1.
HIGH RESOLUTION CT : LUNG
PATTERNS
DR. SABHILASH SUGATHAN
Aquino SL, Gamsu G, Webb WR, Kee SL. Thoracic
imaging: pattern frequency and significance on HRCT , 3rd
edition 2018.

2.
FUNDAMENTAL TECHNICAL PROTOCOLS
• Slice thickness: 0.625 – 1.25mm
• Scan time :0.5 – 1 sec
• Kv: 120
• mAs:100-200
• Reconstruction algorithm: high spatial frequency algorithm
• Window: lung window
• Patient position: supine(routinely) or prone(if suspect ild)
• Level of inspiration: full inspiration(routinely) expiratory hrct scans in patients with
obstructive lung diseases

3.
HRCT VS ROUTINE CT

4.
WE WILL DISCUSS THE FOLLOWING SUBJECTS:
• ANATOMY OF THE SECONDARY LOBULE
• BASIC HRCT PATTERNS
• DISTRIBUTION OF ABNORMALITIES
• DIFFERENTIAL DIAGNOSIS OF INTERSTITIAL LUNG DISEASES

5.
ANATOMY OF SECONDARY LOBULE

6.
• The secondary lobule is the basic anatomic unit
of pulmonary structure and function.
• It is the smallest lung unit that is surrounded by
connective tissue septa.
• It measures about 1-2.5 cm and is made up of 5-
15 pulmonary acini, that contain the alveoli for
gas exchange.
• The central portion of secondary lobule referred
to as CENTRILOBULAR, contains Pulmonary A
and terminal bronchiole that supply the lobule.
• the Pulmonary Artery can be seen in normal
lung as a dot or branching structure 5-10mm
from the pleural surface
• The centrilobular bronchi is normally invisible

7.
• The pulmonary veins and lymphatics run in the
periphery of the lobule within the interlobular septa.
• There are two lymphatic systems: a central network,
that runs along the bronchovascular bundle towards
the centre of the lobule and a peripheral network,
that is located within the interlobular septa and
along the pleural linings.
• Under normal conditions only a few of these very thin
septa can be seen.

8.
Irregular polygonal in shape

9.
The normal pulmonary vein branches are seen marginating
pulmonary lobules.
The centrilobular artery branches are visible as a rounded dot

10.
• ACINUS: Portion of lung parenchyma supplied by a single
respiratory bronchiole 6-10mm in diameter
• PRIMARY LOBULE: Lung parenchyma associated with a single
Alveolar duct
4-5 Primary Lobules  Acinus
6-12 Acini  Secondary Lobule

11.
• CENTRILOBULAR AREA is the central part of the
secondary lobule.
• It is usually the site of diseases, that enter the
airways ( i.e. Hypersensitivity pneumonitis,
respiratory bronchiolitis, centrilobular emphysema
• PERILYMPHATIC AREA is the peripheral part of the
secondary lobule.
• It is usually the site of diseases, that spread through
Sarcoid, lymphangitic carcinomatosis, pulmonary
These diseases are usually also located in the central
lymphatics that surround the broncho vascular bundle.

12.
LUNG INTERSTITUM
Lung
interstitium
Peribronchovascul
ar interstitium
Centrilobul
ar
interstitium
Subpleural
interstitium
Interlobular
septa
Axial fiber
system
Peripheral
fiber
system
* Generally it is not visible on HRCT unless
• IntraLobular

13.
BASIC INTERPRETATION
A STRUCTURED APPROACH
• What is the dominant HRCT - pattern:
• Reticular
• Nodular
• High attenuation (ground-glass, consolidation)
• Low attenuation (emphysema, cystic)
• Where is it located within the secondary lobule HRCT-pattern:
• Centrilobular
• Perilymphatic
• Random
• Is there an upper versus lower zone or a central versus peripheral predominance

14.
HRCT FINDINGS IN LUNG DISEASES:
•LINEAR & RETICULAR OPACITIES
• NODULES & NODULAR
OPACITIES
• INCREASED LUNG OPACITY
• DECREASED LUNG OPACITY

