponding to alveolar collapse adjacent to septa
Areas of consolidation are also present but are usually less extensive and
limited to the dependent area of the lung .
In the early phase, airspace consolidation results from intraalveolar edema
and hemorrhage.
However, consolidations are also present in the fibrotic phase and then result
from intraalveolar fibrosis .
In the late phase of AIP, architectural distortion, traction bronchiectasis, and
honeycombing are the most striking CT features and are more severe in the
nondependent areas of the lung
The CT features of AIP are similar but not identical to those of ARDS
The main differences were a higher prevalence of honeycombing and lower
prevalence of septal thickening in AIP. The abnormalities of AIP were more
likely to be symmetric, and to have lower lung predominance, than those of
ARDS

104. Distribution (a), CT image (b), and CT pattern (c) of AIP. AIP has a basal
predominance (red area in a). CT shows airspace consolidation (dark gray
areas in c), ground-glass opacities (light gray areas in c), and bronchial
dilatation (red areas in c).

105. Exudative phase of AIP in a 22-year-old
man. bilateral ground-glass opacities
(arrowheads) and consolidation (arrow) in
the dependent areas of the lungs. The
anterior zones of the lungs are relatively
spared.
Fibrotic phase of AIP in a 53-year-old
woman who survived the acute phase of
the disease. CT image shows fibrotic
changes with traction bronchiectasis and
architectural distortion predominantly in
the nondependent areas of the lungs
(arrow

106. 5. Respiratory bronchiolitis-interstitial lung disease (RB-
ILD)
RB-ILD is a smoking-related interstitial lung disease and is thought to
represent an exaggerated and symptomatic form of the histologically common
and incidental finding of respiratory bronchiolitis.
Because of the significant overlap in clinical, imaging, and histologic features
between RB-ILD and DIP, these entities are considered a pathomorphologic
continuum, representing different degrees of severity of the same disease
process
Patients with RB-ILD are usually 30–40 years old and have an average
smoking history of 30 pack-years . Men are affected nearly twice as often as
women and present with mild dyspnea and cough
Histological pattern
• Bronchiolocentric (peribronchiolar) distribution
• Intra-alveolar macrophages
• Minimal fibrosis

107. RB-ILD HRCT findings
• Normal
• Centrilobular or patchy ground-glass opacity
• Upper lobe predominance in 60%-75%
• Bronchial wall thickening
• Coexisting moderate centrilobular emphysema is common, given that
most patients have a smoking history.

108. Distribution (a), CT image (b)of RB-ILD. RB-ILD has an upper lung predominance
(red area in a). CT shows ground-glass opacity (gray area in c) and centrilobular
nodules (red areas in c)

109. . RB-ILD in a 44-year-old woman with a 20 pack-year smoking history. High-
resolution CT image of the upper lung lobes shows centrilobular nodules
(white arrows) and patchy ground-glass opacities (black arrow). Mild
coexisting centrilobular emphysema is seen (arrowhead)

110. 6. DESQUAMATIVE INTERSTITIAL PNEUMONIA (DIP)
DIP is strongly associated with cigarette smoking and is considered to
represent the end of a spectrum of RB-ILD. However, DIP also occurs in
nonsmokers and has been related to a variety of conditions, including lung
infections and exposure to organic dust.
Histological pattern
• Diffuse distribution ( as opposed peribronchiolar to RB-ILD )
• Intra-alveolar macrophages
• Minimal fibrosis
HRCT findings
• Diffuse or patchy ground-glass opacity
• Posterior, lower lobe predominance in 60%-75%
• Fibrosis rare
• Cystic lucencies or emphysema
• Air trapping on expiratory scans

111. CT shows bilateral peripheral predominant ground-glass abnormality.
The areas of ground-glass contain multiple small cysts.

