HRCT findings in Diffuse lung disease, HRCT findings in Occupational lung disease, HRCT in Environmental lung disease. HRCT Chest Anatomy

1. BASICS OF HRCT CHEST &
IMAGING OF INTERSTITIAL
LUNG DISEASES
Presenter: Dr. SHAROJ KHAN
MD Radiology Resident
NMCTH

2. HRCT anatomy of the lung.
■ HRCT demonstrate the normal anatomy of the
secondary pulmonary lobule(Reid Lobule).
■ SPL is defined as the subsegment of the lung
supplied by the 3-5 terminal bronchioles.
■ Smallest unit of lung surrounded by connective
tissue.
■ Polyhedral in shape measuring 10-30mm on
each side.
■ 1 terminal bronchiole is subtended to single
pulmonary acinus distally.
■ So a single SPL contains 3-5 such acini

3. Components (SPL):
 Interlobular septa- Pulmonary veins and
lymphatics run in the periphery of the
lobule.
 Lobular core structure- Small bronchiole
parallelled by the centrilobular artery.
 Lobular parenchyma

4. ■ Centrilobular area central part
site of diseases, that enter the lung through the
airways ( i.e. hypersensitivity pneumonitis,
respiratory bronchiolitis, centrilobular
emphysema).

5. ■ Perilymphatic area peripheral part
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.

6. Acinus
■ The pulmonary acinus is smaller
than a secondary lobule.
■ Defined as the portion of lung distal
to a terminal bronchiole (the last
purely conducting airway) and
supplied by a first-order respiratory
bronchiole or bronchioles.
■ Because respiratory bronchioles are
the largest airways that have alveoli
in their walls, an acinus is the largest
lung unit in which all airways
participate in gas exchange.
■ Ranges from 6 to 10 mm in
diameter and average 7 to 8 mm in
adults.
■ Number of acini counted in lobules
of varying sizes ranged from 3 to 24.

7. Pulmonary Interstitium
■ Interstitium of lung is a structural framework
of the lung through which course,,,, the blood
vessels and airways.

8. TYPES
The interstitium is divided into following
interconnecting spaces which is useful for HRCT
interpretation:
1. Central (axial ) interstitium/peribronchovascular-
bronchovascular sheaths and lymphatics.
2. Peripheral /subpleural interstitium - pleura,
subpleural connective tissues, interlobular septa
with pulmonary veins and lymphatics.
3. Centrilobular interstitium-connective tissues
surrounding the centrilobular artery and
bronchiole.
4. Intralobular/parenchymal/alveolar interstitium-
alveolar wall(interalveolar septum).

9. Basic Interpretation of HRCT patterns
■
A structured approach to interpretation of HRCT involves the following
questions:
■ What is the dominant HRCT-pattern:
– reticular
– nodular
– high attenuation (ground-glass, consolidation)
– low attenuation (emphysema, cystic)
■ Where is it located within the secondary lobule HR-pattern:
– centrilobular
– perilymphatic
– random
■ Is there an upper versus lower zone or a central versus peripheral
predominance
■ Are there additional findings HR-pattern:
– pleural fluid
– lymphadenopathy

10. Reticular pattern
■ Thickening of the lung interstitium by fluid,
fibrous tissue, or because of cellular infiltration
results in an increase in reticular or linear
opacities .
■ Reticular abnormalities characterized as
belonging to one of three recognizable patterns,
(may be seen together also).
(a) interlobular septal thickening,
(b) Honeycombing, and
(c) Intralobular interstitial thickening, also
described as intralobular lines by its HRCT
appearance
The first two of these are most easily recognized
and have a limited differential diagnosis. The
last is less specific.

11. a. Interlobular septal thickening

12. a. Smooth interlobular septal thickening in a
patient with pulmonary edema
b. Smooth interlobular septal thickening in a
child with lymphangiomatosis.

13. ■ Interlobular septal thickening in alveolar proteinosis.
■ Thickened septa are associated with ground-glass
opacity.
■ The combination of interlobular septal thickening
and ground-glass opacity in the same lung region is
typical of alveolar proteinosis and is termed crazy
paving

14. Irregular septal thickening in UIP

15. ■ “Beaded” or nodular septal
thickening in two patients with
sarcoidosis

16. Honeycoombing
■ Second type of reticular pattern
■ Pathologically, honeycombing is defined by the presence of small cystic spaces
lined by bronchiolar epithelium with thickened walls composed of dense fibrous
tissue.
Honeycombing is the typical feature of usual interstitial pneumonia (UIP).

