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DR. HARSHIL A. KALARIA
RESIDENT,.
DEPARTMENT OF RADIOLOGY
TECHNICAL ASPECT OF HRCT;
NORMAL LUNG ANATOMY &
HRCT FINDINGS OF LUNG DISEASE
HRCT ------ MEANING
o It is often used for anything and everything to do
with “high resolution”.
o Resolution : Means ability to resolve small object
that are close together ,as separate form.
Actual meaning
o A scan performed using high- spatial frequency
algorithm to accentuate the contrast between tissue
of widely differing densities, eg.,
- air & vessels (lung)
- air & bone (temporal & paranasal sinus)
3
INTRODUCTION
• HRCT -- 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.
• Superior to chest radiography for detection of lung disease,
points a specific diagnosis and helps in identification of
reversible disease.
4
HISTORY
• 1982– The term HRCT was first used by TODO et. Al
• 1985 – Nakata et.al and Naidich et.al published first
report on HRCT
Since then has been an important tool in
pulmonary medicine
• Recent development of MDCT scanner capable of
volumetric high resolution scanning has improved the
investigation
5
TECHNICAL ASPECT
Parameters
o Slice thickness
o Kvp
o mAs
o Scan time
o FoV
o Interslice gap (collimation)
o Filming.
6
SLICE THICKNESS
• Thin sections 0.5 – 1.5 mm is essential for optimal spatial
resolution
• Thicker slices are prone for volume averaging and reduces
ability to resolve smaller structure
• Better for delineation of bronchi, wall thickness and
diameter
7
8
Reconstruction Algorithm
• Denotes the frequency at which the acquired scan data are
recorded when creating the image.
• Using a high-resolution algorithm is critical element in
performing HRCT.
• High spatial frequency or sharp algorithm -- bone algorithm
is used which reduces image smoothing and better depicts
normal and abnormal parenchymal interface.
9
Standard algorithmHigh resolution algorithm 10
Kilovolts (Peak), Milliamperes, and Scan Time
• In HRCT image, noise is more apparent than
standard CT.
• Noise – 1/√ mAs X Kvp X scan time
• As increasing scan time is not feasible, mAs and
Kvp are altered to reduce noise
• Noise decreases with increase in Kvp and mAs.
11
• For routine technique –
Kvp -- 120-140
mAs -- 200- 300
• Increased patient and chest wall thickness are associated
with increase image noise, may be reduced by increasing
mAs and Kvp
• Scan Time : As low as possible (1-2 sec) to minimize motion
artifact.
12
WINDOW SETTINGS
Lung window
 Window level setting ranging from – 600 to – 700 HU and
window widths of 1000 to 1500 HU are appropriate for a
routine lung window.
Soft tissue window
 Window level/width setting of 40-50/ 350-450 HU are best
for evaluation of the mediastinum, hila, and pleura.
13
LOW DOSE HRCT
• Low dose HRCT uses Kvp of 120- 140 and mA of 30-20 at 2
sec scan time.
• Equivalent to conventional HRCT in 97 % of cases
• Disadvantage : Fails to identify GGO in few cases and have
more prominent streak artifact.
• Not recommended for initial evaluation of patients with lung
disease.
• Indicated in following up patients with a known lung
abnormality or in screening large populations at risk for lung
dz.
14
Matrix size, Field of View, and Target reconstruction
• Matrix size : Largest available matrix s/b used – 512 x 512
• Field of view : smallest FOV that will encompass the patient is
used as it will reduce the pixel size. (commonly 35 to 40)
• Retrospectively targeting image reconstruction to a single
lung instead of the entire thorax significantly reduces the FOV
and image pixel size, and thus increases spatial resolution.
15
16
• INTERSLICE GAP – varies from examination to examination,
but is usually 10- 20 mm
• INSPIRATORY LEVEL : Routine HRCT is obtained in
suspended full inspiration, which
 optimizes contrast between normal structures,
various abnormalities and normal aerated lung
parenchyma; and
 reduces transient atelectasis, a finding that may
mimic or obscure significant abnormalities.
• EXPIRATORY SCAN : valuable in obstructive lung disease
or airway abnormality
17
Patient Position and the Use of Prone Scanning
• Supine adequate in most instances.
• Prone for diagnosing subtle lung abnormalities.
e.g., asbestosis, suspected early lung fibrosis
• Prone scan is useful in differentiating dependent lung
atelectasis from early lung fibrosis
18
Axial CT image shows opacity in the posterior part of the lung which could represent
dependent opacity or pulmonary inflammation. The prone images shows complete
resolution of the opacity suggesting dependent atelectasis.
19
Persistent opacity in the posterior lung in a
patient with pulmonary fibrosis.
20
TECHNIQUE OF SCAN ACQUISITION:
1. Spaced axial scans :
 Obtained at 1cm intervals from lung apices to
bases. In this manner, HRCT is intended to “sample”
lung anatomy
 It is assumed that the findings seen at the levels
scanned will be representative of what is present
throughout the lungs
 Results in low radiation dose as the individual
scans are widely placed
21
2. Volumetric HRCT -
 MDCT scanner are capable of rapid scanning and thin slice
acquisition.
Advantages :
1. Viewing of contagious slice for better delineation of lung
abnormality
2. Complete imaging of lung and thorax
3. Reconstruction of scan data in any plane using MIPs or MinIPs.
4. diagnosis of other lung abnormalities
Disadvantage : greater radiation dose. It delivers 3-5 times greater
radiation.
22
Multidetector Helical HRCT
 Multidetector CT is equipped with a multiple row
detector array
 Multiple images are acquired due to presence of multiple
detectors
 Advantages : - shorter acquisition times and
retrospective creation of both thinner and thicker
sections from the same raw data
 Acquisition time is so short that whole-lung HRCT can
be performed in one breath-hold.
23
Which is better HRCT or MD- HRCT
 Various study shows the image quality of axial HRCT
with multi-detector CT is equal to that with
conventional single-detector CT.
 HRCT performed with spaced axial images results
in low radiation dose as compared with MD-HRCT.
 Increased table speed may increase the volume-
averaging artifact and may result in indistinctness of
subtle pulmonary abnormalities.
 MDCT provides for better reconstruction in Z axis
24
Radiation dose
 PA CHEST Radiograph ----- ----- ----- 0.05 mSv
 Spaced axial HRCT (10mm space) ----- 0.7 mSv ( 14 X ray)
 Spaced axial HRCT (20 mm space) ------ 0.35 mSv ( 7 X ray)
 Low Dose Spaced axial HRCT -------- 0.02 mSV
 MD-HRCT ---- ------- 4 - 7 msv ( 60-80 x ray)
Combining HRCT scan at 20 mm interval with low mAs scan
(40 mAs) would result in radiation comparable to
conventional X ray.
25
Summary of HRCT protocol
 Collimation: thinnest available collimation (1.0-1.5 mm).
 Reconstruction algorithm: high-spatial frequency or
“sharp” algorithm (i.e., GE “bone”).
 Scan time: as short as possible (1 sec or less).
 kV(p), 120-140; mA, 240.
 Matrix size: largest available (512 × 512).
Optional
 kV(p)/mA: Increased kV(p)/mA (i.e., 140/340).
Recommended in large patients. Otherwise optional.
 Targeted reconstruction: (15- to 25-cm field of view).
 Reduced mA (low-dose HRCT): 40-80 mA.
HRCT ARTIFACT
• Streak ArtIfacts :
 Fine, linear, or netlike opacities
 Radiate from the edges of sharply
marginated , high-contrast structures
such as bronchial walls, ribs, or vertebral
bodies.
 More evident on low mA
 Mechanisms: beam hardening, photon
starvation, and aliasing.
27
Motion-related artIfacts
• Pulsation / Star artefacts
• Doubling artefacts.
• Stair-step artefacts in sag/coro
reconstruction.
28
MODIFICATION OF SCAN PROTOCOL
Scan protocol can be modified in relation to disease or patients
comfort.
If a disease has basal predominance, it may be wise to begin
scanning near the diaphragm and proceed cephalic .
Caudad for disease with an upper-lobe predominance (e.g.,
sarcoidosis)
An alternative approach - cephalad in all patients.
29
MAXIMUM INTENSITY PROJECTION
 maximum intensity projection (MIP) is a volume
rendering method for 3D data that projects in the
visualization plane thevoxels with maximum intensity
that fall in the way of parallel rays traced from the
viewpoint to the plane of projection
Volume Rendering
VS
Maximum Intensity Projection
(a) Volume-rendered image provides clear definition of individual vessels. (b) MIP
image reconstructed from the same volume data shows all of the vessels, but their
outlines merge; it is impossible to visualize the spatial relationships between the vessels or
to delineate individual
MAXIMUM INTENSITY PROJECTION
 Maximum-intensity projection (MIP) image in a
patient with small lung nodules obtained using a
multidetector-row spiral CT scanner with 1.25-mm
detector width and a pitch of 6. A: A single HRCT
image shows two small nodules (arrows) that are
difficult to distinguish from vessels. B: An MIP image
consisting of eight contiguous HRCT images,
including A, allows the two small nodules to be easily
distinguished from surrounding vessels.
 first step in HRCT interpretation of diffuse lung
diseases is a good quality scan
. Resolution and size or orientation of structures. The tissue plane, 1 mm thick, and the
perpendicular cylinder, 0.2 mm in diameter, are visible on the HRCT scan because they
extend through the thickness of the scan volume or voxel. The horizontal cylinder cannot
be seen.
MDCT Techniques
 Combined “routine” and HRCT studies
 5 mm sections q 5 mm (separate lung and mediastinal
reconstruction algorithms):
 1 – 1.25 mm sections q 10 mm (lung algorithm)
 Optional image acquisitions
 Supine and prone 1 – 1.25 mm sections
 Inspiratory/expiratory 1 -1.25 mm sections
 Low dose technique (mAs 40 – 80)
 Optional Reconstruction techniques
 Sliding maximum and minimum intensity projection images
(MIPs/ MINIPs): 5 mm’s q 5 mm
INDICATIONS
 Detect interstitial lung disease not seen on chest x-ray
 Abnormal pulmonary function tests
 Characterize lung disease seen on X-ray
 Determine disease activity
 Find a biopsy site
INDICATIONS
 Hemoptysis
 Diffusely abnormal CXR
 Normal CXR with abnormal PFT’s
 Baseline for pts with diffuse lung disease
 Solitary pulmonary nodules
 Reversible (active) vs. non-reversible (fibrotic) lung
disease
 Lung biopsy guide
 F/U known lung disease
 Assess Rx response
LUNG ANATOMY Right lung is divided by
major and minor fissure
into 3 lobes and 10
bronchopulmonary
segments
 Left lung is divided by
major fissure into 2 lobes
with a lingular lobe and 8
bronchopulmonary
segments
ANATOMY The trachea (windpipe) divides into left and the
right mainstem bronchi, at the level of the
sternal angle (carina).
 The right main bronchus is wider, shorter, and
more vertical than the left main bronchus.
 The right main bronchus subdivides into three
lobar bronchi, while the left main bronchus
divides into two.
 The lobar bronchi divide into tertiary bronchi, also
known as segmentalinic bronchi, each of which
supplies a bronchopulmonary segment.
ANATOMY
The segmental bronchi divide into many
primary bronchioles which divide into
terminal bronchioles, each of which
then gives rise to several respiratory
bronchioles, which go on to divide into
two to 11 alveolar ducts. There are five or
six alveolar sacs associated with each
alveolar duct. The alveolus is the basic
anatomical unit of gas exchange in the
lung.