112. Lymphoid Interstitial Pneumonia ( LIP)
As an idiopathic disease, LIP is exceedingly rare.
LIP is substantially more common in women, and most commonly presents in
the fourth to seventh decades. Dyspnea and a nonproductive cough are
common and may be present for months to years. Constitutional symptoms of
fever, weight loss, and arthralgia may occur.
Diseases associated with LIP include dysproteinemias (such as common
variable immunodeficiency),autoimmune disorders (particularly SjS),
autologous bone marrow transplantation, and viral, mycobacterial, and HIV
infections.
HIV-related LIP occurs much more commonly in children than in adults.
Histologic pattern
Diffuse interstitial and alveolar wall involvement
Infiltration by lymphocytes, plasma cells, and histiocytes
Lymphoid hyperplasia

113. HRCT findings
• Diffuse or patchy areas of ground-glass opacity
• Poorly defined centrilobular nodules
• Small well-defined nodules or septal thickening
• Isolated cystic air spaces , predominantly perivascular
• Diffuse cystic disease
HRCT through the upper lobes shows thin-walled cysts also
typical of lymphoid interstitial pneumonia.

114. HYPERSENSITIVITY PNEUMONITIS
Hypersensitivity pneumonitis, also known as extrinsic allergic alveolitis, is a
group of pulmonary syndromes caused by repeated inhalation of and
sensitization to a wide variety of organic aerosols and some chemical
antigens.

115. ACUTE
• Exposure to large amounts of antigen
• Acute dyspnea
• Acute lung injury with diffuse alveolar damage, edema,or hemorrhage
• Air-space consolidation on radiographs and HRCT
SUBACUTE
Ongoing or recurrent exposure to antigen
Interstitial infiltrates, poorly defined granulomas, cellular bronchiolitis
• HRCT
• Patchy ground-glass opacity
• Centrilobular nodules round, poorly defined, and less than 5 mm in
diameter.
• Diffuse but mid- to lower lung zone predominance has been variably
reported and are usually of ground glass attenuation compared to soft
tissue attenuation of silicosis and other inhalational lung disease.
• Mosaic perfusion ( lobular decreased attenuation involves several
lobules in more than four lobes)
• "Headcheese" sign( consolidation, GGO and mosaic pattern )
• Air trapping
• Lung cysts
• May progress to fibrosis

116. CHRONIC
• Fibrosis
HRCT
• Irregular reticular opacities
• Traction bronchiectasis
• Honeycombing
• Distribution usually different than idiopathic pulmonary fibrosis
• Often appears patchy and parahilar rather than subpleural
• Superimposed findings of subacute hypersensitivity
pneumonitis may be present

117. Subacute hypersensitivity pneumonitis with patchy ground-glass opacity.
Scans through the upper and lower lobes show patchy areas of ground-
glass opacity.

118. Subacute hypersensitivity pneumonitis with air trapping. A: Inspiratory
scan shows diffuse ground-glass opacity and centrilobular nodules, with
numerous focal, lobular areas of lucency (arrows) due to mosaic perfusion.
The combination of ground-glass opacity and mosaic perfusion constitutes
the headcheese sign. B: Expiratory scan at the same level shows air trapping
in the lucent lung regions.

119. HRCT at the lung bases shows extensive
lung fibrosis with mild subpleural
honeycombing, traction bronchiectasis,
and irregular reticulation.
At the lung bases, areas of fibrosis (arrows)
are patchy and lack the subpleural
predominance of idiopathic pulmonary
fibrosis. Lobular lucencies are also visible.
CHRONIC HP

120. Radiographic differential diagnosis
Subacute
RB-ILD - in this condition the nodules are usually more patchy and sparse
Sarcoidosis, chronic beryllium disease, or pneumoconiosis - nodules are soft
tissue
attenuation
Infection – usually unilateral or patchy distribution
Chronic
UIP and NSIP - lack of lower lung predominance, presence of centrilobular
nodules, ground-glass abnormality or lobular air-trapping, and
absence of honeycombing.

