Gamal Rabie Agmy, MD, FCCP
Professor of Chest Diseases, Assiut University
Types of Collapse
6-Compression Atelectasis
Flat waist Sign
This sign refers to flattening of the contours of the aortic knob and adjacent
main pulmonary artery .
It is seen in severe collapse of the left lower lobe and is caused by leftward
displacement and rotation of the heart
Juxtaphrenic peak sign
The juxtaphrenic peak sign refers to the peaked or
tented appearance of a hemidiaphragm which can
occur in the setting of lobar collapse. It is caused by
retraction of the lower end of diaphragm at an inferior
accessory fissure (most common), major fissure
or inferior pulmonary ligament. It is commonly seen
in upper lobe collapse but may also be seen in middle
lobe collapse.
Fallen Lung Sign
This sign refers to the appearance
of the collapsed lung occurring
with a fractured bronchus .
The bronchial fracture results in
the lung to fall away from the
hilum, either inferiorly and laterally
in an upright patient or posteriorly,
as seen on CT in a supine patient.
DD:
Pneumothorax causes a lung to
collapse inward toward the hilum.
Luftsichel Sign
•German for sickle of air (luft: air sichel:
crescent)
•Paramediastinal lucency due to
interposition of lower lobe apex between
mediastinum and shrunken upper lobe
•Occurs more commonly on the left than in
the right
Comet Tail Sign
•Seen on CT of the chest
•Consists of curvilinear opacity extending
from subpleural mass toward hilum
•Produced by the distortion vessels and
bronchi that lead to adjacent rounded
atelectasis
(posterioranterior) position. Note
that the x-ray tube is 72 inches
away.
the supine AP (anteriorposterior)
position the x-ray tube is 40 inches
from the patient.
Dee method for approximating the position o f the carina can
be used. This involves defining the aortic arch and then
drawing a line Inferomedially through the middle of the arch
at a 45 degree angle to t he midline
The Ideal position for endotracheal tubes is in the
mid trachea, 5cm from the carina, when the head is
neither flexed nor extended. This allows for
movement of the tip with head movements. The
minimal safe distance from the carina is 2cm.
Notice the increased lucency of the cardiophrenic sulci in this patient
with inferior anteromedial pneumothoraces. A CT scan confirms the
diagnosis
 a hyperlucent upper
quadrant with
visualization of the
superior surface of the
diaphragm and
visualization of the
inferiorvena cava.
 double-diaphragm
sign
 Antero lateral air may
increase the
radiolucency at the
costo phrenicsulcus.
This is called the deep
sulcus sign.
 Apicolateral
pneumothorax
(arrows) with right
upper lobe collapse
(arrowheads)
 shifting of the heart
border,
 the superior vena cava,
and the inferior vena
cava.
 The shifting of these
structures can lead to
decreased venous return.
•Mediastinal shifT is
usually
seen in a tension
pneumothorax.
•The most reliable sign of
tension pneumothorax is
depression of a
hemidiaphragm.
Radiographic Signs of Pneumomediastinum
Subcutaneous emphysema
Thymic sail sign
Pneumoprecardium
Ring around the artery sign
Tubular artery sign
Double bronchial wall sign
Continuous diaphragm sign
Extrapleural sign
Ginkgo leaf sign
• The ginkgo leaf sign is a chest plain radiography
appearance which is seen at extensive subcutaneous
emphysema of the chest wall. Air outlines the fibers of
the pectoralis major muscle and creates a branching
pattern that resembles the branching pattern in the
veins of a ginkgo leaf.
Nodular Patternitie
Secondary pulmonary lobular
anatomy
The terminal bronchiole in the center
divides into respiratory bronchioles with
acini that contain alveoli.
Lymphatics and veins run within the
interlobular septa
Centrilobular area in blue (left)
and perilymphatic area in yellow
(right)
Nodular Pattern
Perilymphatic distribution
Centrilobular distribution
Random distribution
ARE NODULES IN CONTACT
WITH PLEURA
NO
CENTRILOBULAR
YES
PERILYMPHATIC RANDOM
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
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 lymphatic
CENTRILOBULAR: related to centrilobular structuresDistribution
75
Disseminated histoplasmosis and nodular ILD.
CT scan shows multiple bilateral round circumscribed
pulmonary nodules.
Notice the nodules along the fissures indicating a
perilymphatic distribution (red arrows).
The majority of nodules located along the bronchovascular
bundle (yellow arrow).
Sarcoidosis
The majority of nodules located
along the bronchovascular bundle
(yellow arrow).
PERILYMPHATIC NODULES
Perilymphatic and Random distribution of
nodules , seen in sarcoidosis.