18. Honeycombing in association with paraseptal
emphysema in a patient with IPF
1.Sub-pleural nodules of Rheumatoid lung disease
1. Sub-pleural honeycombing in Rheumatoid lung disease

19. Nodular Pattern
Perilymphatic distribution
Nodules are seen in relation to pleural surfaces,
interlobular septa and the peribronchovascular
interstitium.
Nodules are almost always visible in a subpleural
location, particularly in relation to the fissures.
Centrilobular distribution
Nodules are limited to the centrilobular region.
Unlike perilymphatic and random nodules,
centrilobular nodules spare the pleural surfaces.
The most peripheral nodules are centered 5-10mm
from fissures or the pleural surface.
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.

20. Algorithm for nodular pattern
■ The algorithm to distinguish perilymphatic, random and centrilobular nodules is the
following:
– Look for the presence of pleural nodules.
These are often easiest to see along the fissures.
If pleural nodules are absent or few in number, the distribution is likely
centrilobular.
– If pleural nodules are visible, the pattern is either random (miliary) or
perilymphatic.
– If there are pleural nodules and also nodules along the central bronchovascular
interstitium and along interlobular septa, represents periplymphatic distribution.
– If the nodules are diffuse and uniformly distributed, it is likely a random
distribution.

21. ALGORITHMIC APPROACH TO NODULE
PATTERN AND DIAGNOSIS

22. ■ Perilymphatic nodules in case of
Sarcoidosis.

23. Centrilobular distribution
The pathogens enter the central area of the
secondary lobule via the terminal bronchiole:
• Hypersensitivity pneumonitis
• Respiratory bronchiolitis in smokers
• Infectious airways diseases (endobronchial
spread of tuberculosis or nontuberculous
mycobacteria, bronchopneumonia)
• In many cases centrilobular nodules are of
ground glass density and ill defined

24. Random distribution
■ On the right a HRCT of patient with random
nodules as a result of miliary TB.
The random distribution is a result of the
hematogenous spread of the infection.
Small random nodules are seen in:
– Hematogenous metastases
– Miliary tuberculosis
– Miliary fungal infections
– Sarcoidosis
– Langerhans cell histiocytosis (early
nodular stage)

25. High Attenuation pattern
Increased lung attenuation is called
ground-glass-opacity (GGO) if there
is a hazy increase in lung opacity
without obscuration of underlying
vessels
and consolidation if the increase in
lung opacity obscures the vessels.

26. Ground glass attenuation
Ground-glass opacity (GGO) represents:
• Filling of alveolar spaces with pus, edema,
hemorrhage, inflammation or tumor cells.
• Thickening of the interstitium or alveolar walls
below the spatial resolution of the HRCT as seen
in fibrosis.
So ground-glass opacification may either be the
result of air space disease (filling of the alveoli)
or interstitial lung disease (i.e. fibrosis).
The location of the abnormalities in ground glass
pattern can be helpfull:
• Upper zone predominance: Respiratory
bronchiolitis, Pneumocystis pneumonia.
• Lower zone predominance: UIP, NSIP, DIP.
• Centrilobular distribution: Hypersensitivity
pneumonitis, Respiratory bronchiolitis

27. CONSOLIDATION
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
Most patients who are evaluated with HRCT, will have
chronic consolidation, which limits the differential diagnosis.

28. cases with chronic
consolidation.
There are patchy
non-segmental
consolidations in
a subpleural and
peripheral
distribution.

29. Mosaic attenuation
■ Term mosaic attenuation is used to
describe density differences between
affected and non-affected lung areas.
■ Patchy areas of black and white lung.
Role of the radiologist is to determine which part is
abnormal: the black or the white lung.
When ground glass opacity presents as mosaic
attenuation consider:
• Infiltrative process adjacent to normal lung.
• Normal lung appearing relatively dense adjacent
to lung with air-trapping.
• Hyperperfused lung adjacent to hypoperfused
lung due to chronic thromboembolic disease.