TRACHEAL ANATOMY
 10-12 cm in length
 Extrathoracic (2-4cm) and Intrathoracic(6-9cm beyond
manubrium)
 In men, tracheal diameter averages 19.5 mm and in
women, tracheal diameter is slightly less, averaging 17.5
mm
 The posterior portion of the tracheal wall is a thin
fibromuscular membrane termed the posterior tracheal
membrane
 There is marked variability in the cross-sectional
appearance of the trachea, which may appear convex
posteriorly, flat, or convex anteriorly
The membranous posterior membrane allows
esophageal expansion during expiration
Contains
glands, small
arteries,
nerves,
lymph vessels
and elastic
fibers
Trachealis
muscle
overlies
esophageal
muscle and
epithelium
BRONCHIAL ANATOMY
 Airways divide by dichotomous branching, with
approximately 23 generations of branches from the trachea
to the alveoli.
 The wall thickness of conducting bronchi and bronchioles
is approximately proportional to their diameter.
 Bronchi with a wall thickness of less than 300 um is not
visible on CT or HRCT.
 As a consequence, normal bronchi less than 2 mm in
diameter or closer than 2 cm from pleural surfaces
equivalent to seventh to ninth order airways are generally
below the resolution even of high-resolution CT
There are approximately 23 generation
of dichotomous branching
From trachea to the alveolar sac
HRCT can identify upto 8th order
central bronchioles
48
BRONCHUS
 BLOOD SUPPLY Bronchial Arteries( 2 on left side i.e.
superior and inferior and 1 on right side)
Left arises from thoracic aorta
Right from either thoracic aorta, sup. lt. bronchial or right 3rd
intercostal artery
 VENOUS DRAINAGE
on right- azygous vein
on left- left superior intercostal or accessory hemiazygous vein
 NERVE SUPPLY Pulmonary plexus at hilum (vagus and
sympathetic)
BRONCHOARTERIAL RATIO (B/A)
 Internal diameter of both bronchus and
accompanying arterial diameter calculated and ratio
measured.
 If obliquely cut section seen, then the LEAST diameter
is considered.
 Normal ratio is 0.65-0.70
 B/A ratio more than 1.0 indicates bronchiactasis.
BRONCHIAL WALL THICKNESS
(T/D)
 Wall thickness proportionately decreases as the
airway divides further as according to the diameter of
the airway.
 T/D ratio approximates to 20% at any generation of
airway.
The Nomenclature Adopted by the Ad HOC lnternational Committee Meeting at
the Time of the lnternational Congress of Otorhinolaryngology in 1949 [I]"
International
Nomenclature
Brock Jackson and Huber
Right upper lobe
bronchus
Apical (RB1)
Posterior (RB2)
Anterior (RB3)
Middle lobe bronchus
Lateral (RB4)
Medial (RB5)
Right lower lobe
bronchus
Apical (RB6)
Medial basal (cardiac)
(RB7)
Anterior basal (RB8)
Lateral basal (RB9)
Posterior basal (RB10)
Pectoral
Subapical
Apical
Lateral
Medial
Apical
Cardiac
Anterior basal
Middle basal
Posterior basal
Anterior
Postenor
Apical
Lateral
Medial
Superior
Medial basal
Anterior basal
Lateral basal
Posterior basal
The Nomenclature Adopted by the Ad HOC lnternational Committee Meeting at
the Time of the lnternational Congress of Otorhinolaryngology in 1949 [I]"
International
Nomenclature
Brock Jackson and Huber
Left upper lobe
bronchus
Upper division
Apical (LB1)
Apicoposterior LB1 and
LB2
Posterior (LB2)
Anterior (LB3)
Lingula
Superior (LB4)
Inferior (LB5)
Left lower lobe
bronchus
Apical (LB6)
Anterior basal (LB8)
Lateral basal (LB9)
Posterior basal (LB10)
Apicopectoral
Apical
Subapical
Pectoral
Upper
Lower
Apical
Anterior basal
Middle basal
Posterior basal
Apical
Apical-posterior
Posterior
Anterior
Superior
Inferior
Superior
Anterior medial basal
Lateral basal
Posterior basal
MEDIASTINUM
 Broad central portion that separate the two laterally
placed pleural cavities.
 Imaginary plane passes through T4 divides it into
Superior & Inferior mediastinum
 Inferior mediastinum is further divided-
Heart enclosed in pericardium (M)
Sternum to anterior pericardium (A)
Posterior pericardium to vertebrae (P)
INTERSTITIAL ANATOMY
 Lung is supported by a network of connective tissue
called interstitium
 Interstitium not visible on normal HRCT but visible
once thickened.
 Interstitium is constituted by AXIAL fibre system
(peribronchovascular & centrilobular), PERIPHERAL
fibre system (subpleural & interlobular septa) and
SEPTAL fibre system (intralobular septa)
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 center, that is parallelled
by the centrilobular artery.
 Pulmonary veins and lymphatics run in the periphery
of the lobule within the interlobular septa.
SECONDARY PULMONARY
LOBULE
 Smallest lung unit that is
surrounded by connective
tissue septa (Miller)
 The basic anatomic unit
 Irregular polyhedral in
shape.
 Measures 1 to 2.5 cm
60
Anatomy of the Secondary Lobule
and Its Components
1. Interlobular septa
and contiguous
subpleural
interstitium,
2. Centrilobular
structures, and
3. Lobular parenchyma
and acini.
61
Interlobular septa and contiguous subpleural interstitium
The secondary pulmonary lobule is marginated by septa which
extends from the pleural surface.
They measure 0.1 mm in thickness.
They are less well defined in central lung
Lobular core :
The secondary lobule is supplied by arteries and bronchioles
that measures approximately 1 mm in diameter.
It consists of functioning lung parenchyma namely the alveoli,
alveolar duct and vessels. The parenchyma is supported by
network of central and peripheral fibers of interstitium.
62
PULMONARY ACINUS
Portion of lung parenchyma
supplied by a single respiratory
Bronchiole.
Size is 7 to 8 mm in adults
3 to 24 acini = Sec Pul. Lobule
Primary Lobule: Lung
parenchyma associated with a
single Alveolar duct.
4-5 Primary Lobules  Acinus
63
64
A group of terminal bronchioles
65
Accompanying
pulmonary
arterioles
66
Surrounded by
lymph vessels
67
Pulmo
nary
veins
68
Pulmo
nary
lymph
atics
69
70
Connective Tissue Stroma
LUNG INTERSTITUM
Lung
interstitium
Axiel fiber
system
Peribronchovascular
interstitium
Centrilobular
interstitium
Peripheral fiber
sysem
Subpleural
interstitium
Interlobular
septa
71
 The peribronchovascular interstitum invests the bronchi
and pulmonary artery in the perihilar region.
 The centrilobular interstitium are associated with small
centrilobular bronchioles and arteries
 The subpleural interstitium is located beneath the
visceral pleura; envelops the lung into fibrous sac and
sends connective tissue septa into lung parenchyma.
 Interlobular septa constitute the septas arising from the
subpleural interstitium.
72
The normal pulmonary vein branches
are seen marginating pulmonary
lobules. The centrilobular artery
branches are visible as a rounded dot
73
Anatomy of pleural surfaces and chest wall.
74
 Every CT scan starts with a scout view, a projection
image that looks like a second rate X-ray.
 A line on scout view tells you the level of axial cut.
HOUNSFIELD UNIT (HU)
 HU scale is a linear transformation of the original
linear attenuation coefficient measurement into one in
which radio density of distilled water at STP is defined
as zero HU, while radio density of air at STP is
defined as -1000 HU.
 Fat  -50 to -100 HU
 Blood  +30 to 45 HU
 Bone  >+400 HU
 Muscle  +40HU
 Contrast  +130 HU
APPEARANCE ON CT SCAN
 AIR  JET BLACK
 FAT  MODERATELY BLACK
 WATER  GRAY
 MUSCLES  SLIGHT WHITE
 BONES  WHITE
 CALICIFICATION  DENSE WHITE
LUNG
WINDOW
MEDIASTINAL
WINDOW
BONE
WINDOW
NORMAL LUNG
ATTENUATION
 Normal lung attenuation : –700 to – 900 HU
 Attenuation gradient : densest at dependent region
of lung as a result of regional difference in blood and
gas density due to gravity
Difference in attenuation of anterior and posterior
lung ranges from 50 – 100 HU
 In children, lung attenuation is greater than adults.
81
NORMAL EXPIRATORY HRCT
 Performed to detect air trapping in small airway
obstruction
 Attenuation increases with expiration (ranges from 100
to 130 HU)
 60 % of normal individual shows air trapping in the
superior segment of lower lobe and involving single
lobule, normal variant.
82
LOBAR AND BRONCHIAL
ANATOMY ON HRCT THORAX
RIGHT
APICAL
SEGMENT
LEFT
APICAL
SEGMENT
TRACHE
A
ESOPHAG
USRB1 LB1
CARIN
A
LEFT
MAIN
BRONCH
US
RIGHT
MAIN
BRONCHUS
RB2 RB1
RB3
LB3
LB1,2
BRONCHUS
INTERMEDI
US
LEFT UL
BRONCHU
S
RIGHT ML
BRONCHU
S
RB5
LUL
LLLRLL
RM
L
RB5
LB4
LB5
RLL
BRONCHU
S
LLL
BRONCH
US
LB6
LINGULA
R
BRONCH
US
RB6
RB7
LB6
RLL
BRONCHUS
LLL
BRONCHUS
MAJOR
FISSUR
E
RB8
RB
9
RB10 LB10
LB9
LB
8
RLL
LML
LLL
RM
L
LB2
LB6
LB10
RB7
RB10
RB9
RB6
RB2
RB1
RB2
LB9
LB1,2
U
L
L
L
U
L
L
L
ML
RB1 joining RUL bronchus LB1,2 joining LUL
bronchus
LB8RB8
CARIN
A
RC2
LC2
RB1
RB3
RB8
ML Bronchus
LB4
LB3
RB3
RB5RB4
LB5
LB3
VASCULAR ANATOMY ON CT
THORAX
Rt. CCA
Rt. IJV
Rt. EJV
Lt. IJV
Lt. EJV
Lt. CCA
Rt.
BCV
Rt. SCV
joining Rt.
BCV
Rt.
CCA
Lt.
CCA Lt.
SCV
Rt. SCA
Lt.
SCA
Lt. BCV
joining Rt.
BCV
Rt. BCV
Rt. BCA
Lt. CCA Lt. SCA
SUPRA AORTIC LEVEL
Formation of SVC
Branching from
Aortic Arch
AORTIC
ARCH
SVC
AORTIC ARCH LEVEL
Ascending
AORTA
Main Pulmonary
TrunkSVC
Right Pulmonary
Trunk
Left Pulmonary
Trunk
Descending
AORTA
Aorta arising
from Left
Ventricle
Pulmonary Trunk
arising from Right
Ventricle
SVC draining
into Right
Atrium
Pulmonary Veins
draining into Left
Atrium
Pulmonary Veins
RV
LV
LA
R
A
RV
LV
DA
IVC
RV
LV
DA
LYMPH NODE STATIONS ON CT
THORAX
THORAX
1. SUPRACLAVICULAR NODES
• LOW CERVICAL
• SUPRACLAVICULAR
• STERNAL NOTCH
Extends from the lower margin of the
cricoid cartilage to the clavicles and the
upper border of the manubrium.
The midline of the trachea serves as border
between 1R and 1L.
