Hrct ii

PRESENTED BY : DR SHAMIM

GUIDED BY : DR A PATIL (MD)

GMC BHOPAL

Interpretation of interstitial lung diseases is
based on the type of involvement of the
secondary lobule.

 Centrilobular area diseases, that enter the lung
through the airways
 ( i.e. hypersensitivity pneumonitis, respiratory
bronchiolitis,).

 Perilymphatic area 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.

This exhibit was displayed
at the 72nd scientific
assembly and annual
meeting of the
Radiological Society of
North America 30th Nov –
5th Dec
, 1986, Chicago, Illinois. It
was recommended by the
Panel and was accepted
for publication on august
3. 1987.

LINEAR AND RETICULAR
OPACITIES

NODULES AND NODULAR
INCREASED LUNG OPACITIES
ATTENUATION

PARENCHYMAL Consolidation
OPACIFICATION

Ground glass
HRCT PATTERN
CYSTIC
LESIONS, EMPHYSEMA, AND
BRONCHIEACTASIS

MOSAIC ATTENUATION AND
PERFUSION

DECREASED LUNG
ATTENUATION
AIR TRAPPING ON
EXPIRATORY SCANS

OPACITIES

NODULES AND NODULAR
ATTENUATION

OPACIFICATION

Ground glass
HRCT PATTERN
CYSTIC LESIONS,
EMPHYSEMA, AND
BRONCHIEACTASIS

MOSAIC ATTENUATION AND
PERFUSION

DECREASED LUNG
ATTENUATION
AIR TRAPPING ON
EXPIRATORY SCANS

OPACITIES

NODULES AND NODULAR
ATTENUATION

OPACIFICATION

Ground glass
HRCT PATTERN
CYSTIC LESIONS,
EMPHYSEMA, AND
BRONCHIEACTASIS

MOSAIC ATTENUATION
AND PERFUSION

DECREASED LUNG
ATTENUATION
AIR TRAPPING ON
EXPIRATORY SCANS

LINEAR AND
RETICULAR
OPACITIES

 Represents thickening of interstitial fibers of lung by
- fluid or
- infiltration by cells or
- fibrous tissue

 Either as a result of thickening of
 peribronchovascular interstitium
 interlobular septa
 Or as a result of fibrosis as in honeycombing.

SMOOTH • Pulmonary edema/ hemorrhage
• Lymphoma / leukemia
(Venous, lymphatic ) • Lymphangitic spread of carcinoma

NODULAR • Sarcoidosis
(lymphatic or infiltrative • Lymphangitic spread of carcinoma
diseases)

IRREGULAR • TB
(Due to adjacent lung • Sarcoidosis,
fibrosis ) • Silicosis, talcosis

 Outline secondary pulmonary lobule,
 Often well depicted in the apices
 Perpendicular to the pleura if present in periphery

 Most Common Causes
1. pulmonary edema
2. pulmonary hemorrhage
3. lymphangitic cancer spread

 Smooth

 Nodular

 Irreguar

D/D are similar to that of PBIT.

Thickened
Septa

Pulmonary
veins

SMOOOOTHHH...

Interlobular septal
thickening associated
with several septal
nodules giving
beaded appearance

Irregular reticular opacities
(arrows) in a patient with
idiopathic pulmonary fibrosis
shows

smooth thickening
of interlobular
septa

Peribronchovascular
Interstitium thickening
SMOOOOTHHH...
Effusion

 Lymphangitic Carcinomatosis results from
hematogenous spread to the lung, with subsequent
invasion of interstitium and lymphatics.

 Seen in carcinoma of the
lung, breast, stomach, pancreas, prostate, cervix, th
yroid and metastatic adenocarcinoma from an
unknown primary

Histologic specimen in patient
with lymphangitic spread of
tumor shows secondary
pulmonary lobule with nodules
of tumor (large arrows) in the
interlobular septa. Tumor (small
arrow) is also visible in
centrilobular
peribronchovascular region.