15.
LINEAR AND RETICULAR OPACITIES
• INTER LOBULAR SEPTAL THICKENING
• INTRA LOBULAR SEPTAL THICKENING
• HONEYCOMBING

16.
INTER LOBULAR SEPTAL THICKENING
abnormal widening of an inter lobular septum or septa, usually caused
by edema, cellular infiltration or fibrosis may be:
• smooth
• Nodular / irregular
Associated findings of septal thickening regardless of cause
include:
• Peri- bronchial interstial thickening – Peribronchial cuffing
• Thickening of fissures

17.
SMOOTH SEPTAL THICKENING
Septal thickening and ground-glass opacity with a gravitational distribution in a patient
with cardiogenic pulmonary edema.
Thickening of the
peribronchovascular interstitium,
which is called peribronchial cuffing,
and fissural thickening are also
common.
Common additional findings are an
enlarged heart and pleural fluid.

18.
NODULAR SEPTAL THICKENING
SARCOIDOSIS :
right lung base shows interlobular
septal thickening associated with
several septal nodules giving beaded
LYMPHANGITIC CARCINOMATOSIS :
show diffuse smooth and nodular
septal thickening.

19.
PULMONARY LYMPHANGITIC CARCINOMATOSIS
(PLC)
• In 50% of patients the septal thickening is focal or
unilateral (distinguishing PLC from other causes
like sarcoidosis or cardiogenic pulmonary edema).
• Hilar lymphadenopathy is visible in 50% and
usually there is a history of malignancy.

20.
HONEYCOMBING
Honeycombing reflects extensive lung fibrosis with alveolar destruction and results in a
characteristic reticular appearance. On HRCT, necessary findings for the diagnosis of
Honeycombing are
1. Air-filled (Black) cysts
2. The cysts have a thick (Easily recognizable) wall
3. The cysts are usually from 3 mm to 1 cm in diameter (although they may be larger or
Smaller in some cases)
4. Cysts are immediately beneath the pleural surface
5. Cysts share walls
Three cysts in a row, at the pleural surface, is a minimum for the diagnosis of
honeycombing

21.
Associated findings of fibrosis include:
reticular opacities, traction
bronchiestasis
UIP - basal and peripheral
predominance

22.
Identification of honeycombing on HRCT:
1. It indicates fibrotic lung disease, although further progression can be seen in patients with
honeycombing.
2. It indicates that a lung biopsy probably will not prove diagnostic
3. In a patient without an associated disease (e.g., Collagen-vascular disease) or exposure
(e.g., Asbestos, drugs, organic antigens), IPF is likely the diagnosis.
4. It points to a poor prognosis in patients with IPF
Honeycombing in a patient with UIP
associated with
rheumatoid arthritis.

23.
INTRALOBULAR INTERSTITIAL
THICKENING (INTRALOBULAR LINES)
• Results in a fine reticular pattern on
HRCT, with the visible lines separated
by a few millimeters
• Fine lace- or netlike appearance
• Causes : Pulmonary fibrosis
Asbestosis
Chronic eosinophilic
pneumonitis.

24.
NODULAR PATTERN

25.
• Round opacity atleast moderately well marginated and not greater than 3cm in
maximum diameter.
• Small < 1cm
Micro < 7mm
Miliary<2mm
• Smooth
• Irregular
• cavitating
• Noncavitating
• Centrilobular
• Perilymphatic
• random
NODULAR PATTERN

26.
PERILYMPHATIC DISTRIBUTION
CENTRILOBULAR DISTRIBUTION
RANDOM DISTRIBUTION

27.
PERILYMPHATIC DISTRIBUTION
Nodules are seen in relation to pleural surfaces,
interlobular septa and the peribronchovascular
interstitium.
Nodules are almost always visible in a subpleural
location, particularly in relation to the fissures.
Nodules in
• subpleural regions
• peribronchovascular regions
• in relation to interlobular
septa

28.
Notice the overlap in differential diagnosis of perilymphatic nodules and the nodular septal
thickening in the reticular pattern.
Sometimes the term reticulonodular is used.