121. EOSINOPHILIC LUNG DISEASE
The term eosinophilic lung disease describes a group of entities
characterized by an abundant accumulation of eosinophils in the pulmonary
interstitium and air spaces..
Diagnostic criteria include (1) radiographic or CT findings of lung disease in
association with peripheral eosinophilia, {2) biopsy-confirmed lung tissue
eosinophilia, and (3) increased eosinophils at bronchoalveolar lavage.
Idiopathic eosinophilic lung disease
• Simple pulmonary eosinophilia (Loeffler's syndrome)
• Chronic eosinophilic pneumonia
• Acute eosinophilic pneumonia
• Hypereosinophilic syndrome
• Churg-Strauss syndrome
• Bronchocentric granulomatosis
Idiopathic eosinophilic lung disease and angiitis
• Wegener's granulomatosis
• Polyarteritis
• Collagen-vascular diseases
• Drugs
Parasitic disease and tropical
pulmonary eosinophilia
• Fungi
• Bronchocentric granulomatosis
Classification

123. Chronic eosinophilic pneumonia
HRCT shows patchy areas of
consolidation involving the
peripheral lungs in the upper lobe
As opposed to COP usually seen in
lower lobe.
Acute eosinophilic pneumonia.
extensive ground-glass opacity and
consolidation with a lower lobe
predominance. Interlobular septal
thickening in also seen (arrows).

124. • Stage 0 – normal chest radiograph
• Stage I – nodal enlargement only
• Stage II – nodal enlargement and parenchymal opacity
• Stage III – parenchymal opacity without adenopathy or evidence of fibrosis
• Stage IV – lung fibrosis (parenchymal distortion, lobar volume
loss, bullae).
SARCOIDOSIS
Sarcoidosis is a common systemic disease characterized by widespread
development of noncaseating epithelioid cell granulomas that eventually
either resolve or convert into fibrous tissue.

125. Small sharply defined nodules
• Typical of active lung disease
• Perilymphatic distribution
• Patchy upper lobe predominance
• Calcification may occur
Large nodules and masses
• 15%-25% of patients
• Due to confluence of small granulomas
• With or without air bronchograms
• Commonly parahilar.
• Associated with satellite nodules
• (galaxy sign)
Ground-glass opacity
• Uncommon
• Due to numerous very small granulomas
• Small nodules may be associated
Reticular opacities and fibrosis
• Develops in 15% of patients
• Peribronchovascular fibrosis with
traction bronchiectasis
• Upper lobe volume loss
• Air-filled cysts
• Honeycombing in some
• Mycetoma may develop
Bronchial or bronchiolar
abnormalities
• Endobronchial granulomas
• Atelectasis in some
• Mosaic perfusion and air trapping
HRCT FINDINGS

126. Perilymphatic distribution of nodules
Confluence of peribronchovascular
nodules on the left(*) results in a large
mass. Discrete satellite nodules are visible
on the edge of the mass. Air bronchograms
(arrows) are visible within the mass. 'This
appearance has been termed alveolar
sarcoidosis

128. Upper lobe
• Sarcoidosis
• Pneumoconioses
• Langerhans cell histiocytosis
• Eosinophilic pneumonia
• Tuberculosis
• RB-ILD
• Centrilobular emphysema
• Cystic fibrosis
• ABPA
Lower lobe
• Usual interstitial pneumonia
• Asbestosis
• Cryptogenic organizing pneumonia
• Nonspecific interstitial pneumonia
• Aspiration pneumonia
• Idiopathic bronchiectasis
Peripheral
• Usual interstitial pneumonia
• Asbestosis
• Cryptogenic organizing pneumonia
• Chronic eosinophilic pneumonia
• Nonspecific interstitial pneumonia
Central
• Sarcoidosis
• Pulmonary edema
Bronchocentric
• Sarcoidosis
• Lymphangitis carcinomatosa
• Lymphoma/leukemia
• Organizing pneumonia (particularly
in association with poly/
dermatomyositis)
• Follicular bronchiolitis
• Tracheobronchial amyloidosis
Pattern of distribution