 Thickening of fissures and peribronchovascular
interstitium (bronchial cuffing).
 Interlobular septal thickening,
 Focal or unilateral abnormalities in 50% of patients.
 Depending on filling with fluid or with tumor cells,
septal thickening is irregular or smooth.
 Hilar lymphadenopathy in 50%
 Pleural effusion due to pleuritic carcinomatosis ( > 50%
of patients).

 Identical findings can be seen in Lymphoma and in
children with HIV infection, who develop
Lymphocytic interstitial pneumonitis (LIP) , a rare
benign infiltrative lymphocytic disease.

Focal Distribution.
This finding distinguishing
from other causes of
interlobular septal
thickening like pulmonary
edema or sarcoid.
There is also
lymphadenopathy

A central bronchogenic carcinoma (blue arrow) is producing unilateral interstitial edema (blue
circles) characteristic of lymphangitic carcinomatosis with a pleural effusion (red
arrow), thickening and irregularity of the bronchovascular bundles (yellow arrow) and thickening
of the interlobular septa (light blue arrow).

 Bilateral septal thickening
 Ground-glass opacity.
 Perihilar and gravitational distribution predominatly
in the dependent lung.
 Pleural fluid.
 Cardiomegaly

There is smooth septal thickening and ground glass opacity in the
dependent part of the lungs.
Bilateral pleural fluid.

 Lymphangitic carcinomatosis

 Interstitial pneumonia (viral, mycoplasma)

 ARDS

 Pulmonary hemorrhage

 Results in a fine
reticular pattern, with
the visible lines
separated by a few mm
 Fine lace- or netlike
appearance
 Causes :
Pulmonary fibrosis
Asbestosis
Chronic Eosinophilic
pneumonitis.
58

 Non tapering , reticular
opacity usually 1 to 3 mm in
thickness and from 2 to 5
cm in length.

 Is often peripheral and
generally contracts the
pleural surface

 D/D :
1. Tuberculosis with scar.
2. Asbestosis
3. Silicosis/ coal worker
4. Sarcoidosis 60

 Clustered cystic air spaces, of comparable
diameters (3–10 mm) characterized by well-defined
walls composed of dense fibrous tissue.

 Honeycombing suggests extensive lung fibrosis with
alveolar destruction .

 Honeycombing is the typical feature of usual
interstitial pneumonia (UIP).

 Often predominate in the peripheral and sub-
pleural lung regions regardless of their cause.

 Typically occur in several contiguous layers.
 This finding can allow honeycombing to be distinguished
from paraseptal emphysema in which subpleural cysts
usually occur in a single layer.

Typical UIP pattern with honeycombing and traction bronchiectasis in
a patient with idiopathic pulmonary fibrosis

HONEYCOMBING

Lower lobe Upper lobe
predominance : predominance :
• UIP • End stage
• IPF sarcodosis
• Connective • Radiation
tissue disorders • End stage ARDS
• Asbestosis
• NSIP (rare)

LINEAR AND
RETICULAR
OPACITIES

NODULES AND
INCREASED LUNG NODULAR
ATTENUATION OPACITIES

OPACIFICATION

Ground glass
HRCT PATTERN CYSTIC
LESIONS, EMPHYSE
MA, AND
BRONCHIEACTASIS
MOSAIC
ATTENUATION AND
PERFUSION
DECREASED LUNG
ATTENUATION
AIR TRAPPING ON
EXPIRATORY SCANS

Nodules can be classified according to their ,

 Distribution in relation to other lung structures
 Centrilobular,
 Perilymphatic,
 Random.
 Appearance
 Well-defined (likely interstitial) or
 Ill -defined (likely air-space)

 Centrilobular

 Perilymphatic

 Random

IS IT IN CONTACT WITH PLEURA

NO YES

CENTRILOBULAR PERILYMPHATIC RANDOM

 Distributed primarily within
the centre of the secondary
pulmonary lobule

 Reflect the presence of
either airspace or
interstitialabnormalities

 Sub pleural lung(5-10mm
from fissures or the pleural
surface) is typically
spared, distinguishes from
diffuse random nodules.
86

 Infectious airways diseases
 endobronchial spread of mycobacteria ( tuberculosis or
nontuberculous)
 bronchopneumonia
 Hypersensitivity pneumonitis
 Respiratory bronchiolitis
 Uncommon in
 Bronchioloalveolar carcinoma,
 Pulmonary edema,
 Vasculitis

 Centrilobular nodules may be further characterized
by presence or absence of ‘‘tree-in-bud.’’

