HRCT in Lung Diseases: A Guide to Patterns and Interpretation

HRCT in Lung Diseases
Dr.Tinku Joseph
MD, DM, FCCP
Consultant Pulmonologist
AIMS, Kochi

Reference
 Radiopedia.com
 Lunghouse.com
 Chestradiology.com
 Radiologyassistant.com
 Various journals & text
books
 Google images

CONTENTS
1. Introduction to HRCT chest
2. Technichal aspects of HRCT
3. Relevant anatomy for HRCT
interpretation
4. Pattern of lung disease in HRCT
5. HRCT pattern in various ILD’s
3

HRCT -: Meaning
 High resolution CT imaging
 Resolution : Means ability to resolve small object that are close
together ,as separate form.
Actual meaning
 A scan performed using high- spatial frequency algorithm to
accentuate the contrast between tissue of widely differing
densities, eg:
- air & vessels (lung)
• (Radiopedia.com)
4

INTRODUCTION
 HRCT - Use of thin section CT images (0.25 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
 Detection of lung disease
 Points a specific diagnosis
 Helps in identification of reversible disease.
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
6

Technical aspects of HRCT Chest
PART- 1
7

Technical aspect
Parameters
 Slice thickness
 Filming
 Patient position
 Types of HRCT
 Artifacts
8

Slice thickness
 Thin sections 0.25 – 1.5 mm is essential for optimal spatial
resolution
 Thicker slices are prone for reduction in ability to resolve
smaller structure
 Better for delineation of bronchi, wall thickness and diameter
9

Window settings
Lung window
 window widths of 1000 to 1500 HU are appropriate for a
routine lung window.
Mediastinal & Soft tissue window
 Window level/width setting of 40-50/ 350-450 HU are best for
evaluation of the mediastinum, hila, and pleura.
11

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
Lateral decubitus CT : Mainly in children
12

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
13

The prone images shows complete resolution of the opacity suggesting dependent
atelectasis.
14

Persistent opacity in the posterior lung in a
patient with pulmonary fibrosis.
15

Normal lung
Attenuation
 Attenuation gradient : densest at dependent region of lung as
a result of regional difference in blood and gas density due to
gravity
 In children, lung attenuation is greater than adults.

Normal expiratory HRCT
 Performed to detect air trapping in small airway obstruction
 Attenuation increases with expiration.
 60 % of normal individual shows air trapping in the superior
segment of lower lobe and involving single lobule, normal
variant.

-
• MDCT scanner are capable of rapid scanning and thin slice
acquisition.
Advantages :
1. Viewing of contiguous 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.
Disadvantage : greater radiation dose.
19
Volumetric HRCT
Technique of scan acquisition

Multidetector Helical HRCT
 Multidetector CT is equipped with a multiple row detector array
 Multiple images are acquired
Advantages -
 Shorter acquisition times
 whole-lung HRCT can be performed in one breath-hold.
 Retrospective creation of both thinner and thicker sections from
the same raw data
20

Low dose HRCT
 Low dose HRCT uses Kvp of 120- 140 and mA of 20-30 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 ds.
 Ongoing trials -: Screening tool for CA lung
21

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)
22

HRCT artifact
 Streak Artefacts :
 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
23

The streak artifacts emanating from the implant

Motion-related artifacts
 Pulsation / Star/ Doubling artifacts
 Visible at lung base
 Adjacent to heart due to cardiac
pulsation
26

Patient related artifacts
 Motion artifacts (Resp, Cardio or both)
-: create pseudobronchiectasis, pseudo-
GGO and star artifacts
 Dependent atlectasis-: sub-pelural lung
disease
27

Interpretive artifacts
 Incorrect window width and level
 Failure to detect bronchiectasis due to mucous
plugging.
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 .
29

Post processing techniques
Maximum intensity projection
 High attenuation films
 Improves detection of pulmonary
nodules.
 Characterize distribution of small
nodules.
 Assessing the size and location of
vessels.
30

Post processing techniques
Minimum intensity projection
 Lowest attenuation films
 Enables detection of low-density
structures
 Optimal tool for the detection,
localization, and quantification of
ground-glass and linear attenuation
patterns.
32

HRCT Technique- Summary
 In all cases:
 Breath hold
 Full Inspiration
 Expiratory images –
Emphysema
 Prone images
 HRCT types
 Artefacts
 MIP/ Min MIP

Lung anatomy
 Right lung is divided by
major and minor fissure into
3 lobes and 10 broncho-
pulmonary segments
 Left lung is divided by
major fissure into 2 lobes
with a lingular lobe and 8/9
bronchopulmonary segments
36

There are approximately 23
generation of dichotomous
branching
From trachea to the alveolar sac
HRCT can identify upto 8th
order central bronchioles
38

Tracheal anatomy
 10-12 cm in length, from C6 level to upper border of D5.
 Extrathoracic (2-4cm) and Intrathoracic(6-9 cm beyond
manubrium)
 In men, tracheal diameter – 25-27 mm
 women – 21- 23 mm
 The posterior portion of the tracheal wall is a thin
fibromuscular membrane----- allows for oesophageal
expansion.