29.
SARCOIDOSIS:
peribronchovascular and subpleural
predominance of Nodules with more
extensive abnormalities in the upper lobes
and may be symmetrical or asymmetrical.
SILICOSIS AND CWP
subpleural and centrilobular
peribronchovascular
But with
• symmetrical, posterior, upper lobe
predominance of nodules.
• exposure history usually is available.

30.
LYMPHANGITIC SPREAD OF TUMOR
which typically predominates in relation to interlobular septa and the
peribronchovascular interstitium
most severe at the lung bases and often is asymmetrical

31.
CENTRILOBULAR DISTRIBUTION
• Unlike perilymphatic and random nodules, centrilobular nodules spare the pleural surfaces.
The most peripheral nodules are centered 5-10mm from fissures or the pleural surface.
• Centrilobular nodules are seen in diseases, that enter the lung through the airways.
The pathogens enter the central area of the secondary lobule via the terminal bronchiole
(Although abnormalities occurring in relation to small vessels also may result in this finding.)
• Hypersensitivity pneumonitis
• Respiratory bronchiolitis in smokers
• Infectious airways diseases (endobronchial spread of tuberculosis or nontuberculous mycobacteria,
bronchopneumonia)
• Uncommon in bronchioloalveolar carcinoma, pulmonary edema, vasculitis

32.
Centrilobular Nodules: Differential
Diagnosis

33.
Bacterial bronchopneumonia - patchy
centrilobular
Centrilobular nodules in hypersensitivity
pneumonitis.

34.
TREE-IN-BUD
• Irregular and often nodular branching structure,
most easily identified in the lung periphery.
It represents dilated and impacted (mucus or pus-
filled) centrilobular bronchioles.
• It almost always indicate presence of infection

35.
tree-in-bud (arrows) in patient with airway infection.

36.
RANDOM DISTRIBUTION
• Nodules are randomly distributed relative to structures of the lung and secondary lobule.
Nodules can usually be seen to involve the pleural surfaces and fissures, but lack the
subpleural predominance often seen in patients with a perilymphatic distribution.
• Small random nodules are seen in:
• Hematogenous metastases
• Miliary tuberculosis
• Miliary fungal infections
• Sarcoidosis
• Langerhans cell histiocytosis (early nodular stage)

37.
Nodules may involve the pleural surfaces, peribronchovascular interstitium, and interlobular septa
but do not show a predominance in relation to these structures as is present with a perilymphatic
pattern.
The overall distribution appears diffuse and uniform.

38.
Random nodules in a patient with miliary
tuberculosis. The nodules are small,
sharply defined, and diffuse and uniform in
distribution. Some nodules are seen at the
pleural surface.

39.
HIGH ATTENUATION PATTERN

40.
• GROUND GLASS
OPACITIES
• CONSOLIDATION
• Increased lung attenuation is called ground-glass-opacity (GGO) if there is a hazy
increase in lung opacity without obscuration of underlying vessels and is called
consolidation if the increase in lung opacity obscures the vessels.
• In both ground glass and consolidation the increase in lung density is the result of
replacement of air in the alveoli by fluid, cells or fibrosis.
• In ggo the density of the intrabronchial air appears darker as the air in the
surrounding alveoli - dark bronchus sign.
• In consolidation, there is exclusively air left in the bronchi.
This is called the air bronchogram.

41.
GGO consolidation

42.
CONSOLIDATION
• Consolidation is synonymous with airspace
disease.
When you think of the causes of consolidation,
think of 'what is replacing the air in the alveoli'?
Is it pus, edema, blood or tumor cells
• Even fibrosis as in UIP, NSIP and long standing
sarcoidosis can replace the air in the alveoli and
cause consolidation.
Patchy areas of consolidation with air bronchogram in
a patient with organizing pneumonia (OP).