WITH TREE-IN-BUD OPACITY WITHOUT TREE-IN-BUD OPACITY
 All causes of tree-in-bud
 Typical and atypical opacity
mycobacteria infections  Hypersensitivity
 Bacterial pneumonia pneumonitis
 Diffuse panbronchiolitis  COP
 Bronchiolitis  Pneumoconioses
 Aspiration  Langerhans’ cell
 ABPA histiocytosis
 Cystic fibrosis  Pulmonary edema
 Endobronchial-neoplasms  Vasculitis
(particularly broncho  Pulmonary hypertension
alveolar carcinoma)

90

 Impaction of centrilobular bronchus with
mucous, pus, or fluid, resulting in dilation of the
bronchus, with associated peribronchiolar
inflammation .

 Dilated, impacted bronchi produce Y- or V-shaped
structures
 Centrilobular dots and linear branching opacities

 This finding is almost always seen with pulmonary
infections

Tree-in-bud
opacities,
consisting of
branching
structures (black
arrows) and buds
(white arrows).

 Endobronchial spread of infection (TB, MAC, any
bacterial bronchopneumonia)
 Airway disease (cystic fibrosis, bronchiectasis)
 Less often, an airway disease associated primarily
with mucus retention (allergic bronchopulmonary
aspergillosis, asthma).

 Infections  Aspiration or inhalation of
 Bacterial foreign substances
 Fungal  Immunologic disorders
 Viral  Connective tissue disorders
 Congenital disorders  Rheumatoid arthritis
 Cystic fibrosis  Sjögren syndrome
 Kartagener syndrome  Peripheral pulmonary
 ABPA vascular disease

 Obliterative bronchiolitis  Idiopathic disorders
 Diffuse panbronchiolitis

Typical Tree-in-bud appearance in a patient with active TB

Impacted mucus- and pus-
filled bronchioles (arrows)
are visible throughout the
lung; this is the pathologic
examination equivalent of
the tree-in-bud sign.

WITH TREE-IN-BUD OPACITY WITHOUT TREE-IN-BUD OPACITY
 All causes of tree-in-bud
 Typical and atypical opacity
mycobacteria infections  Hypersensitivity
 Bacterial pneumonia pneumonitis
 Diffuse panbronchiolitis  COP
 Bronchiolitis  Pneumoconioses
 Aspiration  Langerhans’ cell
 ABPA histiocytosis
 Cystic fibrosis  Pulmonary edema
 Endobronchial-neoplasms  Vasculitis
(particularly broncho  Pulmonary hypertension
alveolar carcinoma)

109

 In many cases centrilobular nodules are of ground
glass density and ill defined
They are called acinar nodules.

•The nodules are poorly defined
and have ground-glass
attenuation.

•Measure 3-5 mm in diameter

•Typically appear as clusters.

•Centered a few millimeters
away from the pleural
surfaces, interlobar fissures, and
interlobular septa .

Small arrows - Interlobular septa .
Large arrows- Ill-defined peribronchiolar and alveolar infiltrates that
predominate in center of a secondary lobule

Diffuse panbronchiolitis

Small arrows outline a secondary lobule. Peribronchiolar infiltrates (large arrow)
predominate in centers of several secondary lobules. Centrilobular bronchioles are
dilated.

Ill defined centrilobular nodules of ground glass density in a patient with
hypersensitivity pneumonitis

25-year-old man with severe dyspnea after attic renovation. Chest
radiographs (not shown) were normal. Thin-section CT (1.0-mm
collimation), initially interpreted as normal, shows, in
retrospect, subtle centrilobular nodules (arrowhead).