Centrilobular distribution
Hypersensitivity pneumonitis
Respiratory bronchiolitis in
smokers
infectious airways diseases
(endobronchial spread of
tuberculosis or
nontuberculous
mycobacteria,
bronchopneumonia)
Uncommon in
bronchioloalveolar
carcinoma, pulmonary
edema, vasculitis
Random distribution
Small random nodules
are seen in:
 Hematogenous
metastases
 Miliary tuberculosis
 Miliary fungal infections
 Sarcoidosis may mimick
this pattern, when very
extensive
 Langerhans cell
histiocytosis (early
nodular stage)
Langerhans cell histiocytosis: early nodular stage before the typical
cysts appear.
Differential diagnosis of a nodular
pattern of interstitial lung disease
SHRIMP
Sarcoidosis
Histiocytosis (Langerhan cell
histiocytosis)
Hypersensitivity pneumonitis
Rheumatoid nodules
Infection (mycobacterial, fungal, viral)
Metastases, Miliary TB
Microlithiasis, alveolar
Pneumoconioses (silicosis, coal
worker's, berylliosis)
Cystic Lung Lesions
By
Gamal Rabie Agmy , MD , FCCP
Professor of Chest Diseases ,Assiut University
DECREASED
LUNG
ATTENUATION
Lung Cysts
Pulmonary fibrosis (Honeycombing)
Lymphangiomyomatosis
Langerhanscell histiocytosis
Lymphocytic Interstitial Pneumonia (LIP)
Differential Diagnosis
Rough Reticular Fine Reticular
Traction
Bronchiectasis
and
Interface
sign
Honey
combing
UIP UIP or NSIP
Usual Interstitial Pneumonia UIP
HRCT Findings
Reticular opacities, thickened intra- and
interlobular septa
Irregular interfaces
Honey combing and parenchymal distorsion
Ground glass opacities (never prominent)
Basal and subpleural predominance
Basal and subpleural distribution
UIP
Inconsistent with UIP
pattern (any one of
seven features
Possible UIP pattern (all
three features)
UIP pattern (all four
features)
•Upper or mid lung
predominance
subpleural basal
predominance
•subpleural basal
predominance
•peribronchovascular
predominance
reticular abnormality•reticular abnormality
•extensive ground glass
abnormality (extent > reticular
abnormality)
•honeycombing with or
without traction
bronchiectasis
•profuse micronodules
(bilateral, predominantly upper
lobes
Absence of features
listed as inconsistent
with UIP pattern
Absence of features
listed as inconsistent
with UIP pattern
•discrete cysts (multiple
bilateral, away from areas of
honeycombing)
•diffuse mosaic attenuation/air
trapping (bilateral in three or
more lobes)
•consolidation in broncho-
pulmonary segment(s)/lobe(s)
Radiological features of idiopathic pulmonary fibrosis: 2011
Lymphangioleiomyomatosis (LAM)
HRCT Morphology
Thin-walled cysts (2mm - 5cm)
Uniform in size / rarely confluent
Homogeneous distribution
Chylous pleural effusion
Lymphadenopathy
in young women
Lymphangioleiomyomatosis (LAM)
Tuberous Sclerosis (young man)
Langerhans Cell Histiocytosis
HRCT Findings
Small peribronchiolar nodules (1-5mm)
Thin-walled cysts (< 1cm),
Bizarre and confluent
Ground glass opacities
Late signs: irreversible / parenchymal fibrosis
Honey comb lung, septal thickening,
bronchiectasis
1 year later
Peribronchiolar NodulesCavitating nodules and cysts
Langerhans Cell Histiocytosis
Langerhans Cell Histiocytosis
Langerhans Cell Histiozytosis
Key Features
Upper lobe predominance
Combination of cysts and noduli
Characteristic stages
Increased Lung volume
Sparing of costophrenic angle
S
M
O
K
I
N
G
Langerhans Cell Histiocytosis
Langerhans Cell Histiocytosis
Differential Diagnosis
Only small nodules
Sarkoidosis, Silikosis
Only cysts
idiopathic Fibrosis
LAM
Destruktive emphysema
Benign lymphoproliferative
disorder
Diffuse interstitial infiltration of
mononuclear cells
Not limited to the air ways as
in follicular Bronchiolitis
LIP
= Lymphocytic Interstitial Pneumonia
Sjögren: LIP
LIP
= Lymphocytic Interstitial Pneumonia
Rarely idiopathic
In association with:
Sjögren’s syndrome
Immune deficiency syndromes, AIDS
Primary biliary cirrhosis
Multicentric Castlemean’s disease
Sjoegren disease
Dry eye and dry mouth
Fibrosis, bronchitis and bronchiolitis
LIP
Overlap
Sarcoid, DM/PM, MXCT
SLE, RA (pleural effusion)
Up to 40 x increased risk for lymphoma (mediastinal
adenopathy) and
2 x times increased risk for neoplasma
Young woman Dry mouth Smoker
LAM LIP Histiocytosis
Wegener‘s disease
Rheumatoid Arthritis
Honeycombing
HRCT showing
subpleural
broncheolectasis
Honeycombing and traction bronchiectasis in UIP.