30. There are two diagnostic hints for further
differentiation:
– Look at the vessels
– If the vesses are difficult to see in the 'black' lung as
compared to the 'white' lung, than it is likely that the
'black' lung is abnormal.
Then there are two possibilities: obstructive
bronchiolitis or chronic pulmonary embolism.
Sometimes these can be differentiated with an
expiratory scan.
If the vessels are the same in the 'black' lung and
'white' lung, then you are looking at a patient with
infiltrative lung disease, like the one on the right with
the pulmonary hemmorrhage.

31. Low Attenuation Pattern
■ Includes abnormalities that result in decreased lung attenuation or air-filled
lesions.
These include:
– Emphysema
– Lung cysts (LAM, LIP, Langerhans cell histiocytosis)
– Bronchiectasis
– Honeycombing

32. Diffuse lung disease
■ Diffuse lung disease represents a broad spectrum of disorders that primarily effect the
pulmonary interstitium.
■ Chronic interstitial lung disease
Chronic interstitial pulmonary edema
Connective tissue disease
Idiopathic chronic interstitial pneumonias
Other chronic interstitial lung disease.
■ Inhalational Disease
Pneumoconiosis
Hypersensitivity pneumonitis

33. ■ Granulomatous Disease
Sarcoidosis
Beryliosis
Langerhans cell histiocytosis of lung
Wegener granulomatosis
■ Eosinophillic lung disease
Idiopathic eosinophillic lung disease
Eosinophillic lung disease of identifiable etiology
Eosinophillic lung disease associated with autoimmune disease.

34. Interstitial Lung Disease
■ ILD presents a broad spectrum of diseases that primarily affects the pulmonary
interstitium.
■ Clinically present with chronic dyspnoea, non- productive cough
■ HRCT may demonstrate abnormal findings when CXR is normal in 10-30% pts of
ILD.

35. Classification (according to the
involvement of structures)
1. SUPPORTING CONNECTIVE TISSUE NETWORK
 Interstitial edema
 Chronic interstitial pneumonia
 Pneumoconioses
 Collagen-vascular disease
 Interstitial fibrosis
 Amyloid
 Tumor infiltration within connective tissue
 Desmoplastic reaction to tumor

36.  MAJOR LYMPHATIC TRUNKS
 Lymphangitic carcinomatosis
 Congenital pulmonary lymphangiectasia
 Pulmonary edema
 Alveolar proteinosis
 PULMONARY VEINS (increased pulmonary venous pressure)
 Left ventricular failure
 Venous obstructive disease

37. Pathogenesis:
■ Inflammatory response of alveolar wall to injury
(a) acute phase: fluid + inflammatory cells exude into alveolar space,
mononuclear cells accumulate in edematous alveolar wall.
(b) organizing phase: hyperplasia of type II pneumocytes attempt to regenerate
alveolar epithelium, fibroblasts deposit collagen
(c) chronic stage: dense collagenous fibrous tissue remodels normal
pulmonary architecture

38. Classification scheme:
■ Terminology for the IIPs with the various subentities according to the ATS-ERS
classification.

39. ■ Diffuse infiltrative disease with granulomas
– Sarcoidosis
– Hypersensitivity pneumonitis
■ Pneumoconioses
■ Interstitial lung disease with cysts
– Langerhans cell histiocytosis
– Lymphangioleiomyomatosis

40. ■ Connective Tissue Diseases
– Rheumatoid Disease
– Sjogren’s Syndrome
– Progressive systemic sclerosis.
– Polymyositis/ Dermatomyositis
– Systemic Lupus Erythematosus

41. ■ Systemic Vasculitides
– Eosinophilic Granulomatosis with Polyangitis (Formerly k/a Churg-strauss
Syndrome)
– Microscopic Polyangitis.
 Drug Induced Lung Diseases
 Occupational Lung Disease
 Silicosis (Coal Worker’s Pneumoconiosis)
 Asbestos related disease

42. IDIOPATHIC PULMONARY FIBROSIS
(UIP)
■ Age> 50
■ More common in men
■ Presents with dyspnea and cough
■ Smoking association is Gradual Currently under discussion
■ Prognosis Poor (median survival, 2.5– 3.5 y)
■ Response to Steroid is Poor, if any

43. Classical HRCT Findings
■ • Subpleural basal honeycombing
■ • Ground-glass opacity not
predominant
■ • Subpleural disease in the upper lobes
(if present) tends to be anterior
■ • Traction bronchiectasis and
bronchiolectasis