129. 1.Sarcoidosis
2.Neoplasm (lymphangitic
carcinomatosis, lymphoma,
metastases)
3. infection (viral, mycobacterial, or
fungal)
4. silicosis
••Asbestosis••1.pulmonary edema
••2.lymphangitic carcinomatosis
••3.lymphoma
••4.collagen vascular disease
••Lymphangioleiomyomatosis
••LCH
➢ Associated with lymphadenopathy
➢ Associated with effusion ➢ Associated with pleural thickening
➢ Associated with pneumothorax

130. THE SOLITARY PULMONARY NODULE
1. It is relatively well-defined.
2. It is surrounded, at least partially, by lung.
3. It is roughly spherical in shape.
4. It is 3 cm or less in diameter
It is evaluated for
• Calcification
• Fat density within a nodule
• Ground-glass opacity
• Contrast enhancement
• Rate of growth
• Size and shape
• Air bronchograms and bubble like lucencies
• Cavities and air crescent sign
• The CT halo sign
• Adjacent bone destruction
• Management considerations

131. Neoplastic
• Lung cancer
• Metastasis
• Pulmonary lymphoma
• Pulmonary carcinoid
• Hamartoma
• Connective tissue and neural tumors,
Inflammatory
• Infective
– Granuloma
– Round pneumonia, acute or chronic*
– Lung abscess
– Septic emboli
– Hydatid cyst
• Noninfective
– Rheumatoid arthritis
– Wegener granulomatosis
– Lymphomatoid granulomatosis
– Sarcoidosis
– Lipoid pneumonia
– Behçet disease
Miscellaneous
• Organizing pneumonia
• Pulmonary infarct*
• Round atelectasis
• Intrapulmonary lymph node
• Progressive massive fibrosis*
• Mucoid impaction*
• Hematoma*
• Amyloidosis*
• Pulmonary artery aneurysm or venous varix
• First costochondral junction
Congenital
• Arteriovenous malformation
• Sequestration
• Lung cyst
• Bronchial atresia with mucoid impaction

132. Calcification
• Concentric (laminated) calcification is suggestive of tuberculous
or fungal granulomas .
• Popcorn calcifications, which are randomly distributed, often
overlapping, small rings of calcification,seen only when there is cartilage
in the nodule, are a feature specific to hamartoma and cartilage tumors .
• Punctate calcification occurs in a variety of malignant
lesions( punctate eccentric ) and benign: granuloma, hamartoma,
amyloid deposit, carcinoid, and metastases ( diffuse), particularly
osteosarcoma
• Cloud like calcification widespread calcification of a nodule
substantially reduces the probability of bronchial carcinoma, it does not
exclude the diagnosis entirely.
• Uniform calcification of an SPN is virtually diagnostic of a calcified
granuloma and excludes the diagnosis of bronchial carcinoma

133. Benign patterns of calcification.
Indeterminate patterns of calcification. These may be seen in
benign or malignant lesions

134. FAT DENSITY WITHIN A NODULE
Unequivocal demonstration of fat within a solitary pulmonary nodule is
virtually pathognomonic of a hamartoma .
Lipoid pneumonia and metastatic liposarcoma are comparatively rare
alternatives.
On CT, care must be taken not to include adjacent aerated lung in the section,
because the density reading may then be a mixture of air and cancer and lie
within the fat range.

135. Ground-glass opacity
Some nodules appear to be of ground glass opacity.
Many focal opacities of ground-glass opacity are inflammatory and resolve on
follow-up.
However. BAC may present as a nodule entirely of ground-glass opacity, and
a high degree of suspicion should be maintained .
Follow-up of such a lesion is appropriate.
Bronchioloalveolar carcinoma