Typical UIP with honeycombing and traction
bronchiectasis in a patient with idiopathic
pulmonary fibrosis (IPF)
Distribution within the lung
Reticular Pattern
Gamal Rabie Agmy, MD, FCCP
Professor of chest Diseases,
Assiut university
Linear Pattern
A linear pattern is seen when there is
thickening of the interlobular septa,
producing Kerley lines.
Kerley B lines
Kerley A lines
The interlobular septa contain
pulmonary veins and lymphatics.
The most common cause of interlobular
septal thickening, producing Kerley A
and B lines, is pulmonary edema, as a
result of pulmonary venous
hypertension and distension of the
lymphatics.
Kerley B lines
Kerley A lines
DD of Kerly Lines:
Pulmonary edema is the most common cause
Mitral stenosis
Lymphangitic carcinomatosis
Malignant lymphoma
Congenital lymphangiectasia
Idiopathic pulmonary fibrosis
Pneumoconiosis
Sarcoidosis
HRCT of the lung
Reticular pattern – HRCT
numerous, clearly visible interlobular septa
outlining lobules of characteristic size and shape
interlobular septal thickening
very fine network of lines within visible lobules
intralobular interstitial thickening
several layers of air-filled cysts, 3-10 mm in diameter,
with thick walls (1-3 mm)
honeycombing
Reticular pattern
Interlobular septal thickening – dd
smooth
thickening
pulm. edema
pulm. hemorrhage
lymphangitic carc.
lymphoma
nodular
thickening
lymphangitic carc.
sarcoidosis
amyloidosis
irregular
thickening
fibrosis
Reticular pattern
Interlobular septal thickening – pulmonary edema
 smooth septal thickening, isolated or in combination
with ground-glass opacity
 peribronchovascular and subpleural interstitial th.
 perihilar and gravitational distribution, bilateral
 findings of CHF
Reticular pattern
Interlobular septal th. – lymphangitic carcinomatosis
 smooth or nodular septal thickening
 smooth or nodular thickening of peribronchovascular
interstitium and fissures
 thickening of the intralobular axial interstitium
 focal or asymmetric distribution
Reticulation or not reticulation ……
“crazy paving”
Reticular pattern
Honeycombing – significance
air-containing cystic spaces having thick,
fibrous walls lined by bronchiolar
epithelium

fibrosis is present
UIP is likely the histologic pattern
IPF is very likely, in the absence of a
known disease
Reticular pattern
Honeycombing – differential diagnosis
basal
distribution
middle/upper
distribution
chronic HP
sarcoidosis
IPF
collagen vasc. dis.
asbestosis
drugs
Reticular pattern
adapted from: Webb RW – HRCT of the lung, III ed; 2001
interlobular septal thickening
irregular, lung
distorsion
nodularsmooth
•fibrosis
(sarcoidosis,
asbestosis)
•pulm. edema
•linf. carc.
•hemorrhage
•sarcoidosis
•linf. carc.
Reticular pattern
adapted from: Webb RW – HRCT of the lung, III ed; 2001
honeycombing
•IPF (60%)
•collagen vascular dis.
•drug reaction
•asbestosis (uncommon)
subpleural, posterior
LL predominance
•sarcoidosis
•chronic HP
•radiation
other distribution
(UL; parahilar)
Head cheese sign
It refers to mixed
densities which includes
# consolidation
# ground glass
opacities
# normal lung
# Mosaic perfusion
• Signifies mixed
infiltrative and
obstructive disease
Head cheese sign
Common cause are :
1. Hypersensitive pneumonitis
2. Sarcoidosis
3. DIP
127
Headcheese sign
Headcheese sign in
hypersensitivity
pneumonitis.
HRCT scan shows lung with
a geographic appearance,
which represents a
combination of patchy or
lobular ground-glass opacity
(small arrows) and mosaic
perfusion (large arrows).