Bronchial Anatomy
 Approximately 23 generations of branches from the trachea to
the alveoli.
 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

Bronchus
BLOOD SUPPLY Bronchial Arteries—
2 on left side i.e. superior and inferior
1 on right side
Left arises from thoracic aorta
Right from either thoracic aorta, sup. left 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)

Broncho-arterial ratio (B/A)
 Internal diameter of both bronchus and accompanying arterial
diameter calculated and ratio measured.
 Normal ratio is 1:1
 B/A ratio >1.5 indicates bronchiectasis.
NB:: B/A ratio increases with age and may exceed 1 in normal
patients > 40 years.
42

Increased broncho-arterial ratio
 Ageing
 High altitude
Pathological conditions -
 Bronchiectasis
 Chronic asthma
Conditions that can reduce pulmonary arterial calibres
 Chronic embolism
Decreased broncho-arterial ratio
 < 0.65 conditions that cause bronchoconstriction

Secondary pulmonary lobule
 Smallest lung unit that is
surrounded by connective
tissue septa.
 The basic anatomic unit
 Irregular polyhedral in
shape.
 Measures 1 to 2.5 cm
45

Anatomy of the Secondary Lobule and Its
Components
1. Interlobular septa and
contiguous subpleural
interstitium,
2. Centrilobular
structures, and
3. Lobular parenchyma
and acini.

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.

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
49

A group of terminal bronchioles

Accompanying pulmonary arterioles

Lung interstitum
Lung
interstitium
Axial fiber
system
Peribronchovascular
interstitium
Centrilobular
interstitium
Peripheral fiber
system
Subpleural
interstitium
Interlobular
septa

 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.

Lymphangitic carcinomatosis : show
diffuse smooth and nodular septal
thickening.
• Focal septal thickening in
lymphangitic carcinomatosis
Sarcoidosis :
right lung base shows interlobular septal
thickening associated with several septal
nodules giving beaded appearance

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

Anatomy of pleural surfaces and chest wall.
63

Pattern of lung disease in HRCT
PART - 3

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) ?
Structured approach

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

Linear and reticular opacities
 Represents
thickening of
interstitial fibers
of lung by
- fluid or
- fibrous tissue
or
- infiltration by
cells
67

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.
Described by Zerhouni et al

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

sarcoidosis
Unilateral lymphangitic spread of
carcinoma

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.

Smooth Septal thickening
Septal thickening and ground-glass opacity with a
gravitational distribution in a patient with cardiogenic
pulmonary edema.

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

Intralobular interstitial thickening (Intralobular lines)
 Results in a fine reticular pattern
on HRCT, with the visible lines
separated by a few millimeters
 Fine lace/ netlike appearance
 Causes :
 Pulmonary fibrosis
 Asbestosis
74

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
contacts the pleural surface
 D/D :
 1. Asbestosis
 2. Sarcoidosis
 3. Silicosis/ coal worker pneumoconiosis
 4. Tuberculosis with associated scarring.
75

Subpleural Interstitial Thickening
 Mimic thickening of fissure.
 DD similar to that of interlobular
septal thickening.

Honeycombing
 Small cystic spaces with irregularly thickened bronchiolar walls
composed of fibrous tissue.
 Predominate in the peripheral and subpleural lung regions
 Indicates the presence of “END stage” disease regardless of the
cause.
The Fleischner Society definition is clustered cystic air spaces (between 3-10 mm in
diameter but occasionally as large as 2.5 cm) which are usually subpleural and basal
in distribution. The walls of the cysts are well-defined and often thick (1-3 mm)

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
78

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 79

Interstitial nodules
Air space opacity
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
81

Perilymphatic distribution
Nodules in relation to pulmonary lymphatics at
 Perihilar peribronchovascular interstitium,
 Interlobular septa,
 Sub-pleural regions, and
 Centrilobular interstitium.
82

Perilymphatic nodules: D/D
 Sarcoidosis
 Lymphangitic carcinomatosis
 Lymphocytic interstitial
pneumonia (LIP)
 Lymphoproliferative disorders
 Amyloidosis, Silicosis
83

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.

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

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.

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 Broncho alveolar
cell 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

Random nodules
 Random nodules – No definable distribution
 Are usually distributed uniformly throughout the lung parenchyma
in a bilaterally symmetric distribution.
Random nodules: Miliary
tuberculosis.

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. Sarcoidosis ( extensive)
7. Langerhans’ cell histiocytosis (early
nodular stage)

Parenchymal Opacification
Ground-glass opacity
Consolidation
Lung calcification &
high attenuation
opacities.