44. Diagnostic Categories of Usual Interstitial
Pneumonitis by High-Resolution Computed
Tomography Pattern

46. Non-Specific Interstitial Pneumonia
■ Age 40 to 50
■ Male=Female
■ Presents with dyspnea,cough and fatigue
■ Gradual or subacute onset
■ Smoking association is not present
■ Prognosis better than UIP
■ Response to Steroid is good

47. Classical HRCT Findings
■ Bilateral ground-glass opacities and
superimposed fine reticulation
■ Predominantly peripheral, but also patchy or
band-like
■ Honeycomb pattern minimal or absent
■ Traction bronchiectasis and bronchiolectasis

48. Comparison Between UIP and NSIP

49. Cryptogenic Organising Pneumonia
■ Mean Age around 55
■ Male=Female
■ Presents with cough, mild dyspnea, Fever
■ subacute onset
■ More common in non smoker
■ Complete recovery in most patient
■ Excellent response to Steroid is good

50. Findings
■ Patchy bilateral airspace
consolidation
■ Ground-glass opacity or
crazy paving
■ Subpleural and/or
peribronchovascular
distribution
■ Perilobular opacities
■ Combination of first four
findings
Other findings:
• Reversed halo sign
• Focal, mild irregular
linear opacities
• Pleural effusion
• Mediastinal
lymphadenopathy

51. Respiratory Bronchiolitis–Interstitial
Lung Disease
■ Mean age of onset is 30 to 40
■ More common in Men
■ Mild dyspnea and cough
■ Gradual in onset
■ Smoking association is very important for diagnosis.
■ Prognosis is good after smoking cessation
■ Good response to steroid.

52. Classical HRCT Finding
Inconspicuous poorly defined centrilobular nodules of
ground-glass opacification in symptomatic smokers are
suggestive of RB–ILD
combination of a fine reticular pattern
representing fibrosis and ground-glass
opacification on a background of
emphysema suggests a diagnosis of
smoking related-interstitial lung
disease.

53. Desquamative Interstitial Pneumonia
■ Mean age of onset is 30 to 40 years
■ More common in smokers
■ Presents with dyspnea and cough
■ Insidious in onset
■ Most cases are associated with smoking
■ Generally good prognosis after smoking cessation
■ Good response to steroid

54. Classical HRCT findings
■ Non-specific extensive ground-
glass opacities, usually lower
zone, with or without associated
mild reticulation, are typical
features of DIP
several areas of non-
specific reticulation
and groundglass
opacification in both
lower lobes

55. Acute Interstitial Pneumonia/Diffuse
Alveolar Damage
■ Mean age of onset is 50
■ Men=Female
■ Dyspnea is presenting complaint
■ Acute in onset
■ No association with smoking
■ High Mortality rate(>50%)
■ Response to corticosteroid is not proved.

56. Classical HRCT Findings
■ Patchy or diffuse ground-glass
opacities and
consolidation/collapse (the latter
mainly in dependent lung)
■ Traction bronchiectasis and
reticulation may become evident
after several days
a combination of ground-glass
opacification, consolidation,
bronchial dilatation and
architectural distortion.

57. Lymphoid Interstitial Pneumonia
■ Mean age of onset 40 to 50 years
■ More common in Women
■ Presents with cough, Dyspnea
■ Slow onset
■ No association with smoking
■ Variable association with smoking
■ Variable prognosis
■ Variable response to Corticosteroid.

58. Classic HRCT Finding
Patchy ground-glass
opacities, indistinct
nodules and thin-walled
cysts

59. Idiopathic Pleuroparenchymal
Fibroelastosis
■ Previous recurrent infection/ bone
marrow or lung transplantation
■ Classical finding is Bilateral upper lobe
irregular pleural thickening with
posterior continuity and subjacent
reticular pattern

60. SARCOIDOSIS
■ multisystem granulomatous disorder of unknown aetiology.
■ diagnosis of this syndrome is defined by the presence of characteristic clinical and
radiological data along with histological evidence of non-caseating granuloma.
■ Granulomas in the lung have a characteristic distribution along the lymphatics in
the bronchovascular sheath and, to a lesser extent, in the interlobular septa and
subpleural lung regions.
■ disease of young adults, with a peak incidence in the second to fourth decades.
■ Pulmonary involvement accounts for most of the morbidity and mortality
associated with sarcoidosis.