2. UPPER PARATRACHEAL NODES
2R. Upper Right Paratracheal
Extends to the left lateral border of the trachea.
From upper border of manubrium to the
intersection of caudal margin of innominate (left
brachiocephalic) vein with the trachea.
2L. Upper Left Paratracheal
From the upper border of manubrium to the
superior border of aortic arch.
2L nodes are located to the left of the left lateral
border of the trachea.
3A. Pre-vascular
These nodes are not adjacent to the
trachea like the nodes in station 2, but
they are anterior to the vessels.
3P. Pre-vertebral
These nodes are not adjacent to the
trachea like the nodes in station 2, but
behind the esophagus, which is
prevertebral.
4. LOWER PARATRACHEAL NODES
4R. Lower Right Paratracheal
From the intersection of the caudal margin of
in nominate (left brachiocephalic) vein with
the trachea to the lower border of the azygos
vein.
4R nodes extend from the right to the left
lateral border of the trachea.
4L. Lower Left Paratracheal
From the upper margin of the aortic arch to
the upper rim of the left main pulmonary
artery.
5-6. AORTIC NODES
5. Subaortic nodes
These nodes are located in the AP window
lateral to the ligamentum arteriosum.
These nodes are not located between the
aorta and the pulmonary trunk but lateral to
these vessels.
6. Para-aortic nodes
These are ascending aorta or phrenic nodes
lying anterior and lateral to the ascending
aorta and the aortic arch.
Inferior Mediastinal Nodes 7-9
7. Subcarinal nodes
Nodes below carina
8. Paraesophageal nodes
Nodes lateral to esophagus
9. Pulmonary Ligament nodes
Nodes lying within the pulmonary
ligaments.
Hilar, Lobar and (sub)segmental Nodes 10-
14
These are all N1-nodes.
10. Hilar nodes
These include nodes adjacent to the main stem
bronchus and hilar vessels.
On the right they extend from the lower rim of
the azygos vein to the interlobar region.
On the left from the upper rim of the
pulmonary artery to the interlobar region.
DR. HARSHIL A. KALARIA
RESIDENT,.
DEPARTMENT OF RADIOLOGY
Part II: HRCT FINDINGS OF LUNG DISEASE
Q.1. What is the dominant HR-pattern ?
Q.2. Where is it located within the secondary lobule
(centrilobular, Perilymphatic or random) ?
Q.3. Is there an upper versus lower zone or a central
versus peripheral predominance ?
Q.4. Are there additional findings (pleural fluid,
lymphadenopathy, traction bronchiectasis) ?
STRUCTURED APPROACH
158
HRCT
PATTERN
INCREASED
LUNG
ATTENUATION
LINEAR AND
RETICULAR
OPACITIES
NODULES AND
NODULAR
OPACITIES
PARENCHYMAL
OPACIFICATION
consolidation
Ground glass
DECREASED
LUNG
ATTENUATION
CYSTIC LESIONS,
EMPHYSEMA, AND
BRONCHIEACTASIS
MOSAIC
ATTENUATION
AND PERFUSION
AIR TRAPPING ON
EXPIRATORY
SCANS
160
Attenuation pattern
 High Attenuation pattern
 GROUND GLASS
 CONSOLIDATION
 Low Attenuation pattern
 Emphysema
 Lung cysts
 Bronchiectasis
 Honeycombing
LINEAR AND RETICULAR OPACITIES
 Represents
thickening of
interstitial fibers of
lung by
- fluid or
- fibrous tissue or
- infiltration by
cells
162
Interface sign
Irregular interfaces between the
aerated lung parenchyma and
bronchi, vessels, or visceral pleural
surfaces.
Represent thickened interlobular
septa, intralobular lines, or
irregular scars.
Nonspecific.
Common in patients with an interstitial abnormality, fibrotic
lung disease.
163
Peribronchovascular Interstitial Thickening
PBIT
Smooth
Pulmonary
edema/
hemorrhage
Lymphoma /
leukemia
Lymphangitic
spread of
carcinoma
Nodular
Sarcoidosis
Lymphangitic
spread of
carcinoma
Irregular
Due to
adjacent
lung fibrosis
Sarcoidosis,
silicosis, TB
and talcosis
Venous, lymphatic
or infiltrative
disease
lymphatic or
infiltrative
diseases
164
sarcoidosis
UNILATERAL LYMPHANGITIC SPREAD
OF CARCINOMA
165
INTERLOBULAR SEPTAL THICKENING
 Normally, only a few septa seen
 On HRCT, if numerous
interlobular septas are seen, it
almost always indicate
abnormality.
 Septal thickening d/t -interstitial
fluid, cellular infiltration or
fibrosis.
 The thickened interstitium outline
the secondary pulmonary lobules
and are perpendicular to the
pleura.
 D/D are similar to that of PBIT.
166
Smooth Septal thickening
Septal thickening and ground-glass opacity with a
gravitational distribution in a patient with
cardiogenic pulmonary edema.
167
Nodular Septal thickening
Focal septal thickening in
lymphangitic carcinomatosis
Lymphangitic carcinomatosis :
show diffuse smooth and nodular
septal thickening. Sarcoidosis :
right lung base shows interlobular
septal thickening associated with
several septal nodules giving
beaded appearance
168
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.
169
PARENCHYMAL BANDS
 Non tapering , reticular opacity usually
1 to 3 mm in thickness and from 2 to 5
cm in length.
 Is often peripheral and generally
contracts the pleural surface
 D/D : 1. Asbestosis
2. Sarcoidosis
3. Silicosis/ coal worker
pneumoconiosis
4. Tuberculosis with associated
scarring.
170
Subpleural Interstitial
Thickening
 Mimic thickening of fissure.
 DD similar to that of interlobular
septal thickening.
 more common than septal
thickening in Idiopathic
Pulmonary Fibrosis or UIP of any
cause.
171
Size, Distribution, Appearance
Nodules and Nodular Opacities
Size
Small Nodules: <10 mm Miliary - <3 mm
Large Nodules: >10 mm Masses - >3 cms
Appearance
Interstitial opacity:
 Well-defined, homogenous,
Soft-tissue density
Obscures the edges of vessels or adjacent structure
Air space:
Ill-defined, inhomogeneous.
Less dense than adjacent vessel – GGO
small nodule is difficult to identify
172
Interstitial nodules Air space opacity
173
Miliary tuberculosis
sarcoidosis
in a lung transplant patient with
bronchopneumonia
RANDOM: no consistent relationship to any structures
PERILYMPHATIC: corresponds to distribution of lymphatics
CENTRILOBULAR: related to centrilobular structuresDistribution
174
Perilymphatic distribution
Nodules in relation to pulmonary lymphatics at
# perihilar peribronchovascular interstitium,
# interlobular septa,
# subpleural regions, and
# centrilobular interstitium.
175
Perilymphatic nodules: D/D
Sarcoidosis
Lymphangitic carcinomatosis
Lymphocytic interstitial
pneumonia (LIP)
Lymphoproliferative disorders
Amyloidosis
176
Centrilobular nodules
 Distributed primarily within the
centre of the secondary pulmonary
lobule
 Reflect the presence of either
interstitial or airspace
abnormalities
 Dense or ground-glass opacity
 Subpleural lung is typically spared-
distinguishes from
diffuse random nodules.
177
Tree-in-bud
Centrilobular nodules m/b further characterized by presence or
absence of ‘‘tree-in-bud.’’
Tree-in-bud -- Impaction of centrilobular bronchus with
mucous, pus, or fluid, resulting in dilation of the bronchus, with
associated peribronchiolar inflammation .
 Dilated, impacted bronchi produce Y- or V-shaped structures
This finding is almost always seen with pulmonary infections.
178
179
180
Centrilobular nodules with or without tree-in-bud opacity: D/D :
With tree-in-bud opacity
 Bacterial pneumonia
 Typical and atypical
mycobacteria infections
 Bronchiolitis
 Diffuse panbronchiolitis
 Aspiration
 Allergic bronchopulmonary
aspergillosis
 Cystic fibrosis
 Endobronchial-neoplasms
(particularly
 Bronchioloalveolar
carcinoma)
Without tree-in-bud opacity
 All causes of centrilobular
nodules with tree-in-bud
opacity
 Hypersensitivity
pneumonitis
 Respiratory bronchiolitis
 Cryptogenic organizing
pneumonia
 Pneumoconioses
 Langerhans’ cell
histiocytosis
 Pulmonary edema
 Vasculitis
 Pulmonary hypertension
181
Random nodules
Random nodules – No definable distribution
Are usually distributed uniformly throughout the lung parenchyma
in a bilaterally symmetric distribution.
Random nodules: Miliary
tuberculosis.
Axial HRCT image shows
multiple nodules scattered uniformly
throughout the lung parenchyma.
184
Random nodules: D/D
1. Haematogenous metastases
2. Miliary tuberculosis
3. Miliary fungal infection
4. Disseminated viral infection
5. Silicosis or coal-worker’s pneumoconiosis
6. Langerhans’ cell histiocytosis
185
Parenchymal Opacification
Ground-glass opacity
Consolidation
Lung calcification &
high attenuation
opacities.
186
GROUND GLASS
OPACITIES
 Hazy increased attenuation of lung, with
preservation of bronchial and vascular
margins
 Pathology : it is caused by
# partial filling of air spaces,
# interstitial thickening,
# partial collapse of alveoli,
# normal expiration, or
# increased capillary blood volume
 D/t volume averaging of morphological
abnormality too small to be resolved by
HRCT
187
IMPORTANCE OF GGO
 Can represent - microscopic interstitial disease
(alveolar interstitium)
- microscopic alveolar space disease
- combination of both
 In the absence of fibrosis, mostly indicates the presence
of an ongoing, active, potentially treatable process
 Ground Glass opacity should be diagnosed only on scans
obtained with thin sections : with thicker sections volume
averaging is more - leading to spurious GGO, regardless
of the nature of abnormality
188
DIFFERNTIAL DIAGNOSIS : GGO
189
The location of the abnormalities in ground glass
pattern can be helpful:
 Upper zone predominance:
Respiratory bronchiolitis
PCP.
 Lower zone predominance: UIP, NSIP, DIP.
 Centrilobular distribution:
Hypersensitivity pneumonitis,
Respiratory bronchiolitis
190
GGO with few cystic and reticular
lesion in HIV + ve patient -- PCP
Combination of GGO with
fibrosis and tractional
bronchiectasis-- NSIP
191
CRAZY PAVING PATTERN
 It is scattered or diffuse ground-glass attenuation with
superimposed interlobular septal thickening and
intralobular lines.
 Causes:
192
Combination of ground glass
opacity and septal thickening :
Alveolar proteinosis.
193
194
CONSOLIDATION
 Consolidation is defined as increased attenuation, which results in
obscuration of the underlying vasculature, usually producing air
bronchogram.
 The presence of consolidation implies that the air within affected
alveoli has been replaced by another substance, such as blood, pus,
oedema, or cells.
 When consolidation is evident on a chest radiograph, HRCT does
not usually provide additional diagnostically useful information.