43.
Air-Space Consolidation: Differential
Diagnosis

44.
GROUND-GLASS OPACITY
• Ground-glass opacity (GGO) represents:
GGO is a nonspecific term referring to a hazy increase in lung opacity that is not associated
with obscuration of underlying vessels
The location of the abnormalities in ground glass pattern can be helpful:
• Upper zone predominance: respiratory bronchiolitis, pneumocystis pneumonia.
• Lower zone predominance: UIP, NSIP, DIP.
• Centrilobular distribution: hypersensitivity pneumonitis, respiratory bronchiolitis

45.
A peripheral increase in lung attenuation represents
ground-glass opacity. Vessels remain visible in the dense
lung regions. This patient had acute dyspnea due to
pulmonary edema..
B: Patchy ground-glass opacity is visible in the upper
lobes. This immunosuppressed patient had symptoms of
acute fever and cough.
Bronchoscopy revealed cytomegalovirus pneumonia

46.
TREATABLE OR NOT TREATABLE
• Ground-glass opacity is nonspecific, but a highly significant
finding since 60-80% of patients with ground-glass opacity
on HRCT have an active and potentially treatable lung
disease.
• In the other 20-40% of the cases the lung disease is not
treatable and the ground-glass pattern is the result of
fibrosis.
• In those cases there are usually associated HRCT findings of
fibrosis, such as traction bronchiectasis and honeycombing.
• The images show two cases with GGO, one without fibrosis
and potentially treatable and the other with traction
bronchiectasis indicating fibrosis.
LEFT: No fibrosis, so potentially treatable lung
disease. RIGHT: Fibrosis, so no treatable lung
disease.

47.
CRAZY PAVING
• Crazy paving is a combination of ground glass opacity with superimposed septal
thickening
It was first thought to be specific for alveolar proteinosis, but later was also seen in other
diseases.
• Crazy paving can also be seen in:
• Alveolar proteinosis
• Sarcoid
• NSIP
• Organizing pneumonia (COP/BOOP)
• Infection (PCP, viral, mycoplasma, bacterial)
• Neoplasm (bronchoalveolar ca (BAC)
• Pulmonary haemorrhage
• Oedema (heart failure, ARDS, AIP)

48.
CRAZY PAVING IN A PATIENT WITH ALVEOLAR PROTEINOSIS.

49.
MOSAIC ATTENUATION
• A patchwork of regions of varied attenuation interpreted as secondary to regional differences in
perfusion
• There are patchy areas of black and white lung.
• Differential Diagnosis

50.
MOSAIC PERFUSION:
In homogenous lung opacity resulting from regional differences in lung perfusion
MOSAIC PERFUSION GROUND GLASS OPACITY
relatively smaller Pulmonary vessels pulmonary vessels are equal throughout
in lucent areas
Airway abnormality may be enlarged pulmonary arteries may be
appreciated seen in lucent areas
Accentuated on expiratory scans remains the same on expiratory scans

51.
 It can be difficult to distinguish these entities.
 There are two diagnostic hints for further differentiation:
 Look at the vessels
• If the vessels are difficult to see in the 'black' lung as compared to the 'white' lung, than it is likely that the
'black' lung is abnormal.
 Look at expiratory scans for air trapping
• Accentuation of attenuation differences in airway diseases
• Uniform increase in attenuation in infiltrative and vascular disorders

52.
LOW ATTENUATION PATTERN

53.
• It includes abnormalities that result in decreased lung attenuation
or air-filled lesions.
These include:
• Emphysema
• Lung cysts (LAM, LIP, langerhans cell histiocytosis)
• Bronchiectasis
• Honeycombing
• Most diseases with a low attenuation pattern can be readily
distinguished on the basis of HRCT findings.