 Also known as extrinsic allergic alveolitis (EAA).
 Allergic lung disease caused by the inhalation of a
variety of antigens (farmer's lung, bird fancier's
lung, 'hot tub' lung, humidifier lung).
 Classified into acute, subacute, and chronic stages.
 Mostly HRCT is performed in the subacute stage of
HP, weeks to months following the first exposure to
the antigen or in the chronic phase.

Centrilobular nodules in hypersensitivity pneumonitis.
Histologic specimen shows ill-defined peribronchiolar and alveolar infiltrates
(large arrows) that predominate in center of a secondary lobule.
Interlobular septa (small arrows) outline parts of three lobules.

Subacute hypersensitivity pneumonitis with ill-defined centrilobular nodules

The key findings are:

 Ill-defined centrilobularground-glass nodules (80%
of cases)
 Mosaic pattern : combination of patchy ground-
glass opacity due to lung infiltration and patchy
lucency due to bronchiolitis with air trapping

Subtle opacity in the centre of the secondary lobules (arrows)
with sparing of the subpleural region.

Subtle ill-defined centrilobular opacity in a patient with subacute HP.

Sometimes the centrilobular opacities are more nodular in appearance

Mosaic Pattern.
Some secondary lobules demonstrate ground-glass opacity due to lung
infiltration, while others are more lucent due to bronchiolitis with air
trapping

Patient who presented with acute dyspnoe and a normal chest film (not shown).
The HRCT at presentation (left) shows lobular areas of ground glass attenuation.
A control HRCT ten days later demonstrated, that the findings had resolved without any
treatment. The findings were thought to be due to hypersensitivity pneumonitis

The key findings in chronic hypersensitivity
pneumonitis are:

 Mosaic pattern with areas of ground-glass
atenuation and areas of low attenuation.
 Fibrosis and parenchymal distortion in a mid zone
distribution.

The HRCT shows a mosaic pattern with hyperaerated secondary
lobule and secondry lobule of increased attenuation.
Additionally there is septal and intralobular reticular
thickening, indicating already existing irreversible fibrosis

 Inspiratory and expiratory scan: the mosaic pattern
with areas of ground-glass attenuation and areas of low
attenuation, that become more evident on the
expiratory scan, indicating air trapping.
 Signs of fibrosis such as distorted vessels and bronchi as
well as septal thickening are more pronounced in the
mid and lower lung zones, but not limited to the
subpleural area.
 The images on the left suggest the diagnosis
hypersensitivity pneumonitis.
Based on the imaging findigs alone, alveolar proteinosis
and other diseases with a mozaic pattern should be
included in the differential diagnosis.

 Subacute stage:
 RB-ILD: seen in smokers, upper lobe predilection, usually
associated with centrilobular emphysema.
 Alveolar proteinosis.
 Chronic stage:
 UIP: may show very similar HRCT findings.
UIP has a strong lower zone distribution.
In chronic HP fibrotic changes are typically seen
throughout the whole lung parenchyma from the
periphery towards the centrum.

Centrilobular area in blue
Perilymphatic area in yellow

Nodules in relation to pulmonary lymphatics at
# perihilar peribronchovascular interstitium,
# interlobular septa,
# subpleural regions, and
# centrilobular interstitium.

140

 Perilymphatic nodules are most commonly seen in
sarcoidosis.
 They also occur in
 Silicosis,
 Coal-worker's pneumoconiosis and
 Lymphangitic spread of carcinoma.

Notice the overlap in differential diagnosis of perilymphatic
nodules and the nodular septal thickening .

Nodules along bronchi & septum + nodes

In addition to the perilymphatic nodules, there are multiple
enlarged lymph nodes, which is also typical for sarcoidosis

 Sarcoidosis is a multi-organ granulomatous disease of
unknown origin.
 It is characterized by non-caseating granulomas that
may resolve spontaneously or progress to fibrosis
 Systemic symptoms : fatigue, night sweats and weight
loss.
 Pulmonary manifestations are present in 90%.

Two photomicrographs demonstrating characteristic non-caseating granulomata (arrows):
(A) centred on the bronchovascular bundle and (B) along an interlobular septum.