D/D on the basis of
presentation
Acute consolidation is seen in:
- Pneumonias (bacterial, mycoplasma , PCP)
- Pulmonary edema due to heart failure or ARDS
- Hemorrhage
- Acute eosinophilic pneumonia
Chronic consolidation is seen in:
- Organizing Pneumonia
- Chronic eosinophilic pneumonia
- Fibrosis in UIP and NSIP
- Bronchoalveolar carcinoma or lymphoma
195
196
Patchy ground-glass opacity,
consolidation, and nodule mainly with
peribronchovascular distribution with
reversed halo signs (central ground-glass
opacity and surrounding air-space
consolidation)
Peripheral consolidations with
upper lobe predominance (photo
negative of pulmonary edema)
Lung calcification & high attenuation
opacities
Multifocal lung calcification
• Infectious granulomatous ds - TB, histoplasmosis, and
varicella, pneumonia;
• Sarcoidosis , silicosis, Amyloidosis
 Fat embolism associated with ARDS
Diffuse & dense lung calcification
• Metastatic calcification,
• Disseminated pulmonary ossification, or
• Alveolar microlithiasis
197
High attenuation opacity
• Talcosis asso with fibrotic mass,
• inhalation of metals (tin/barium)
Small focal areas of increased attenuation
• injection and embolized radiodense materials such as
mercury or acrylic cement
Diffuse, increased lung attn in absence of calcification
• amiodarone lung toxicity or
• embolization of iodinated oil after chemoembolization
198
199
HRCT findings manifesting as
decreased lung opacity
Lung Cysts,
Emphysema,
and
Bronchiectasis
200
HONEYCOMBING
 Defined as - small cystic spaces with irregularly thickened
walls composed of fibrous tissue.
 Predominate in the peripheral and subpleural lung
regions
 Subpleural honeycomb cysts typically occur in several
contiguous layers. D/D- paraseptal emphysema in which
subpleural cysts usually occur in a single layer.
 Indicates the presence of “END stage” disease regardless
of the cause.
201
Causes
Lower lobe predominance :
1. UIP or interstitial fibrosis
2. Connective tissue disorders
3. Hypersensitivity pneumonitis
4. Asbestosis
5. NSIP (rare)
Upper lobe predominance :
1. End stage sarcodosis
2. Radiation
3. Hypersensitivity Pneumonitis
4. End stage ARDS
202
Honeycombing and traction bronchiectasis in UIP.
Lung cysts
 Thin walled (less than 3mm) , well defined and
circumscribed air containing lesions
 They are lined by cellular epithelium, usually fibrous or
epithelial in nature.
 Common cause are : 1. Lymphangiomyomatosis
2. Langerhans Histiocytosis
3. Lymphoid interstitial pneumonia
They need to be differentiated from emphysematous bullae,
blebs and pneumatocele.
204
Axial HRCT image through the upper
lobes shows multiple bilateral bizarre-
shaped cysts and small centrilobular
nodules in a smoker with Langerhans’
cell histiocytosis.
Axial HRCT image through the
upper lobes shows multiple bilateral
uniform, thin-walled cysts.
205
BRONCHIEACTASIS
Bronchiectasis is defined as localized, irreversible dilation of
the bronchial tree.
HRCT findings of the bronchiectasis include
# Bronchial dilatation
# Lack of bronchial tapering
# Visualization of peripheral airways.
206
BRONCHIAL DILATATION
# The broncho-arterial ratio (internal diameter of the
bronchus /pulmonary artery) exceeds 1.
# In cross section it appears as “Signet Ring
appearance”
LACK OF BRONCHIAL TAPERING
# The earliest sign of cylindrical bronchiectasis
# One indication is lack of change in the size of an
airway over 2 cm after branching.
VISUALIZATION OF PERIPHERAL AIRWAYS
# Visualization of an airway within 1 cm of the costal
pleura is abnormal and indicates potential bronchiectasis
207
Coned axial HRCT image shows bronchial
dilation with lack of tapering . Bronchial
morphology is consistent with varicose
bronchiectasis.
208
A NUMBER OF ANCILLARY FINDINGS ARE ALSO
RECOGNIZED:
# Bronchial wall thickening : normally wall of bronchus
should be less than half the width of the accompanying
pulmonary artery branch.
# Mucoid impaction
# Air trapping and mosaic perfusion
Extensive, bilateral mucoid impaction
Mosaic perfusion caused by large and small
airway obstruction.
Small centrilobular nodules are visible in the
right lower lobe
209
Types
1. CYLINDRICAL BRONCHIECTASIS
# mildest form of this disease,
# thick-walled bronchi that extend
into the lung periphery and fail to
show normal tapering
2. VARICOSE BRONCHIECTASIS
# beaded appearance of bronchial
walls - dilated bronchi with areas of
relative narrowing
# string of pearls.
# Traction bronchiectasis often
appears varicose.
210
3. CYSTIC BRONCHIECTASIS :
# Group or cluster of air-filled
cysts,
# cysts can also be fluid filled,
giving the appearance of a cluster
of grapes.
4.TRACTION BRONCHIECTASIS :
# Defined as dilatation of
intralobular bronchioles because
of surrounding fibrosis
# due to fibrotic lung diseases
211
Tram Tracks
ABPA: glove-finger shadow due to mucoid impaction in central
bronchiectasis in a patient with asthma.
Differential diagnosis
1. Infective causes : specially childhood pneumonia,
pertusis, measles, tuberculosis
2. Non- infective causes : Bronchopulmonary
aspergillosis, inhalation of toxic fumes
3. Connective tissue disorder : Ehlers-Danlos Synd,
Marfan synd , tracheobronchomeglay
4. Ciliary diskinesia : Cystic fibrosis, Kartangener
synd, agammaglobulinemia .
5. Tractional bronchiectasis in interstitial fibrosis.
214
EMPHYSEMA
 Permanent, abnormal enlargement of air spaces distal
to the terminal bronchiole and accompanied by the
destruction of the walls of the involved air spaces.
215
Centrilobular (proximal or
centriacinar) emphysema
 Found most commonly in the upper lobes
 Manifests as multiple small areas of low attenuation without a
perceptible wall, producing a punched-out appearance.
 Often the centrilobular artery is visible within the centre of
these lucencies.
216
PANLOBULAR EMPHYSEMA
 Affects the entire secondary pulmonary lobule and is
more pronounced in the lower zones
 Complete destruction of the entire pulmonary lobule.
 Results in an overall decrease in lung attenuation and a
reduction in size of pulmonary vessels
217
Paraseptal (distal acinar)
emphysema
 Affects the peripheral parts of the secondary
pulmonary lobule
 Produces subpleural lucencies.
218
Cicatricial Emphysema/ irregular air
space enlargement previously known as irregular or cicatricial emphysema
• can be seen in association with fibrosis
• with silicosis and progressive massive fibrosis or
sarcoidosis
BULLOUS EMPHYSEMA :
• Does not represent a specific histological abnormality
• Emphysema characterized by large bullae
• Often associated with centrilobular and paraseptal
emphysema
219
Paraseptal Emphysema vs
Honeycombing
Paraseptal emphysema Honeycomb cysts
occur in a single layer at the
pleural surface
may occur in several layers in the
subpleural lung
predominate in the upper lobes predominate at the lung bases
unassociated with significant
fibrosis
Asso with other findings of
fibrosis.
Associated with other findings of
emphysema
Absent
220
Bullae
A sharply demarcated area of emphysema ≥ 1 cm in
diameter
a thin epithelialized wall ≤ 1 mm.
uncommon as isolated findings, except in the lung
apices
Usually asso with evidence of extensive centrilobular or
paraseptal emphysema
When emphysema is associated with predominant
bullae, it may be termed bullous emphysema
221
Pneumatocele
 Defined as a thin-walled, gas-filled space within the lung,
 Associated with acute pneumonia or hydrocarbon
aspiration.
• Often transient.
• believed to arise from lung necrosis and bronchiolar
obstruction.
• Mimics a lung cyst or bulla on HRCT and cannot be
distinguished on the basis of HRCT findings.
222
CAVITARY NODULE
 Thicker and more irregular
walls than lung cysts
• In diffuse lung diseases - LCH,
TB, fungal infections, and
sarcoidosis.
 Also seen in rheumatoid lung
disease, septic embolism,
pneumonia, metastatic tumor,
tracheobronchial
papillomatosis, and Wegener
granulomatosis
Cavitary nodules or cysts in
tracheobronchial papillomatosis.
fungal pneumonia 223
Mosaic attenuation & perfusion
 Lung density and attenuation depends partially on amount
of blood in lung tissue.
 The term 'mosaic attenuation' is used to describe density
differences between affected and non-affected lung areas.
 It is seen as inhomogeneous attenuation of lung
parenchyma with focal region of lucency which show
smaller size of vessels
 May be due to vascular obstruction, abnormal ventilation
or airway disease/
224
Mosaic attenuation due to small airway disease
# Air trapping and bronchial dilatation commonly seen.
# Areas of increased attenuation have relatively large
vessels, while areas of decreased attenuation have small
vessels.
# Causes include: Bronchiectasis, cystic fibrosis and
bronchiolitis obliterans.
Mosaic attenuation due to vascular disease
# common in patients with acute or chronic pulmonary
embolism (CPE), and
# decreased vessel size in less opaque regions is often
visible
225
MOSIAC PATTERN
DEPENDENT LUNG ONLY
PRONE
POSITION
RESOLVE
PLATE
ATELECTASIS
NOT
RESOLVE
GROUND
GLASS
NONDEPENDENT LUNG
EXPIRATION
NO AIR
TRAPPING
VESSEL SIZE
DECREASED
VASCULAR
NORMAL
GROUND
GLASS
AIR
TRAPPING
AIRWAYS
DISEASE
226
Inhomogeneous lung
opacity: mosaic
perfusion in a patient
with bronchiectasis.
central bronchiectasis with
multifocal, bilateral
inhomogeneous lung opacity.
The vessels within the areas of
abnormally low attenuation are
smaller than their counterparts
in areas of normal lung
attenuation.
227
Air trapping on expiration
 Most patients with air trapping seen on expiratory scans
have inspiratory scan abnormalities, such as
bronchiectasis, mosaic perfusion, airway thickening, or
nodules suggest the proper differential diagnosis.
 Occasionally, air trapping may be the sole abnormal
finding on an HRCT study.
 The differential diagnosis include ---
bronchiolitis obliterans; asthma; chronic
bronchitis; and hypersensitivity pneumonitis
228
Air trapping on expiratory imaging
in the absence of inspiratory scan
findings in a patient with
bronchiolitis obliterans.
(A) Axial inspiratory image through
the lower lobes shows no clear
evidence of inhomogeneous lung
opacity.
(B) Axial expiratory image shows
abnormal low attenuation
(arrows) caused by air trapping,
representing failure of the
expected increase in lung
attenuation that should normally
occur with expiratory imaging.
229
Head cheese sign
 It refers to mixed densities which includes presence of-
# consolidation
# ground glass opacities
# normal lung
# Mosaic perfusion
• Signifies mixed infiltrative and obstructive disease
• Common cause are : Hypersensitive pneumonitis
Sarcoidosis
DIP
230
Axial HRCT image in a patient with
hypersensitivity pneumonitis shows a
combination of ground-glass opacity, normal
lung, and mosaic perfusion (arrow) on the same
inspiratory image.
231
Distribution within the lung
Upper lung zone preference is seen in:
1.Inhaled particles: pneumoconiosis (silica or
coal)
2.Smoking related diseases (centrilobular
emphysema
3. Respiratory bronchiolitis (RB-ILD)
4.Langerhans cell histiocytosis
5.Hypersensitivity pneumonitis
6.Sarcoidosis
Lower zone preference is seen in:
1. UIP
2. Aspiration
3. Pulmonary edema
232
Central vs peripheral zone
 Central Zone Peripheral zone
1. Sarcoidosis 1. COP
2. Cardiogenic pulmonary 2. Ch Eosinophilic
Pneumonia
edema 3. UIP
3. Bronchitis 4. Hematogenous mets
233
Additional findings
Pleural effusion is seen in:
 Pulmonary edema
 Lymphangitic spread of carcinoma - often unilateral
 Tuberculosis
 Lymphangiomyomatosis (LAM)
 Asbestosis
234
Hilar and mediastinal
lymphadenopathy
# In sarcoidosis the common pattern is right paratracheal
and bilateral hilar adenopathy ('1-2-3-sign').