61. ■ Chest radiography was traditionally used for sarcoidosis staging according to the
modified Scadding method:
– stage I, lymphadenopathy;
– stage II, lymphadenopathy with parenchymal opacity;
– stage III, parenchymal opacity alone;
– stage IV, pulmonary fibrosis.
■ Low stages at presentation are reported to have a better prognosis than high
stages, although this is not a precise method

62. Classical HRCT Findings
■ Well-defined, smooth or irregular nodules, measuring 2–4 mm, in a perilymphatic
distribution (i.e. mainly along interlobar fissures, peribronchovascular interstitium
and interlobular septa), most extensive in the upper lobes
■ Nodules may be grouped in clusters or coalesce to larger nodules
■ Bilateral hilar and mediastinal enlarged lymph nodes
■ Fibrosis may occur and typically involves the upper lobes

64. HYPERSENSITIVITY PNEUMONITIS
■ HP, also called extrinsic allergic alveolitis (EAA),
■ immunologically mediated lung disease characterised by an inflammatory reaction
to specific antigens contained in a variety of organic dusts.
■ Common causes include avian proteins (e.g. bird breeder’s lung) and thermophilic
bacteria present in mouldy hay (farmer’s lung), mouldy grain (grain handler’s lung),
or heated water reservoirs (humidifier or air conditioner lung)

65. Classical HRCT Findings
■ In the subacute phase, poorly defined
centrilobular nodules, background ground-
glass opacification and lobular areas of air
trapping
■ Chronic HP results in a pattern of fibrosis
which may resemble NSIP or UIP; ancillary
findings such as coexisting areas of
mosaic attenuation and air trapping
suggest the diagnosis of chronic HP
■ Axial distribution and upper-lobe
predominant disease and not subpleural
but bronchocentric distribution of fibrosis

66. LANGERHANS CELL HISTIOCYTOSIS
■ Granulomatous disorder characterised histologically by the presence of large
histiocytes containing rod- or racket-shaped organelles
■ male-to-female ratio is about 4 :1
■ strong association with cigarette smoke.

67. Classical HRCT Findings
■ Progression from ill-defined
nodules(which cavitate)to a
combination of cysts and nodules.
■ The typical distribution of
parenchymal abnormalities spares
the costophrenic recesses even in
advanced disease; however, exception
to this is seen in paediatric onset.

68. LYMPHANGIOLEIOMYOMATOSIS
■ LAM can occur with or without evidence of other disease, such as tuberous
sclerosis complex.
■ LAM is a rare disease seen almost exclusively in women, the vast majority of
cases being diagnosed during childbearing age.
■ However, there are case reports of women developing LAM after menopause,
including women in their eighth decade.

69. Diffuse thin-walled cysts throughout the
lungs with no zonal predominance
HRCT may demonstrate interlobular septal
thickening (attributed to dilatation of lymphatic
channels secondary to obstruction of
pleuropulmonary lymphatics and/or septal veins)
or patchy areas of ground-glass attenuation
(presumably the result of pulmonary
haemorrhage).
Generally no signs of fibrosis.

70. Connective tissue diseases.

71. Rheumatoid Disease
■ a broad spectrum of pleural and
pulmonary abnormalities.
■ In a significant minority of patients
with RA, pleuropulmonary disease
antedates the development of
arthritis and
■ In general, pleuropulmonary
involvement is not related to the
severity of the arthritis.

72. Classical HRCT Findings
■ Pleural effusions are common
■ UIP >NSIP
■ Other findings include
necrobiotic nodules,
organising pneumonia,
bronchiectasis and evidence of
small airways disease

73. Sjögren Syndrome
■ chronic autoimmune inflammatory disease characterised by a triad of clinical
features:
■ dry mouth (xerostomia) + dry eyes (keratoconjunctivitis sicca) + arthritis.

74. Classical HRCT Findings
■ most frequent interstitial
pneumonias in SjS are NSIP
and LIP
■ Mild bronchiectasis is
common
■ Lymphoproliferative disease
may occur on a background
of LIP
Fig: Lymphoid interstitial pneumonia and amyloid. There are
numerous thin-walled cysts in association with multiple
irregular solid nodules, some of which are heavily calcified.