136. Contrast enhancement
Most SPNs show peak enhancement at either 3 or 4 minutes.
Using an enhancement of 15 – 20 HU or more to suggest malignancy,
though inflammatory lesions also may show similar enhancement,
Causes of an SPN with Contrast Enhancement
• Carcinoma
• Carcinoid tumor
• Granuloma (active)
• Hamartoma or other benign tumor
• Hemangioma
• Focal pneumonia
• Round atelectasis
• Vascular metastases
Gd-DTPA-enhanced MRI noted that tuberculomas tend to show ring
enhancement of their capsule with slight or no enhancement of the caseous
center, whereas lung cancers below 3 cm in diameter show homogeneous
enhancement, similar to that observed with contrast-enhanced CT
SPN with contrast opacification
• Arteriovenous malformation
• Pulmonary vein varix
• Pulmonary artery aneurysm

137. Rate Of Growth
The growth rate of an SPN has been used to determine its likelihood of
being malignant.
Doubling time- the time required for a lesion to double in volume, is used
to measure the growth rate. For easy reference, a 26% increase in nodule
diameter is one doubling, and a doubling of diameter means that three
volume doublings
have occurred.
Doubling times ranging from 1 month to 200 days encompass most
cancers.
Size

138. Shape
Malignant nodules are much more likely to have an ill-defined, irregular,
lobulated, or spiculated margin.
Benign lesions tend to have a smooth,sharply defined edges.
Nearly 90% of nodules with an irregular or spiculated edge are malignant;
only 20% of nodules with a smooth, sharp margin are malignant.
Malignancies that tend to have a sharp and smooth edge include metastases
and carcinoid tumors.
The terms corona radiate and corona maligna have been used to describe
the appearance of spiculation associated with a nodule or mass. Particularly
in patients with adenocarcinoma and bronchioloalveolar carcinoma (BAC),
this appearance reflects the presence of fibrosis surrounding the tumor,
although tumor invasion of the adjacent lung also may be present
The presence of a pleural tail associated with a peripherally located
nodule
is not overly helpful in the differential diagnosis of an SPN.

139. Edge Appearances and Common Diagnoses
Sharply marginated
• Granuloma
• Hamartoma or benign tumor
• Carcinoid tumor
• Metastasis
Spiculated (corona radiata) or pleural tail
• Bronchioloalveolar carcinoma or adenocarcinoma
• Granuloma or focal scarring
Malignant with CR and PT Benign smooth nodule

140. Air Bronchograms and Pseudocavitation
Causes
• Adenocarcinoma
• Bronchioloalveolar carcinoma
• Conglomerate mass (e.g., silicosis, sarcoidosis)
• Focal pneumonia
• Infarction
• Rounded atelectasis
• Bronchiolitis obliterans with organizing pneumonia
• Lymphoma
• Lymphoproliferative diseases
• Mycetoma (may mimic an air bronchogram)
Bubble like low attenuation areas, similar to air bronchograms but more
spherical in configuration are common in adenocarcinomas on CT,
particularly bronchioloalveolar cell carcinomas.These lucencies may be due
to patent small bronchi within the nodule.

141. Air bronchograms and cyst like lucencies in a bronchioloalveolar cell
carcinoma.

142. Cavities
The term cavity usually is used to describe a lesion with a thicker or more
irregular wall ( compared to cyst ) or a lesion that has cavitated (ie.,evolved
by developing an air-filled space, regardless of how thick the wall is). Thus, a
thin-walled.lesion may be either a
cyst or a cavity, whereas a thick-walled or irregular lesion is a cavity.
The thickness of the wall of a cavity serves as an indicator of its likelihood of
being malignant. Nearly 85% of cavities with a wall measuring more than 15
mm in its thickest portion are malignant . If the thickest part of the wall is
less than 5 mm, 95% are benign. 75 % percent of cavities with a wall 5 to 15
mm in thickness are benign. If the thickest part of the cavity wall measures 1
mm or less. malignancy is rare.