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/ alveolar wall thickening,
# partial collapse of alveoli,
# normal expiration, or
# increased capillary blood volume
93

Importance of GGO
 Can represent - microscopic interstitial/ alveolar disease
 In the absence of fibrosis, mostly indicates the presence of an
ongoing, active, potentially treatable process
 NB :: 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

 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

GGO with few cystic and reticular lesion
in HIV + ve patient -- PCP
Combination of GGO with
fibrosis and tractional
bronchiectasis-- NSIP

Persistent chest
abnormality, weight loss
• Broncho-alveolar cell
carcinoma with ground-glass
opacity & consolidation

Crazy paving pattern
 It is scattered or diffuse ground-glass attenuation with
superimposed interlobular septal thickening and
intralobular lines.
 Causes:

Combination of ground glass
opacity and septal thickening :
Alveolar proteinosis.

 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.
Consolidation

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

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 diseases - 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

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
107

HRCT findings manifesting as decreased lung
opacity
Lung Cysts
Emphysema
Bronchiectasis
109

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.

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.

Bronchiectasis
 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.

 Bronchial dilatation
 The broncho-arterial ratio (internal diameter of the bronchus
/pulmonary artery) exceeds 1 , >1.5
 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

Coned axial HRCT image shows bronchial
dilation with lack of tapering . Bronchial
morphology is consistent with varicose
bronchiectasis.

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
115

Types
1. 1) Cylindrical bronchiectasis
 Mildest form of this disease,
 Thick-walled bronchi that extend into
the lung periphery and fail to show
normal tapering
2. 2) Varicose bronchiectasis
 Beaded appearance of bronchial
walls - dilated bronchi with areas of
relative narrowing
 String of pearls.
 Traction bronchiectasis often appears
varicose. 116

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
117

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 , tracheobronchomegaly
4. Ciliary diskinesia : Cystic fibrosis, Kartangener
synd, agammaglobulinemia .
5. Tractional bronchiectasis in interstitial fibrosis.

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.

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.
120

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
121

Paraseptal (distal acinar) emphysema
 Affects the peripheral parts of the secondary
pulmonary lobule
 Produces subpleural lucencies.
122

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/ sarcoidosis
Bullous emphysema :
 Does not represent a specific histological abnormality
 Emphysema characterized by large bullae
 Often associated with centrilobular and paraseptal emphysema

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

Pneumatocele
 Defined as a thin-walled, air-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.

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

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/

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

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

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.

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

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.

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

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.
134

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

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

Additional findings
Pleural effusion is seen in:
 Pulmonary edema
 Lymphangitic spread of carcinoma -
often unilateral
 Tuberculosis
 Lymphangiomyomatosis (LAM)
 Asbestosis

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 .

Common Interstitial lung diseases
PART 4

COP
1) Patchy consolidation with a predominantly sub-pleural and/or peribronchial
distribution
2)small, ill-defined peribronchial or peribronchiolar nodules
large nodules or masses
3) Bronchial wall thickening or dilatation in the abnormal lung regions
4) Perilobular pattern with ill-defined linear opacities that are thicker than
the thicked interlobular septa and have an arcade or polygonal appearance
5) GGO or crazy paving
6) The reverse halo or Atoll sign is considered to be highly specific, although only
seen in <20% of patients with COP 5.

AIP
 GGO- B/L
 Air space consolidation
 Traction bronchiectasis >80%
 Lung parenchymal architectural
distortion
 Resemblance to ARDS

RB-ILD
 GGO – upper zone
 Centrilobular nodules – poorly
defined
 Smoking related changes:
centrilobular emphysema, bronchial
wall thickening
 Advanced-: fibrosis

DIP
 Extensive GGO
 Linear opacities, cysts
 Fibrotic changes <50%
 Smoking related changes
 Confused with RB-ILD

LIP
 Mid to lower zone
predominance
 Thickening of bronchovascular
bundles
 Interstitial thickening
 Pulmonary nodules
 GGO
 Thin walled cysts
 Mediastinal lymphadenopathy

Idiopathic Pleuro-parenchymal fibroelastosis
 Marked apical pleural thickening
 Architectural distortion
 Reticular abnormality
 Pneumothorax
 Lymphadenopathy –
Mediastinal/ axillary

Combined pulmonary fibrosis and emphysema
 Centrilobular/ paraseptal
emphysema – often upper
zone predominant
 Pulmonary fibrosis –lower
lobes

Golden rules for HRCT interpretation
1. Honeycombing with a basal and sub-pleural predominance is highly
suggestive of UIP. Lung biopsy is rarely performed when HRCT shows these
findings.
2. Concentric lower lobe GGO without honeycombing suggests NSIP. In a
patient with collagen vascular disease ,biopsy is uncommoly performed.
3. Patchy or noular sub-pleural or peribronchial consolidation is typical of COP.
4. Cystic air spaces or GGO may represent LIP. LIP is usually associated with
other diseases.
5. Diffuse or centrilobular GGO in a smoker is typical of DIP or RB-ILD

Conclusion
 A thorough knowledge of the
basic anatomy is of utmost
importance.
 Overall distribution
 Differential diagnosis
 Correlation of history, clinical
findings and radiological pattern
to clinch the diagnosis.

HRCT in Lung Diseases: A Guide to Patterns and Interpretation

HRCT in Lung Diseases: A Guide to Patterns and Interpretation

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