# In lung carcinoma and lymphangitic carcinomatosis
adenopathy is usually unilateral.
#'Eggshell calcification' in lymph nodes occurs in ----
Silicosis and coal-worker's pneumoconiosis and is
sometimes seen in sarcoidosis, post irradiation
Hodgkin disease, blastomycosis and scleroderma .
235
Conclusion
• A thorough knowledge of the basic anatomy is of utmost
importance.
 When attempting to reach a diagnosis or differential diagnosis of
lung disease using HRCT, the overall distribution of pulmonary
abnormalities should be considered along with their morphology,
HRCT appearance, and distribution relative to lobular structures.
Correlation of the radiological findings with patients clinical and
laboratory findings to reach a likely diagnosis

236
237
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DR Harshil Radiology HRCT

  • 1. DR. HARSHIL A. KALARIA RESIDENT,. DEPARTMENT OF RADIOLOGY
  • 2. TECHNICAL ASPECT OF HRCT; NORMAL LUNG ANATOMY & HRCT FINDINGS OF LUNG DISEASE
  • 3. HRCT ------ MEANING o It is often used for anything and everything to do with “high resolution”. o Resolution : Means ability to resolve small object that are close together ,as separate form. Actual meaning o A scan performed using high- spatial frequency algorithm to accentuate the contrast between tissue of widely differing densities, eg., - air & vessels (lung) - air & bone (temporal & paranasal sinus) 3
  • 4. INTRODUCTION • HRCT -- 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. • Superior to chest radiography for detection of lung disease, points a specific diagnosis and helps in identification of reversible disease. 4
  • 5. HISTORY • 1982– The term HRCT was first used by TODO et. Al • 1985 – Nakata et.al and Naidich et.al published first report on HRCT Since then has been an important tool in pulmonary medicine • Recent development of MDCT scanner capable of volumetric high resolution scanning has improved the investigation 5
  • 6. TECHNICAL ASPECT Parameters o Slice thickness o Kvp o mAs o Scan time o FoV o Interslice gap (collimation) o Filming. 6
  • 7. SLICE THICKNESS • Thin sections 0.5 – 1.5 mm is essential for optimal spatial resolution • Thicker slices are prone for volume averaging and reduces ability to resolve smaller structure • Better for delineation of bronchi, wall thickness and diameter 7
  • 8. 8
  • 9. Reconstruction Algorithm • Denotes the frequency at which the acquired scan data are recorded when creating the image. • Using a high-resolution algorithm is critical element in performing HRCT. • High spatial frequency or sharp algorithm -- bone algorithm is used which reduces image smoothing and better depicts normal and abnormal parenchymal interface. 9
  • 11. Kilovolts (Peak), Milliamperes, and Scan Time • In HRCT image, noise is more apparent than standard CT. • Noise – 1/√ mAs X Kvp X scan time • As increasing scan time is not feasible, mAs and Kvp are altered to reduce noise • Noise decreases with increase in Kvp and mAs. 11
  • 12. • For routine technique – Kvp -- 120-140 mAs -- 200- 300 • Increased patient and chest wall thickness are associated with increase image noise, may be reduced by increasing mAs and Kvp • Scan Time : As low as possible (1-2 sec) to minimize motion artifact. 12
  • 13. WINDOW SETTINGS Lung window  Window level setting ranging from – 600 to – 700 HU and window widths of 1000 to 1500 HU are appropriate for a routine lung window. Soft tissue window  Window level/width setting of 40-50/ 350-450 HU are best for evaluation of the mediastinum, hila, and pleura. 13
  • 14. LOW DOSE HRCT • Low dose HRCT uses Kvp of 120- 140 and mA of 30-20 at 2 sec scan time. • Equivalent to conventional HRCT in 97 % of cases • Disadvantage : Fails to identify GGO in few cases and have more prominent streak artifact. • Not recommended for initial evaluation of patients with lung disease. • Indicated in following up patients with a known lung abnormality or in screening large populations at risk for lung dz. 14
  • 15. Matrix size, Field of View, and Target reconstruction • Matrix size : Largest available matrix s/b used – 512 x 512 • Field of view : smallest FOV that will encompass the patient is used as it will reduce the pixel size. (commonly 35 to 40) • Retrospectively targeting image reconstruction to a single lung instead of the entire thorax significantly reduces the FOV and image pixel size, and thus increases spatial resolution. 15
  • 16. 16
  • 17. • INTERSLICE GAP – varies from examination to examination, but is usually 10- 20 mm • INSPIRATORY LEVEL : Routine HRCT is obtained in suspended full inspiration, which  optimizes contrast between normal structures, various abnormalities and normal aerated lung parenchyma; and  reduces transient atelectasis, a finding that may mimic or obscure significant abnormalities. • EXPIRATORY SCAN : valuable in obstructive lung disease or airway abnormality 17
  • 18. Patient Position and the Use of Prone Scanning • Supine adequate in most instances. • Prone for diagnosing subtle lung abnormalities. e.g., asbestosis, suspected early lung fibrosis • Prone scan is useful in differentiating dependent lung atelectasis from early lung fibrosis 18
  • 19. Axial CT image shows opacity in the posterior part of the lung which could represent dependent opacity or pulmonary inflammation. The prone images shows complete resolution of the opacity suggesting dependent atelectasis. 19
  • 20. Persistent opacity in the posterior lung in a patient with pulmonary fibrosis. 20
  • 21. TECHNIQUE OF SCAN ACQUISITION: 1. Spaced axial scans :  Obtained at 1cm intervals from lung apices to bases. In this manner, HRCT is intended to “sample” lung anatomy  It is assumed that the findings seen at the levels scanned will be representative of what is present throughout the lungs  Results in low radiation dose as the individual scans are widely placed 21
  • 22. 2. Volumetric HRCT -  MDCT scanner are capable of rapid scanning and thin slice acquisition. Advantages : 1. Viewing of contagious slice for better delineation of lung abnormality 2. Complete imaging of lung and thorax 3. Reconstruction of scan data in any plane using MIPs or MinIPs. 4. diagnosis of other lung abnormalities Disadvantage : greater radiation dose. It delivers 3-5 times greater radiation. 22
  • 23. Multidetector Helical HRCT  Multidetector CT is equipped with a multiple row detector array  Multiple images are acquired due to presence of multiple detectors  Advantages : - shorter acquisition times and retrospective creation of both thinner and thicker sections from the same raw data  Acquisition time is so short that whole-lung HRCT can be performed in one breath-hold. 23
  • 24. Which is better HRCT or MD- HRCT  Various study shows the image quality of axial HRCT with multi-detector CT is equal to that with conventional single-detector CT.  HRCT performed with spaced axial images results in low radiation dose as compared with MD-HRCT.  Increased table speed may increase the volume- averaging artifact and may result in indistinctness of subtle pulmonary abnormalities.  MDCT provides for better reconstruction in Z axis 24
  • 25. Radiation dose  PA CHEST Radiograph ----- ----- ----- 0.05 mSv  Spaced axial HRCT (10mm space) ----- 0.7 mSv ( 14 X ray)  Spaced axial HRCT (20 mm space) ------ 0.35 mSv ( 7 X ray)  Low Dose Spaced axial HRCT -------- 0.02 mSV  MD-HRCT ---- ------- 4 - 7 msv ( 60-80 x ray) Combining HRCT scan at 20 mm interval with low mAs scan (40 mAs) would result in radiation comparable to conventional X ray. 25
  • 26. Summary of HRCT protocol  Collimation: thinnest available collimation (1.0-1.5 mm).  Reconstruction algorithm: high-spatial frequency or “sharp” algorithm (i.e., GE “bone”).  Scan time: as short as possible (1 sec or less).  kV(p), 120-140; mA, 240.  Matrix size: largest available (512 × 512). Optional  kV(p)/mA: Increased kV(p)/mA (i.e., 140/340). Recommended in large patients. Otherwise optional.  Targeted reconstruction: (15- to 25-cm field of view).  Reduced mA (low-dose HRCT): 40-80 mA.
  • 27. HRCT ARTIFACT • Streak ArtIfacts :  Fine, linear, or netlike opacities  Radiate from the edges of sharply marginated , high-contrast structures such as bronchial walls, ribs, or vertebral bodies.  More evident on low mA  Mechanisms: beam hardening, photon starvation, and aliasing. 27
  • 28. Motion-related artIfacts • Pulsation / Star artefacts • Doubling artefacts. • Stair-step artefacts in sag/coro reconstruction. 28
  • 29. MODIFICATION OF SCAN PROTOCOL Scan protocol can be modified in relation to disease or patients comfort. If a disease has basal predominance, it may be wise to begin scanning near the diaphragm and proceed cephalic . Caudad for disease with an upper-lobe predominance (e.g., sarcoidosis) An alternative approach - cephalad in all patients. 29
  • 30. MAXIMUM INTENSITY PROJECTION  maximum intensity projection (MIP) is a volume rendering method for 3D data that projects in the visualization plane thevoxels with maximum intensity that fall in the way of parallel rays traced from the viewpoint to the plane of projection
  • 31. Volume Rendering VS Maximum Intensity Projection (a) Volume-rendered image provides clear definition of individual vessels. (b) MIP image reconstructed from the same volume data shows all of the vessels, but their outlines merge; it is impossible to visualize the spatial relationships between the vessels or to delineate individual
  • 33.
  • 34.  Maximum-intensity projection (MIP) image in a patient with small lung nodules obtained using a multidetector-row spiral CT scanner with 1.25-mm detector width and a pitch of 6. A: A single HRCT image shows two small nodules (arrows) that are difficult to distinguish from vessels. B: An MIP image consisting of eight contiguous HRCT images, including A, allows the two small nodules to be easily distinguished from surrounding vessels.
  • 35.  first step in HRCT interpretation of diffuse lung diseases is a good quality scan
  • 36. . Resolution and size or orientation of structures. The tissue plane, 1 mm thick, and the perpendicular cylinder, 0.2 mm in diameter, are visible on the HRCT scan because they extend through the thickness of the scan volume or voxel. The horizontal cylinder cannot be seen.
  • 37. MDCT Techniques  Combined “routine” and HRCT studies  5 mm sections q 5 mm (separate lung and mediastinal reconstruction algorithms):  1 – 1.25 mm sections q 10 mm (lung algorithm)  Optional image acquisitions  Supine and prone 1 – 1.25 mm sections  Inspiratory/expiratory 1 -1.25 mm sections  Low dose technique (mAs 40 – 80)  Optional Reconstruction techniques  Sliding maximum and minimum intensity projection images (MIPs/ MINIPs): 5 mm’s q 5 mm
  • 38. INDICATIONS  Detect interstitial lung disease not seen on chest x-ray  Abnormal pulmonary function tests  Characterize lung disease seen on X-ray  Determine disease activity  Find a biopsy site
  • 39. INDICATIONS  Hemoptysis  Diffusely abnormal CXR  Normal CXR with abnormal PFT’s  Baseline for pts with diffuse lung disease  Solitary pulmonary nodules  Reversible (active) vs. non-reversible (fibrotic) lung disease  Lung biopsy guide  F/U known lung disease  Assess Rx response
  • 40. LUNG ANATOMY Right lung is divided by major and minor fissure into 3 lobes and 10 bronchopulmonary segments  Left lung is divided by major fissure into 2 lobes with a lingular lobe and 8 bronchopulmonary segments
  • 41. ANATOMY The trachea (windpipe) divides into left and the right mainstem bronchi, at the level of the sternal angle (carina).  The right main bronchus is wider, shorter, and more vertical than the left main bronchus.  The right main bronchus subdivides into three lobar bronchi, while the left main bronchus divides into two.  The lobar bronchi divide into tertiary bronchi, also known as segmentalinic bronchi, each of which supplies a bronchopulmonary segment.