143. Amyloidosis-solitary or multiple
Aspergillosis, angioinvasive
Carcinoma
Granulomatous infection
Tuberculosis
Nontuberculous mycobacteria
Coccidioidomycosis
Histoplasmosis
Metastatic neoplasm-usually multiple
Mycetoma-aspergilloma
Papillomatosis-usually multiple
Paragonimiasis-usually multiple
Pulmonary gangrene-usually solitary
Pulmonary laceration-traumatic
Sarcoma-solitary
Septic embolism-usually multiple
Wegener's granulomatosis-usually
multiple
Hematoma-solitary or multiple
Lung abscess-solitary or multiple
Lymphoma-solitary or multiple
Causes

144. Cavitary squamous cell carcinoma shown at two levels. 'The wall of the
cavity is irregular, with several thick nodular regions.

145. Air-crescent Sign
In some patients with a cavitatory nodule or lung cyst, a mass or nodule
may be present within the cavity. Air outlining or capping the superior
aspect of the mass results in a crescent-shaped collection of air, termed the
air-crescent sign.
Causes
Aspergilloma (mycetoma)
Angioinvasive aspergillosis with septic infarction
Carcinoma arising in a cyst
Cavitary carcinoma
Echinococcus
Mucous plug in cystic bronchiectasis
Papillomatosis
Pulmonary gangrene
Rasmussen aneurysm

146. Halo Sign
The term ‘CT halo sign’ refers to ground-glass attenuation surrounding
a nodule on CT.
Causes
• Fungi: invasive aspergillosis, candidiasis, cocddioidomycosis
• Bacteria: TB, Nocardia, Legionella
• Viruses: cytomegalovirus, herpes
• Pneumocystis jiroveci
• Organizing pneumonia
• Wegener's granulomatosis
• Infarct
• Metastatic tumor
• Kaposi sarcoma
• Bronchioloalveolar carcinoma
• Adenocarcinoma

147. BAC showing dense central nodule
surrounded by a halo (arrows).
Halo sign in invasive aspergillosis

148. Radiology in the Intensive Care Unit
Direct injury
Pneumonia
Inhalation (smoke andtoxic gases)
Aspiration
Thoracic trauma with contusion or
crush injury
Thoracic radiation
Cardiopulmonary bypass
Fat embolism
Air embolism
Amniotic fluid embolism
Reexpansion or reperfusion edema
Sickle cell crisis
Acute interstitial pneumonia
Indirect injury
Sepsis (particularly gram negative
organisms)
Shock
Toxic shock syndrome
Disseminated intravascular coagulati
Extrathoracic trauma
Burns
Neurogenic edema
Drugs
Anaphylaxis
Transfusion reactions
Diabetic ketoacidosis
Pancreatitis
Uremia
High altitude
Causes
ARDS , Acute Lung Injury, Diffuse Alveolar Damage with ARDS ,
Pulmonary Hemorrhage

149. STAGES OF ACUTE LUNG INJURY AND ARDS

150. ARDS associated with sepsis.HRCT shows patchy peripheral areas of consolidation an
ground-glass opacity these are nonspecific but typical of early ARDS.

151. Diffuse alveolar damage resulting from treatment with doxorubicin
(Adriamycin)

152. Radiation Pneumonias and Fibrosis
Radiation pneumonitis
• 1-3 months after radiation is completed
• Most severe 3-4 months after radiation
• Diffuse alveolar damage
• Radiographs and HRCT
• Homogeneous or patchy ground-glass opacity or
• consolidation
• Edges correspond to radiation ports
Radiation fibrosis
• 6-12 months after radiation is completed
• Fibrosis and traction bronchiectasis
• Radiographs and HRCT
• Persisting abnormalities after 9 months
• Dense consolidation
• Traction bronchiectasis typical
• Honeycombing
• Ipsilateral volume loss

153. Radiation fibrosis 12 months following axillary radiotherapy. A. B: CTs at two
levels
show consolidation in the peripheral lung. Abnormal areas have a straight edge
(white arrows) due to the port used. Dense consolidation is typical of fibrosis.
Traction bronchiectasis (black arrow ) B indicates that fibrosis is present

154. Thank you
NR