Detailed view with nodules along bronchovascular bundle (red
arrow) and fissures (yellow arrow).
This is the typical perilymphatic distribution of the nodules.

 The HRCT appearance of pulmonary sarcoidosis
varies greatly and depend on disease stage and is
known to mimic many other diffuse infiltrative lung
diseases.

 60 to 70% - have characteristic radiologic findings.

 25 to 30% - findings are atypical.

 5 to 10% - are normal.

 Lymphadenopathy in left hilus, right hilus and
paratracheal (1-2-3 sign). Often with calcifications.

 Parenchymal involvement : Small nodules in a
perilymphatic distribution (i.e. along subpleural
surface ; fissures ; interlobular septa and the
peribronchovascular bundle)
 Upper and midlle zone predominence
 With progression : bronchocentric scarring, more
pronounced in the upper zones

Uncommon findings:
 Conglomerate masses in a perihilar location.
 Larger nodules (> 1cm in diameter) in Grouped
nodules or coalescent nodlues surrounded by
multiple satellite nodules (Galaxy sign)
 Nodules so small and dense that they appear as
ground glass or even as consolidations (alveolar
sarcoidosis)

Nodules along fissures(red arrows)- perilymphatic distribution
Nodules located along the bronchovascular bundle (yellow
arrow).
Nodules in the subpleural region and along the fissures, is very
specific for sarcoidosis.

Chest films in sarcoidosis have been classified into four
stages:
1. Bilateral hilar lymphadenopathy

2. Bilateral hilar lymphadenopath + pulmonary
disease
3. Only pulmonary disease

4. Irreversible fibrosis

 These stages do not indicate disease chronicity or correlate
with changes in pulmonary function.

Sarcoidosis stage I: left and right hilar There is hilar and paratracheal
and paratracheal adenopathy (1-2-3 adenopathy and no sign of pulmonary
sign) involvement.

Typical presentation of sarcoidosis with hilar and small nodules along
bronchovascular bundles (yellow arrow) and along fissures (red arrows)

Typical presentation of sarcoidosis .

Always look for small nodules along the fissures, because this is a very specific
and typical sign of sarcoidosis

 Progressive fibrosis in sarcoidosis may lead to
peribronchovascular (perihilar) conglomerate
masses of fibrous tissue.
 The typical location is posteriorly in the upper
lobes, leading to volume loss of the upper lobes
with displacement of the interlobar fissure.

 Other diseases that result in this appearance are:
 Tuberculosis
 Silicosis
 Talcosis

Typical chest film of long standing sarcoidosis with fibrosis in the
upper zones and volume loss of the upper lobes resulting in hilar
elevation.

Notice the distribution of the conglomerate masses of fibrosis in the posterior part
of the lungs. In addition there are multiple small well-defined nodules. Some of
these nodules have the typical subpleural distribution.

Sarcoidosis with conglomerate masses of fibrous tissue

Nodules so small and dense that they appear
as ground glass or even as consolidations

In this case the appearance resembles a ground glass attenuation, but with a close look you may
appreciate that the increased attenuation is the result of many tiny grouped nodules.
Also notice the hilar lymphadenopathy

 Nodular pattern:
 Silicosis / Pneumoconiosis: predominantly centrilobular and
subpleural nodules.
 Miliary TB: random nodules.
 Fibrotic pattern:
 Usual Interstitial Pneumonia (UIP): basal and peripheral
fibrosis, honeycombing.
 Chronic Hypersensitivity Pneumonitis: mid zone fibrosis with mosaic
pattern.
 Tuberculosis (more unilateral)
 Lymphadenopathy:
 Primary TB: asymmetrical adenopathy
 Histoplasmosis
 Lymphoma
 Small cell lung cancer with nodal metastases

 Pathologically distinct entities
 differing histology,
 resulting from the inhalation of different inorganic dusts.
 The radiographic and HRCT appearances
 may not be distinguishable from each other
 may be similar to sarcoidosis.
 These diseases are rare compared to sarcoidosis
and occur in a specific patient group (construction
workers, mining workers, workers exposed to
sandblasting, glass blowing and pottery).