  • 42.
  • 43. ANATOMY The segmental bronchi divide into many primary bronchioles which divide into terminal bronchioles, each of which then gives rise to several respiratory bronchioles, which go on to divide into two to 11 alveolar ducts. There are five or six alveolar sacs associated with each alveolar duct. The alveolus is the basic anatomical unit of gas exchange in the lung.
  • 44.
  • 45. TRACHEAL ANATOMY  10-12 cm in length  Extrathoracic (2-4cm) and Intrathoracic(6-9cm beyond manubrium)  In men, tracheal diameter averages 19.5 mm and in women, tracheal diameter is slightly less, averaging 17.5 mm  The posterior portion of the tracheal wall is a thin fibromuscular membrane termed the posterior tracheal membrane  There is marked variability in the cross-sectional appearance of the trachea, which may appear convex posteriorly, flat, or convex anteriorly
  • 46. The membranous posterior membrane allows esophageal expansion during expiration Contains glands, small arteries, nerves, lymph vessels and elastic fibers Trachealis muscle overlies esophageal muscle and epithelium
  • 47. BRONCHIAL ANATOMY  Airways divide by dichotomous branching, with approximately 23 generations of branches from the trachea to the alveoli.  The wall thickness of conducting bronchi and bronchioles is approximately proportional to their diameter.  Bronchi with a wall thickness of less than 300 um is not visible on CT or HRCT.  As a consequence, normal bronchi less than 2 mm in diameter or closer than 2 cm from pleural surfaces equivalent to seventh to ninth order airways are generally below the resolution even of high-resolution CT
  • 48. There are approximately 23 generation of dichotomous branching From trachea to the alveolar sac HRCT can identify upto 8th order central bronchioles 48
  • 49. BRONCHUS  BLOOD SUPPLY Bronchial Arteries( 2 on left side i.e. superior and inferior and 1 on right side) Left arises from thoracic aorta Right from either thoracic aorta, sup. lt. bronchial or right 3rd intercostal artery  VENOUS DRAINAGE on right- azygous vein on left- left superior intercostal or accessory hemiazygous vein  NERVE SUPPLY Pulmonary plexus at hilum (vagus and sympathetic)
  • 50. BRONCHOARTERIAL RATIO (B/A)  Internal diameter of both bronchus and accompanying arterial diameter calculated and ratio measured.  If obliquely cut section seen, then the LEAST diameter is considered.  Normal ratio is 0.65-0.70  B/A ratio more than 1.0 indicates bronchiactasis.
  • 51. BRONCHIAL WALL THICKNESS (T/D)  Wall thickness proportionately decreases as the airway divides further as according to the diameter of the airway.  T/D ratio approximates to 20% at any generation of airway.
  • 52. The Nomenclature Adopted by the Ad HOC lnternational Committee Meeting at the Time of the lnternational Congress of Otorhinolaryngology in 1949 [I]" International Nomenclature Brock Jackson and Huber Right upper lobe bronchus Apical (RB1) Posterior (RB2) Anterior (RB3) Middle lobe bronchus Lateral (RB4) Medial (RB5) Right lower lobe bronchus Apical (RB6) Medial basal (cardiac) (RB7) Anterior basal (RB8) Lateral basal (RB9) Posterior basal (RB10) Pectoral Subapical Apical Lateral Medial Apical Cardiac Anterior basal Middle basal Posterior basal Anterior Postenor Apical Lateral Medial Superior Medial basal Anterior basal Lateral basal Posterior basal
  • 53. The Nomenclature Adopted by the Ad HOC lnternational Committee Meeting at the Time of the lnternational Congress of Otorhinolaryngology in 1949 [I]" International Nomenclature Brock Jackson and Huber Left upper lobe bronchus Upper division Apical (LB1) Apicoposterior LB1 and LB2 Posterior (LB2) Anterior (LB3) Lingula Superior (LB4) Inferior (LB5) Left lower lobe bronchus Apical (LB6) Anterior basal (LB8) Lateral basal (LB9) Posterior basal (LB10) Apicopectoral Apical Subapical Pectoral Upper Lower Apical Anterior basal Middle basal Posterior basal Apical Apical-posterior Posterior Anterior Superior Inferior Superior Anterior medial basal Lateral basal Posterior basal
  • 54.
  • 55.
  • 56. MEDIASTINUM  Broad central portion that separate the two laterally placed pleural cavities.  Imaginary plane passes through T4 divides it into Superior & Inferior mediastinum  Inferior mediastinum is further divided- Heart enclosed in pericardium (M) Sternum to anterior pericardium (A) Posterior pericardium to vertebrae (P)
  • 57. INTERSTITIAL ANATOMY  Lung is supported by a network of connective tissue called interstitium  Interstitium not visible on normal HRCT but visible once thickened.  Interstitium is constituted by AXIAL fibre system (peribronchovascular & centrilobular), PERIPHERAL fibre system (subpleural & interlobular septa) and SEPTAL fibre system (intralobular septa)
  • 58. 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 center, that is parallelled by the centrilobular artery.  Pulmonary veins and lymphatics run in the periphery of the lobule within the interlobular septa.
  • 59.
  • 60. SECONDARY PULMONARY LOBULE  Smallest lung unit that is surrounded by connective tissue septa (Miller)  The basic anatomic unit  Irregular polyhedral in shape.  Measures 1 to 2.5 cm 60
  • 61. Anatomy of the Secondary Lobule and Its Components 1. Interlobular septa and contiguous subpleural interstitium, 2. Centrilobular structures, and 3. Lobular parenchyma and acini. 61
  • 62. Interlobular septa and contiguous subpleural interstitium The secondary pulmonary lobule is marginated by septa which extends from the pleural surface. They measure 0.1 mm in thickness. They are less well defined in central lung Lobular core : The secondary lobule is supplied by arteries and bronchioles that measures approximately 1 mm in diameter. It consists of functioning lung parenchyma namely the alveoli, alveolar duct and vessels. The parenchyma is supported by network of central and peripheral fibers of interstitium. 62
  • 63. PULMONARY ACINUS Portion of lung parenchyma supplied by a single respiratory Bronchiole. Size is 7 to 8 mm in adults 3 to 24 acini = Sec Pul. Lobule Primary Lobule: Lung parenchyma associated with a single Alveolar duct. 4-5 Primary Lobules  Acinus 63
  • 64. 64
  • 65. A group of terminal bronchioles 65
  • 72.  The peribronchovascular interstitum invests the bronchi and pulmonary artery in the perihilar region.  The centrilobular interstitium are associated with small centrilobular bronchioles and arteries  The subpleural interstitium is located beneath the visceral pleura; envelops the lung into fibrous sac and sends connective tissue septa into lung parenchyma.  Interlobular septa constitute the septas arising from the subpleural interstitium. 72
  • 73. The normal pulmonary vein branches are seen marginating pulmonary lobules. The centrilobular artery branches are visible as a rounded dot 73
  • 74. Anatomy of pleural surfaces and chest wall. 74
  • 75.  Every CT scan starts with a scout view, a projection image that looks like a second rate X-ray.  A line on scout view tells you the level of axial cut.
  • 76. HOUNSFIELD UNIT (HU)  HU scale is a linear transformation of the original linear attenuation coefficient measurement into one in which radio density of distilled water at STP is defined as zero HU, while radio density of air at STP is defined as -1000 HU.  Fat  -50 to -100 HU  Blood  +30 to 45 HU  Bone  >+400 HU  Muscle  +40HU  Contrast  +130 HU
  • 77. APPEARANCE ON CT SCAN  AIR  JET BLACK  FAT  MODERATELY BLACK  WATER  GRAY  MUSCLES  SLIGHT WHITE  BONES  WHITE  CALICIFICATION  DENSE WHITE
  • 81. NORMAL LUNG ATTENUATION  Normal lung attenuation : –700 to – 900 HU  Attenuation gradient : densest at dependent region of lung as a result of regional difference in blood and gas density due to gravity Difference in attenuation of anterior and posterior lung ranges from 50 – 100 HU  In children, lung attenuation is greater than adults. 81
  • 82. NORMAL EXPIRATORY HRCT  Performed to detect air trapping in small airway obstruction  Attenuation increases with expiration (ranges from 100 to 130 HU)  60 % of normal individual shows air trapping in the superior segment of lower lobe and involving single lobule, normal variant. 82
  • 83. LOBAR AND BRONCHIAL ANATOMY ON HRCT THORAX
  • 85.
  • 87.
  • 88.
  • 90.
  • 91.
  • 92.
  • 94.
  • 95.
  • 96.
  • 98.
  • 100.
  • 101.
  • 102.
  • 103.
  • 104.
  • 105.
  • 107.
  • 109.
  • 111.
  • 112. RB1 joining RUL bronchus LB1,2 joining LUL bronchus LB8RB8 CARIN A RC2 LC2
  • 113.
  • 115.
  • 117. VASCULAR ANATOMY ON CT THORAX
  • 118. Rt. CCA Rt. IJV Rt. EJV Lt. IJV Lt. EJV Lt. CCA
  • 119.
  • 120.
  • 121.
  • 123.
  • 124.
  • 125.
  • 126. Lt. BCV joining Rt. BCV Rt. BCV Rt. BCA Lt. CCA Lt. SCA SUPRA AORTIC LEVEL
  • 127. Formation of SVC Branching from Aortic Arch
  • 129.
  • 130.
  • 131.
  • 133.
  • 134.
  • 135. Aorta arising from Left Ventricle Pulmonary Trunk arising from Right Ventricle SVC draining into Right Atrium Pulmonary Veins draining into Left Atrium
  • 136.
  • 138.
  • 141. LYMPH NODE STATIONS ON CT THORAX
  • 142. THORAX
  • 143. 1. SUPRACLAVICULAR NODES • LOW CERVICAL • SUPRACLAVICULAR • STERNAL NOTCH Extends from the lower margin of the cricoid cartilage to the clavicles and the upper border of the manubrium. The midline of the trachea serves as border between 1R and 1L.
  • 144.
  • 145. 2. UPPER PARATRACHEAL NODES 2R. Upper Right Paratracheal Extends to the left lateral border of the trachea. From upper border of manubrium to the intersection of caudal margin of innominate (left brachiocephalic) vein with the trachea. 2L. Upper Left Paratracheal From the upper border of manubrium to the superior border of aortic arch. 2L nodes are located to the left of the left lateral border of the trachea.
  • 146.
  • 147. 3A. Pre-vascular These nodes are not adjacent to the trachea like the nodes in station 2, but they are anterior to the vessels. 3P. Pre-vertebral These nodes are not adjacent to the trachea like the nodes in station 2, but behind the esophagus, which is prevertebral.
  • 148.