54.
EMPHYSEMA
Emphysema : focal region / regions of low attenuation usually without visible walls resulting from actual or
perceived enlarged air spaces & destroyed alveolar walls. May be associated with air trapping.
•CENTRILOBULAR EMPHYSEMA
• Most common type
• Irreversible destruction of alveolar walls in the centrilobular portion of the lobule
• Upper lobe predominance and uneven distribution
• Strongly associated with smoking.
Centrilobular emphysema due to
smoking. The periphery of the lung is
spared (blue arrows). Centrilobular
artery (yellow arrows) is seen in the
center of the hypodense area

55.
• Pulmonary vessels in the affected lung appear fewer and smaller than
normal.
• Panlobular emphysema is diffuse and is most severe in the lower
lobes.
• In severe panlobular emphysema, the characteristic appearance of
extensive lung destruction and the associated paucity of vascular
markings are easily distinguishable from normal lung parenchyma.
• Affects the whole secondary lobule(large area of low attenuation)
• Usually Diffuse and associated with decreased vessel size
• Lower lobe predominance
• In alpha-1-antitrypsin deficiency, but also seen in smokers with advanced emphysema
PANLOBULAR EMPHYSEMA

56.
• Adjacent to the pleura and interlobar
fissures(subpleural lucencies marginated
interlobular septa)
• Can be isolated phenomenon in young
adults, or in older patients with
centrilobular emphysema
• In young adults often associated with
spontaneous pneumothorax
• frequently associated with bullae formation
(area of emphysema larger than 1 cm in
diameter).
PARASEPTAL EMPHYSEMA

57.
CYSTIC LUNG DISEASE
• Lung cysts are defined as radiolucent areas with a wall thickness of less than 4mm.

58.
lymphangiomyomatosis (LAM). Langerhans cell histiocytosis (LCH)
• related to tuberous sclerosis genes 1 and 2
• women, usually of childbearing age
• uniformly distributed cysts, round, and similar in size and
shape
• a neoplastic proliferation of perivascular epithelioid cells
• small percentage of patients with tuberous sclerosis have
LAM.
• irregularly or bizarrely shaped cysts
• upper-lobe predominance,
• associated with nodules and cavitary nodules in
early stages of the disease
• spare the costophrenic angles.
• smokers.

59.
BRONCHIECTASIS
Bronchiectasis is defined as localized, irreversible bronchial dilatation.
The diagnosis of bronchiectasis is usually based on a combination of the following findings:
•bronchial dilatation (signet-ring sign)
•bronchial wall thickening
•lack of normal tapering with visibility of airways in the peripheral lung
•mucus retention in the bronchial lumen
•associated atelectasis and sometimes air trapping
A signet-ring sign represents an axial cut of a dilated bronchus (ring) with its accompanying small
artery (signet).
The most common cause of bronchiectasis is prior infection, usually viral, at an early age.
It also occurs in patients with chronic bronchitis, COPD and cystic fibrosis.

60.
CONED AXIAL HRCT IMAGE SHOWS BRONCHIAL DILATION WITH
LACK OF TAPERING . BRONCHIAL MORPHOLOGY IS CONSISTENT
WITH VARICOSE BRONCHIECTASIS.
75

61.
DISTRIBUTION WITHIN THE LUNG

62.
ADDITIONAL FINDINGS

63.
PLEURAL EFFUSION

64.
LYMPHADENOPATHY
• In sarcoidosis the common
pattern is right paratracheal and
bilateral hilar adenopathy ('1-2-
3-sign’).
• In lung carcinoma and
lymphangitic carcinomatosis
adenopathy is usually unilateral.
Eggshell calcification
This is commonly seen in lymph
nodes in patients with silicosis and
coal-worker's pneumoconiosis and
is sometimes seen in sarcoidosis,
post irradiation Hodgkin disease,
blastomycosis and scleroderma.

65.
EXAMPLES OF RETICULAR PATTERN:
1.Lymphangitic carcinomatosis: irregular septal thickening,
usually focal or unilateral 50% adenopathy', known carcinoma.
2.Cardiogenic pulmonary edema : incidental finding in HRCT,
smooth septal thickening with basal predominance (Kerley B
lines), ground-glass opacity with a gravitational and perihilar
distribution, thickening of the peribronchovascular interstitium
(peribronchial cuffing)
3.Lymphangitic carcinomatosis
4.Lymphangitic carcinomatosis with hilar adenopathy.
5.Alveolar proteinosis: ground glass attenuation with septal
thickening (crazy paving).
6.Cardiogenic pulmonary edema.