 Small well-defined nodules 2 to 5mm in both lungs.
 Nodules may be calcified
 Upper lobe predominance
 Centrilobular and subpleural distribution
 Sometimes random distribution
 Irregular conglomerate masses, known as
progressive massive fibrosis
 Masses may cavitate due to ischemic necrosis.
 Often hilar and mediastinal lymphnodes.

Nodules of varying sizes with a random and subpleural distribution. One nodule
contains calcification (arrow). Note the absence of a lymphatic distribution
pattern (peribronchovascular and along fissures), which would be suggestive of
sarcoidosis.

Conglomerate mass in a perihilar location in the right upper lobe.
The left lobe shows multiple nodules of varying size

 Sarcoidosis : can be difficult to distinguish (look for
distribution of nodules along fissures).
 Infection: miliairy TB, fungus.
 Hematogenous metastases: silicotic nodules in
subpleural and peribronchiolar location up to the level
of the secundary pulmonary lobule, may have a
seemingly random distribution and simulate metastases
and miliary infections.
 Langerhans cell histiocytosis: can be difficult to
distinguish from silicosis in the early stage, when LCH is
solely characterized by the presence of small nodules.
Look for nodules with cavitation

 Nodules are randomly distributed relative to
structures of the lung and secondary lobule.

 Random nodules are usually well-defined and
appear diffuse, but uniform in distribution

 Nodules can involve the pleural surfaces and
fissures, but lack the subpleural predominance

 The random distribution is a result of the
hematogenous spread of the infection.

 Hematogenous metastases
 Miliary tuberculosis
 Miliary fungal infections
 Langerhans cell histiocytosis (early nodular stage)
 Wegener granulomatosis
 Sarcoidosis (when very extensive)

LEFT: miliary TB RIGHT: metastases

 An uncommon disease characterised by multiple
cysts in patients with nicotine abuse.
 Very early stage, show only nodules,
 Later , cavitate and become cysts .
 Upper lobe predominance,as in all smoking related
diseases,

early nodular stage before the typical cysts appear

Early nodular stage before the typical cysts appear

• Random
– touch pleura
– scattered in lung

• Centrilobular
–away from pleura

• Perilymphatic
– around vessels, bronchi
– touch pleura or fissure

Miliary : <3 mm

Small Nodules: <10 mm
Size

Large Nodules: >10 mm

Masses : >3 cms
193

Interstitial opacity:

 Well-defined, homogenous,
Soft-tissue density
Obscures the edges of vessels or adjacent structure

Appearance

Air space:

Ill-defined, inhomogeneous.
Less dense than adjacent vessel – GGO
small nodule is difficult to identify

194

 Hypersensitivity pneumonitis: ill defined
centrilobular nodules.
 Miliary TB: random nodules of the same size.
 Sarcoidosis: nodules with perilymphatic
distribution, along fissures, adenopathy.
 Hypersensitivity pneumonitis: centrilobular
nodules, notice sparing of the subpleural area.

 Lymphangitic carcinomatosis: irregular septal
thickening, usually focal or unilateral, 50%
adenopathy', known carcinoma.
 Cardiogenic pulmonary edema: smooth septal
thickening with basal predominance ,ground-glass
opacity with a gravitational and perihilar
distribution, thickening of the peribronchovascular
interstitium (peribronchial cuffing)
 Lymphangitic carcinomatosis.
 Lymphangitic carcinomatosis with hilar adenopathy.
 Alveolar proteinosis: ground glass attenuation with
septal thickening (crazy paving).
 Cardiogenic pulmonary edema

 Sarcoidosis: nodules with perilymphatic
distribution, along fissures, adenopathy.
 TB: Tree-in-bud appearance in a patient with active
TB.
 Langerhans cell histiocytosis: early nodular stage
before the typical cysts appear.
 Respiratory bronchiolitis: ill defined centrilobular
nodules of ground-glass opacity.

Hrct ii

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Editor's Notes