  • 149. 4. LOWER PARATRACHEAL NODES 4R. Lower Right Paratracheal From the intersection of the caudal margin of in nominate (left brachiocephalic) vein with the trachea to the lower border of the azygos vein. 4R nodes extend from the right to the left lateral border of the trachea. 4L. Lower Left Paratracheal From the upper margin of the aortic arch to the upper rim of the left main pulmonary artery.
  • 150.
  • 151. 5-6. AORTIC NODES 5. Subaortic nodes These nodes are located in the AP window lateral to the ligamentum arteriosum. These nodes are not located between the aorta and the pulmonary trunk but lateral to these vessels. 6. Para-aortic nodes These are ascending aorta or phrenic nodes lying anterior and lateral to the ascending aorta and the aortic arch.
  • 152.
  • 153. Inferior Mediastinal Nodes 7-9 7. Subcarinal nodes Nodes below carina 8. Paraesophageal nodes Nodes lateral to esophagus 9. Pulmonary Ligament nodes Nodes lying within the pulmonary ligaments.
  • 154.
  • 155. Hilar, Lobar and (sub)segmental Nodes 10- 14 These are all N1-nodes. 10. Hilar nodes These include nodes adjacent to the main stem bronchus and hilar vessels. On the right they extend from the lower rim of the azygos vein to the interlobar region. On the left from the upper rim of the pulmonary artery to the interlobar region.
  • 156.
  • 157. DR. HARSHIL A. KALARIA RESIDENT,. DEPARTMENT OF RADIOLOGY Part II: HRCT FINDINGS OF LUNG DISEASE
  • 158. Q.1. What is the dominant HR-pattern ? Q.2. Where is it located within the secondary lobule (centrilobular, Perilymphatic or random) ? Q.3. Is there an upper versus lower zone or a central versus peripheral predominance ? Q.4. Are there additional findings (pleural fluid, lymphadenopathy, traction bronchiectasis) ? STRUCTURED APPROACH 158
  • 159.
  • 160. HRCT PATTERN INCREASED LUNG ATTENUATION LINEAR AND RETICULAR OPACITIES NODULES AND NODULAR OPACITIES PARENCHYMAL OPACIFICATION consolidation Ground glass DECREASED LUNG ATTENUATION CYSTIC LESIONS, EMPHYSEMA, AND BRONCHIEACTASIS MOSAIC ATTENUATION AND PERFUSION AIR TRAPPING ON EXPIRATORY SCANS 160
  • 161. Attenuation pattern  High Attenuation pattern  GROUND GLASS  CONSOLIDATION  Low Attenuation pattern  Emphysema  Lung cysts  Bronchiectasis  Honeycombing
  • 162. LINEAR AND RETICULAR OPACITIES  Represents thickening of interstitial fibers of lung by - fluid or - fibrous tissue or - infiltration by cells 162
  • 163. Interface sign Irregular interfaces between the aerated lung parenchyma and bronchi, vessels, or visceral pleural surfaces. Represent thickened interlobular septa, intralobular lines, or irregular scars. Nonspecific. Common in patients with an interstitial abnormality, fibrotic lung disease. 163
  • 164. Peribronchovascular Interstitial Thickening PBIT Smooth Pulmonary edema/ hemorrhage Lymphoma / leukemia Lymphangitic spread of carcinoma Nodular Sarcoidosis Lymphangitic spread of carcinoma Irregular Due to adjacent lung fibrosis Sarcoidosis, silicosis, TB and talcosis Venous, lymphatic or infiltrative disease lymphatic or infiltrative diseases 164
  • 166. INTERLOBULAR SEPTAL THICKENING  Normally, only a few septa seen  On HRCT, if numerous interlobular septas are seen, it almost always indicate abnormality.  Septal thickening d/t -interstitial fluid, cellular infiltration or fibrosis.  The thickened interstitium outline the secondary pulmonary lobules and are perpendicular to the pleura.  D/D are similar to that of PBIT. 166
  • 167. Smooth Septal thickening Septal thickening and ground-glass opacity with a gravitational distribution in a patient with cardiogenic pulmonary edema. 167
  • 168. Nodular Septal thickening Focal septal thickening in lymphangitic carcinomatosis Lymphangitic carcinomatosis : show diffuse smooth and nodular septal thickening. Sarcoidosis : right lung base shows interlobular septal thickening associated with several septal nodules giving beaded appearance 168
  • 169. 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. 169
  • 170. PARENCHYMAL BANDS  Non tapering , reticular opacity usually 1 to 3 mm in thickness and from 2 to 5 cm in length.  Is often peripheral and generally contracts the pleural surface  D/D : 1. Asbestosis 2. Sarcoidosis 3. Silicosis/ coal worker pneumoconiosis 4. Tuberculosis with associated scarring. 170
  • 171. Subpleural Interstitial Thickening  Mimic thickening of fissure.  DD similar to that of interlobular septal thickening.  more common than septal thickening in Idiopathic Pulmonary Fibrosis or UIP of any cause. 171
  • 172. Size, Distribution, Appearance Nodules and Nodular Opacities Size Small Nodules: <10 mm Miliary - <3 mm Large Nodules: >10 mm Masses - >3 cms Appearance Interstitial opacity:  Well-defined, homogenous, Soft-tissue density Obscures the edges of vessels or adjacent structure Air space: Ill-defined, inhomogeneous. Less dense than adjacent vessel – GGO small nodule is difficult to identify 172
  • 173. Interstitial nodules Air space opacity 173 Miliary tuberculosis sarcoidosis in a lung transplant patient with bronchopneumonia
  • 174. RANDOM: no consistent relationship to any structures PERILYMPHATIC: corresponds to distribution of lymphatics CENTRILOBULAR: related to centrilobular structuresDistribution 174
  • 175. Perilymphatic distribution Nodules in relation to pulmonary lymphatics at # perihilar peribronchovascular interstitium, # interlobular septa, # subpleural regions, and # centrilobular interstitium. 175
  • 176. Perilymphatic nodules: D/D Sarcoidosis Lymphangitic carcinomatosis Lymphocytic interstitial pneumonia (LIP) Lymphoproliferative disorders Amyloidosis 176
  • 177. Centrilobular nodules  Distributed primarily within the centre of the secondary pulmonary lobule  Reflect the presence of either interstitial or airspace abnormalities  Dense or ground-glass opacity  Subpleural lung is typically spared- distinguishes from diffuse random nodules. 177
  • 178. Tree-in-bud Centrilobular nodules m/b further characterized by presence or absence of ‘‘tree-in-bud.’’ Tree-in-bud -- Impaction of centrilobular bronchus with mucous, pus, or fluid, resulting in dilation of the bronchus, with associated peribronchiolar inflammation .  Dilated, impacted bronchi produce Y- or V-shaped structures This finding is almost always seen with pulmonary infections. 178
  • 179. 179
  • 180. 180 Centrilobular nodules with or without tree-in-bud opacity: D/D : With tree-in-bud opacity  Bacterial pneumonia  Typical and atypical mycobacteria infections  Bronchiolitis  Diffuse panbronchiolitis  Aspiration  Allergic bronchopulmonary aspergillosis  Cystic fibrosis  Endobronchial-neoplasms (particularly  Bronchioloalveolar carcinoma) Without tree-in-bud opacity  All causes of centrilobular nodules with tree-in-bud opacity  Hypersensitivity pneumonitis  Respiratory bronchiolitis  Cryptogenic organizing pneumonia  Pneumoconioses  Langerhans’ cell histiocytosis  Pulmonary edema  Vasculitis  Pulmonary hypertension
  • 181. 181 Random nodules Random nodules – No definable distribution Are usually distributed uniformly throughout the lung parenchyma in a bilaterally symmetric distribution. Random nodules: Miliary tuberculosis. Axial HRCT image shows multiple nodules scattered uniformly throughout the lung parenchyma.
  • 182.
  • 183.
  • 184. 184 Random nodules: D/D 1. Haematogenous metastases 2. Miliary tuberculosis 3. Miliary fungal infection 4. Disseminated viral infection 5. Silicosis or coal-worker’s pneumoconiosis 6. Langerhans’ cell histiocytosis
  • 185. 185
  • 186. Parenchymal Opacification Ground-glass opacity Consolidation Lung calcification & high attenuation opacities. 186
  • 187. GROUND GLASS OPACITIES  Hazy increased attenuation of lung, with preservation of bronchial and vascular margins  Pathology : it is caused by # partial filling of air spaces, # interstitial thickening, # partial collapse of alveoli, # normal expiration, or # increased capillary blood volume  D/t volume averaging of morphological abnormality too small to be resolved by HRCT 187
  • 188. IMPORTANCE OF GGO  Can represent - microscopic interstitial disease (alveolar interstitium) - microscopic alveolar space disease - combination of both  In the absence of fibrosis, mostly indicates the presence of an ongoing, active, potentially treatable process  Ground Glass opacity should be diagnosed only on scans obtained with thin sections : with thicker sections volume averaging is more - leading to spurious GGO, regardless of the nature of abnormality 188
  • 190. The location of the abnormalities in ground glass pattern can be helpful:  Upper zone predominance: Respiratory bronchiolitis PCP.  Lower zone predominance: UIP, NSIP, DIP.  Centrilobular distribution: Hypersensitivity pneumonitis, Respiratory bronchiolitis 190
  • 191. GGO with few cystic and reticular lesion in HIV + ve patient -- PCP Combination of GGO with fibrosis and tractional bronchiectasis-- NSIP 191
  • 192. CRAZY PAVING PATTERN  It is scattered or diffuse ground-glass attenuation with superimposed interlobular septal thickening and intralobular lines.  Causes: 192
  • 193. Combination of ground glass opacity and septal thickening : Alveolar proteinosis. 193
  • 194. 194 CONSOLIDATION  Consolidation is defined as increased attenuation, which results in obscuration of the underlying vasculature, usually producing air bronchogram.  The presence of consolidation implies that the air within affected alveoli has been replaced by another substance, such as blood, pus, oedema, or cells.  When consolidation is evident on a chest radiograph, HRCT does not usually provide additional diagnostically useful information.
  • 195. D/D on the basis of presentation Acute consolidation is seen in: - Pneumonias (bacterial, mycoplasma , PCP) - Pulmonary edema due to heart failure or ARDS - Hemorrhage - Acute eosinophilic pneumonia Chronic consolidation is seen in: - Organizing Pneumonia - Chronic eosinophilic pneumonia - Fibrosis in UIP and NSIP - Bronchoalveolar carcinoma or lymphoma 195
  • 196. 196 Patchy ground-glass opacity, consolidation, and nodule mainly with peribronchovascular distribution with reversed halo signs (central ground-glass opacity and surrounding air-space consolidation) Peripheral consolidations with upper lobe predominance (photo negative of pulmonary edema)
  • 197. Lung calcification & high attenuation opacities Multifocal lung calcification • Infectious granulomatous ds - TB, histoplasmosis, and varicella, pneumonia; • Sarcoidosis , silicosis, Amyloidosis  Fat embolism associated with ARDS Diffuse & dense lung calcification • Metastatic calcification, • Disseminated pulmonary ossification, or • Alveolar microlithiasis 197
  • 198. High attenuation opacity • Talcosis asso with fibrotic mass, • inhalation of metals (tin/barium) Small focal areas of increased attenuation • injection and embolized radiodense materials such as mercury or acrylic cement Diffuse, increased lung attn in absence of calcification • amiodarone lung toxicity or • embolization of iodinated oil after chemoembolization 198
  • 199. 199
  • 200. HRCT findings manifesting as decreased lung opacity Lung Cysts, Emphysema, and Bronchiectasis 200
  • 201. HONEYCOMBING  Defined as - small cystic spaces with irregularly thickened walls composed of fibrous tissue.  Predominate in the peripheral and subpleural lung regions  Subpleural honeycomb cysts typically occur in several contiguous layers. D/D- paraseptal emphysema in which subpleural cysts usually occur in a single layer.  Indicates the presence of “END stage” disease regardless of the cause. 201
  • 202. Causes Lower lobe predominance : 1. UIP or interstitial fibrosis 2. Connective tissue disorders 3. Hypersensitivity pneumonitis 4. Asbestosis 5. NSIP (rare) Upper lobe predominance : 1. End stage sarcodosis 2. Radiation 3. Hypersensitivity Pneumonitis 4. End stage ARDS 202
  • 203. Honeycombing and traction bronchiectasis in UIP.