75. Progressive Systemic Sclerosis
(Scleroderma)
■ a collagen vascular disease characterised by the deposition of excessive
extracellular matrix with vascular occlusion involving several organs.
■ . ILD is common in patients with SSc and causes considerable morbidity and
mortality.
■ Nonetheless, absence of parenchymal abnormalities may be associated with
pulmonary hypertension and poor prognosis.

76. Classical HRCT Findings
■ Fibrotic NSIP is the most
common pattern of lung
involvement
■ Dilated oesophagus is usual
■ Signs of pulmonary
hypertension, often without
fibrotic ILD

77. Polymyositis/Dermatomyositis
■ Polymyositis is an idiopathic autoimmune inflammatory myopathy that results in
proximal muscle weakness.
■ Dermatomyositis (DM) is similar, except that it is accompanied by a skin rash.
■ Pulmonary complications of PM/DM are important determinants of the clinical
course.

78. Classical HRCT Findings
■ Diffuse ground-glass opacities
may represent either NSIP or
DAD
■ Consolidation is common and
represents organising
pneumonia frequently
admixed with NSIP and DAD
patterns

79. SYSTEMIC VASCULITIDES
■ Associated with deposition of immune complexes in the walls of blood vessels.
■ The size of the vessels predominantly involved strongly influences the clinical and
radiological features of the different forms of vasculitis

80. Eosinophilic Granulomatosis With
Polyangiitis (Formerly Churg–Strauss
Syndrome)
■ determined by necrotising vasculitis and extravascular granulomatous
inflammation rich in eosinophils.

81. Classical HRCT Findings
■ Non-specific patchy ground-glass
opacities or consolidation
■ Interlobular septal thickening
(particularly with cardiac
involvement)
■ Pleural and pericardial effusion
(A) areas of ground-glass opacification, (B) small cavitating
nodules, (C) thickened interlobular septa and (D) an area of
airspace opacification, likely to be a peripheral infarct

82. Microscopic Polyangiitis
■ a non-granulomatous vasculitis of
small vessels.
■ DAH is the most frequent
manifestation (10%–30%);
■ chest radiography may be negative or
show diffuse parenchymal shadowing.
■ On HRCT, patchy ground glass and
consolidations or centrilobular faint
nodules are seen. Other common
thoracic radiological findings of MPA
are pleural effusion (15%) and
pulmonary oedema (6%).
Classical HRCT Findings
• Patchy ground-glass opacities
• Subsolid centrilobular nodules with faint
margins

83. DRUG-INDUCED LUNG DISEASE

84. OCCUPATIONAL LUNG DISEASE

85. Silicosis/Coal Worker’s
Pneumoconiosis
■ Classical HRCT Findings
– Well-defined dense centrilobular
and subpleural nodules, upper and
posterior lung predominance
– Hilar and mediastinal lymph node
enlargement, with or without
calcification
– Upper lobe irregular masses
Progressive Massive Fibrosis in Coal Worker’s
Pneumoconiosis. Mass-like opacities are seen bilaterally in
the upper lobes in association with multiple small nodules
that cluster into pseudo-plaques

86. Asbestos-Related Disease
■ Asbestosis
– Asbestosis is defined as pulmonary parenchymal
fibrosis secondary to inhalation of asbestos
fibres.
– The time lag between exposure and onset of
symptoms is usually 20 years or longer.
Classical HRCT Findings
- Asbestos-related benign pleural disease consists of
either parietal pleural plaques in characteristic
locations or diffuse visceral pleural thickening
- The presence of such pleural disease in individuals
with HRCT findings compatible with UIP/NSIP pattern
suggests the diagnosis of asbestosis in patients with
an appropriate exposure history
A. early asbestosis include subpleural lines (arrowheads) and fine
reticulation (arrows). These subtle abnormalities persisted on prone
sections.
B. In more advanced disease, a coarse reticular pattern with
honeycombing, often indistinguishable from usual interstitial
pneumonia on HRCT, is seen in the left lower lobe. Note the calcified
pleural plaques in both examples.

87. Refrences:
■ 1. Grainger & Allison’s DIAGNOSTIC RADIOLOGY A
Textbook of Medical Imaging 7th Edition
■ 2. https://pubs.rsna.org/doi/pdf/10.1148/rg.273065130
Idiopathic Interstitial Pneumonia What Every Radiologist
must know.
■ 3.https://radiologyassistant.nl/chest/hrct/basic-
interpretation (Basics of HRCT Chest)
■ 4. W. Richard Webb HRCT 5th edition