66.
EXAMPLES OF NODULAR PATTERN
1.Hypersensitivity pneumonitis: ill defined centrilobular
nodules.
2.Miliary TB: random nodules
3.Sarcoidosis: nodules with perilymphatic distribution,
along fissures, adenopathy.
4.Hypersensitivity pneumonitis: centrilobular nodules,
notice sparing of the area next to pleura and fissure.

67.
MORE NODULAR PATTERN
1.Sarcoidosis: nodules with perilymphatic
distribution, along fissures, adenopathy.
2.TB: Tree-in-bud appearance in a patient with
active TB.
3.Langerhans cell histiocytosis: early nodular
stage before the typical cysts appear.
4.Respiratory bronchiolitis in infection.

68.
EXAMPLES OF HIGH ATTENUATION PATTERN
1.Chronic eosinophilic pneumonia with peripheral
areas of ground glass opacity.
2.Sarcoid end-stage with massive fibrosis in upper
lobes presenting as areas of consolidation. Notice
lymphadenopathy.
3.Chronic eosinophilic pneumonia with peripheral
areas of consolidation.
4.Broncho-alveolar cell carcinoma with both areas
of ground glass opacity and consolidation

69.
HIGH ATTENUATION PATTERN (2)
1.Non specific interstitial pneumonitis (NSIP):
ground glass with traction bronchiectasis, no
honeycombing.
2.Cryptogenic organizing pneumonia (COP).
3.Sarcoidosis end-stage: consolidation as a
result of massive fibrosis perihilar and in upper
lobes.
4.COP.

70.
LOW ATTENUATION PATTERN
1.Lymphangiomyomatosis (LAM): uniform cysts in woman
of child-bearing age; no history of smoking; adenopathy
and pleural effusion; sometimes pneumothorax.
2.LCH: multiple round and bizarre shaped cysts; smoking
history.
3.Honeycombing
4.Centrilobular emphysema: low attenuation areas
without walls.

71.
LOW ATTENUATION PATTERN (2)
1.Centrilobular emphysema: low attenuation
areas without walls. Notice the centrilobular
artery in the center.
2.Langerhans cell histiocytosis (LCH): multiple
thick walled cysts; smoking history.
3.Honeycombing.
4.Lymphangiomyomatosis (LAM): regular cysts
in woman of child-bearing age.

72.
THANK YOU!

73.
DIFFERENTIAL DIAGNOSIS OF
INTERSTITIAL LUNG DISEASES

74.
CHRONIC INTERSTITIAL
PNEUMONITIS:
Do not represent “diseases” per se; rather represent fundamental responses
of lungs to injury/pathological conditions
Histologically 5 types (Liebow):
• usual interstitial pneumonia (UIP)
• desquamative interstitial pneumonia (DIP)
• lymphocytic interstitial pneumonia (LIP)
• giant-cell interstitial pneumonia (GIP)
• bronchiolitis with interstitial pneumonia(BIP) – BOOP/COP

75.
COLLAGEN VASCULAR DISEASES:
All collagen vascular diseases can cause pulmonary disease
frequency & tendency to involve vary among them
Pulmonary involvement is most common in – Rheumatoid arthritis
Scleroderma (PSS)
radiological features are indistinguishable from IPF
HRCT:
interstitial pneumonia & findings of fibrosis
ground glass opacity
irregular interlobular septal thickening
* Peripheral & subpleural
* Lower zone & posterior zone
RA - pleural thickening & effusion
necrobiotic nodules
BOOP
PSS – esophageal dilatation

76.
IDIOPATHIC INTERSTITIAL FIBROSIS – IPF :
40-60 yrs, breathlessness & dry cough, finger
clubbing
late inspiratory crackles(velcro rales)
Restrictive pattern on PFT
Pathologically – UIP and/or DIP
HRCT:
fibrosis-intralobular interstitial thickening
visible intralobular bronchioles
honey combing
traction bronchiectasis
ground glass opacity
irregular interlobular septal thickening
* Patchy distribution
* Peripheral & subpleural
* Lower zone & posterior zone