  • 204. Lung cysts  Thin walled (less than 3mm) , well defined and circumscribed air containing lesions  They are lined by cellular epithelium, usually fibrous or epithelial in nature.  Common cause are : 1. Lymphangiomyomatosis 2. Langerhans Histiocytosis 3. Lymphoid interstitial pneumonia They need to be differentiated from emphysematous bullae, blebs and pneumatocele. 204
  • 205. Axial HRCT image through the upper lobes shows multiple bilateral bizarre- shaped cysts and small centrilobular nodules in a smoker with Langerhans’ cell histiocytosis. Axial HRCT image through the upper lobes shows multiple bilateral uniform, thin-walled cysts. 205
  • 206. BRONCHIEACTASIS Bronchiectasis is defined as localized, irreversible dilation of the bronchial tree. HRCT findings of the bronchiectasis include # Bronchial dilatation # Lack of bronchial tapering # Visualization of peripheral airways. 206
  • 207. BRONCHIAL DILATATION # The broncho-arterial ratio (internal diameter of the bronchus /pulmonary artery) exceeds 1. # In cross section it appears as “Signet Ring appearance” LACK OF BRONCHIAL TAPERING # The earliest sign of cylindrical bronchiectasis # One indication is lack of change in the size of an airway over 2 cm after branching. VISUALIZATION OF PERIPHERAL AIRWAYS # Visualization of an airway within 1 cm of the costal pleura is abnormal and indicates potential bronchiectasis 207
  • 208. Coned axial HRCT image shows bronchial dilation with lack of tapering . Bronchial morphology is consistent with varicose bronchiectasis. 208
  • 209. A NUMBER OF ANCILLARY FINDINGS ARE ALSO RECOGNIZED: # Bronchial wall thickening : normally wall of bronchus should be less than half the width of the accompanying pulmonary artery branch. # Mucoid impaction # Air trapping and mosaic perfusion Extensive, bilateral mucoid impaction Mosaic perfusion caused by large and small airway obstruction. Small centrilobular nodules are visible in the right lower lobe 209
  • 210. Types 1. CYLINDRICAL BRONCHIECTASIS # mildest form of this disease, # thick-walled bronchi that extend into the lung periphery and fail to show normal tapering 2. VARICOSE BRONCHIECTASIS # beaded appearance of bronchial walls - dilated bronchi with areas of relative narrowing # string of pearls. # Traction bronchiectasis often appears varicose. 210
  • 211. 3. CYSTIC BRONCHIECTASIS : # Group or cluster of air-filled cysts, # cysts can also be fluid filled, giving the appearance of a cluster of grapes. 4.TRACTION BRONCHIECTASIS : # Defined as dilatation of intralobular bronchioles because of surrounding fibrosis # due to fibrotic lung diseases 211
  • 213. ABPA: glove-finger shadow due to mucoid impaction in central bronchiectasis in a patient with asthma.
  • 214. Differential diagnosis 1. Infective causes : specially childhood pneumonia, pertusis, measles, tuberculosis 2. Non- infective causes : Bronchopulmonary aspergillosis, inhalation of toxic fumes 3. Connective tissue disorder : Ehlers-Danlos Synd, Marfan synd , tracheobronchomeglay 4. Ciliary diskinesia : Cystic fibrosis, Kartangener synd, agammaglobulinemia . 5. Tractional bronchiectasis in interstitial fibrosis. 214
  • 215. EMPHYSEMA  Permanent, abnormal enlargement of air spaces distal to the terminal bronchiole and accompanied by the destruction of the walls of the involved air spaces. 215
  • 216. Centrilobular (proximal or centriacinar) emphysema  Found most commonly in the upper lobes  Manifests as multiple small areas of low attenuation without a perceptible wall, producing a punched-out appearance.  Often the centrilobular artery is visible within the centre of these lucencies. 216
  • 217. PANLOBULAR EMPHYSEMA  Affects the entire secondary pulmonary lobule and is more pronounced in the lower zones  Complete destruction of the entire pulmonary lobule.  Results in an overall decrease in lung attenuation and a reduction in size of pulmonary vessels 217
  • 218. Paraseptal (distal acinar) emphysema  Affects the peripheral parts of the secondary pulmonary lobule  Produces subpleural lucencies. 218
  • 219. Cicatricial Emphysema/ irregular air space enlargement previously known as irregular or cicatricial emphysema • can be seen in association with fibrosis • with silicosis and progressive massive fibrosis or sarcoidosis BULLOUS EMPHYSEMA : • Does not represent a specific histological abnormality • Emphysema characterized by large bullae • Often associated with centrilobular and paraseptal emphysema 219
  • 220. Paraseptal Emphysema vs Honeycombing Paraseptal emphysema Honeycomb cysts occur in a single layer at the pleural surface may occur in several layers in the subpleural lung predominate in the upper lobes predominate at the lung bases unassociated with significant fibrosis Asso with other findings of fibrosis. Associated with other findings of emphysema Absent 220
  • 221. Bullae A sharply demarcated area of emphysema ≥ 1 cm in diameter a thin epithelialized wall ≤ 1 mm. uncommon as isolated findings, except in the lung apices Usually asso with evidence of extensive centrilobular or paraseptal emphysema When emphysema is associated with predominant bullae, it may be termed bullous emphysema 221
  • 222. Pneumatocele  Defined as a thin-walled, gas-filled space within the lung,  Associated with acute pneumonia or hydrocarbon aspiration. • Often transient. • believed to arise from lung necrosis and bronchiolar obstruction. • Mimics a lung cyst or bulla on HRCT and cannot be distinguished on the basis of HRCT findings. 222
  • 223. CAVITARY NODULE  Thicker and more irregular walls than lung cysts • In diffuse lung diseases - LCH, TB, fungal infections, and sarcoidosis.  Also seen in rheumatoid lung disease, septic embolism, pneumonia, metastatic tumor, tracheobronchial papillomatosis, and Wegener granulomatosis Cavitary nodules or cysts in tracheobronchial papillomatosis. fungal pneumonia 223
  • 224. Mosaic attenuation & perfusion  Lung density and attenuation depends partially on amount of blood in lung tissue.  The term 'mosaic attenuation' is used to describe density differences between affected and non-affected lung areas.  It is seen as inhomogeneous attenuation of lung parenchyma with focal region of lucency which show smaller size of vessels  May be due to vascular obstruction, abnormal ventilation or airway disease/ 224
  • 225. Mosaic attenuation due to small airway disease # Air trapping and bronchial dilatation commonly seen. # Areas of increased attenuation have relatively large vessels, while areas of decreased attenuation have small vessels. # Causes include: Bronchiectasis, cystic fibrosis and bronchiolitis obliterans. Mosaic attenuation due to vascular disease # common in patients with acute or chronic pulmonary embolism (CPE), and # decreased vessel size in less opaque regions is often visible 225
  • 226. MOSIAC PATTERN DEPENDENT LUNG ONLY PRONE POSITION RESOLVE PLATE ATELECTASIS NOT RESOLVE GROUND GLASS NONDEPENDENT LUNG EXPIRATION NO AIR TRAPPING VESSEL SIZE DECREASED VASCULAR NORMAL GROUND GLASS AIR TRAPPING AIRWAYS DISEASE 226
  • 227. Inhomogeneous lung opacity: mosaic perfusion in a patient with bronchiectasis. central bronchiectasis with multifocal, bilateral inhomogeneous lung opacity. The vessels within the areas of abnormally low attenuation are smaller than their counterparts in areas of normal lung attenuation. 227
  • 228. Air trapping on expiration  Most patients with air trapping seen on expiratory scans have inspiratory scan abnormalities, such as bronchiectasis, mosaic perfusion, airway thickening, or nodules suggest the proper differential diagnosis.  Occasionally, air trapping may be the sole abnormal finding on an HRCT study.  The differential diagnosis include --- bronchiolitis obliterans; asthma; chronic bronchitis; and hypersensitivity pneumonitis 228
  • 229. Air trapping on expiratory imaging in the absence of inspiratory scan findings in a patient with bronchiolitis obliterans. (A) Axial inspiratory image through the lower lobes shows no clear evidence of inhomogeneous lung opacity. (B) Axial expiratory image shows abnormal low attenuation (arrows) caused by air trapping, representing failure of the expected increase in lung attenuation that should normally occur with expiratory imaging. 229
  • 230. Head cheese sign  It refers to mixed densities which includes presence of- # consolidation # ground glass opacities # normal lung # Mosaic perfusion • Signifies mixed infiltrative and obstructive disease • Common cause are : Hypersensitive pneumonitis Sarcoidosis DIP 230
  • 231. Axial HRCT image in a patient with hypersensitivity pneumonitis shows a combination of ground-glass opacity, normal lung, and mosaic perfusion (arrow) on the same inspiratory image. 231
  • 232. Distribution within the lung Upper lung zone preference is seen in: 1.Inhaled particles: pneumoconiosis (silica or coal) 2.Smoking related diseases (centrilobular emphysema 3. Respiratory bronchiolitis (RB-ILD) 4.Langerhans cell histiocytosis 5.Hypersensitivity pneumonitis 6.Sarcoidosis Lower zone preference is seen in: 1. UIP 2. Aspiration 3. Pulmonary edema 232
  • 233. Central vs peripheral zone  Central Zone Peripheral zone 1. Sarcoidosis 1. COP 2. Cardiogenic pulmonary 2. Ch Eosinophilic Pneumonia edema 3. UIP 3. Bronchitis 4. Hematogenous mets 233
  • 234. Additional findings Pleural effusion is seen in:  Pulmonary edema  Lymphangitic spread of carcinoma - often unilateral  Tuberculosis  Lymphangiomyomatosis (LAM)  Asbestosis 234
  • 235. Hilar and mediastinal lymphadenopathy # In sarcoidosis the common pattern is right paratracheal and bilateral hilar adenopathy ('1-2-3-sign'). # In lung carcinoma and lymphangitic carcinomatosis adenopathy is usually unilateral. #'Eggshell calcification' in lymph nodes occurs in ---- Silicosis and coal-worker's pneumoconiosis and is sometimes seen in sarcoidosis, post irradiation Hodgkin disease, blastomycosis and scleroderma . 235
  • 236. Conclusion • A thorough knowledge of the basic anatomy is of utmost importance.  When attempting to reach a diagnosis or differential diagnosis of lung disease using HRCT, the overall distribution of pulmonary abnormalities should be considered along with their morphology, HRCT appearance, and distribution relative to lobular structures. Correlation of the radiological findings with patients clinical and laboratory findings to reach a likely diagnosis  236
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