Mosaic Patternitie
By
Gamal Rabie Agmy , MD , FCCP
Professor of Chest Diseases ,Assiut University
Mosiac pattern
Where is the pathology ???????
in the areas with increased density
meaning there is ground glass
in the areas with decreased density
meaning there is air trapping
Pathology in black areas
Airtrapping: Airway
Disease
Bronchiolitis obliterans (constrictive bronchiolitis)
idiopathic, connective tissue diseases, drug reaction,
after transplantation, after infection
Hypersensitivity pneumonitis
granulomatous inflammation of bronchiolar wall
Sarcoidosis
granulomatous inflammation of bronchiolar wall
Asthma / Bronchiectasis / Airway diseases
Bronchiolitis
obliterans
Pathology in white Areas
Alveolitis / Pneumonitis
Ground glass
desquamative intertitial pneumoinia (DIP)
nonspecific interstitial pneumonia (NSIP)
organizing pneumonia
In expiration
both areas (white and black) decrease in
volume and increase in density
DECREASE IN CONTRAST
DIFFERENCES
Mosaic Perfusion
Chronic pulmonary embolism
LOOK FOR
Pulmonary hypertension
idiopathic, cardiac disease, pulmonary
disease
CTEPH =
Chronic thrombembolic
pulmonary hypertension
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology
Radiological Presentation of Pulmonary Pathology

Radiological Presentation of Pulmonary Pathology

  • 2.
    Gamal Rabie Agmy,MD, FCCP Professor of Chest Diseases, Assiut University
  • 14.
  • 36.
    Flat waist Sign Thissign refers to flattening of the contours of the aortic knob and adjacent main pulmonary artery . It is seen in severe collapse of the left lower lobe and is caused by leftward displacement and rotation of the heart
  • 38.
    Juxtaphrenic peak sign Thejuxtaphrenic peak sign refers to the peaked or tented appearance of a hemidiaphragm which can occur in the setting of lobar collapse. It is caused by retraction of the lower end of diaphragm at an inferior accessory fissure (most common), major fissure or inferior pulmonary ligament. It is commonly seen in upper lobe collapse but may also be seen in middle lobe collapse.
  • 40.
    Fallen Lung Sign Thissign refers to the appearance of the collapsed lung occurring with a fractured bronchus . The bronchial fracture results in the lung to fall away from the hilum, either inferiorly and laterally in an upright patient or posteriorly, as seen on CT in a supine patient. DD: Pneumothorax causes a lung to collapse inward toward the hilum.
  • 42.
    Luftsichel Sign •German forsickle of air (luft: air sichel: crescent) •Paramediastinal lucency due to interposition of lower lobe apex between mediastinum and shrunken upper lobe •Occurs more commonly on the left than in the right
  • 43.
    Comet Tail Sign •Seenon CT of the chest •Consists of curvilinear opacity extending from subpleural mass toward hilum •Produced by the distortion vessels and bronchi that lead to adjacent rounded atelectasis
  • 45.
    (posterioranterior) position. Note thatthe x-ray tube is 72 inches away. the supine AP (anteriorposterior) position the x-ray tube is 40 inches from the patient.
  • 47.
    Dee method forapproximating the position o f the carina can be used. This involves defining the aortic arch and then drawing a line Inferomedially through the middle of the arch at a 45 degree angle to t he midline
  • 48.
    The Ideal positionfor endotracheal tubes is in the mid trachea, 5cm from the carina, when the head is neither flexed nor extended. This allows for movement of the tip with head movements. The minimal safe distance from the carina is 2cm.
  • 51.
    Notice the increasedlucency of the cardiophrenic sulci in this patient with inferior anteromedial pneumothoraces. A CT scan confirms the diagnosis
  • 52.
     a hyperlucentupper quadrant with visualization of the superior surface of the diaphragm and visualization of the inferiorvena cava.  double-diaphragm sign
  • 53.
     Antero lateralair may increase the radiolucency at the costo phrenicsulcus. This is called the deep sulcus sign.
  • 54.
     Apicolateral pneumothorax (arrows) withright upper lobe collapse (arrowheads)
  • 55.
     shifting ofthe heart border,  the superior vena cava, and the inferior vena cava.  The shifting of these structures can lead to decreased venous return.
  • 56.
    •Mediastinal shifT is usually seenin a tension pneumothorax. •The most reliable sign of tension pneumothorax is depression of a hemidiaphragm.
  • 57.
    Radiographic Signs ofPneumomediastinum Subcutaneous emphysema Thymic sail sign Pneumoprecardium Ring around the artery sign Tubular artery sign Double bronchial wall sign Continuous diaphragm sign Extrapleural sign
  • 65.
    Ginkgo leaf sign •The ginkgo leaf sign is a chest plain radiography appearance which is seen at extensive subcutaneous emphysema of the chest wall. Air outlines the fibers of the pectoralis major muscle and creates a branching pattern that resembles the branching pattern in the veins of a ginkgo leaf.
  • 66.
  • 67.
  • 68.
    The terminal bronchiolein the center divides into respiratory bronchioles with acini that contain alveoli. Lymphatics and veins run within the interlobular septa Centrilobular area in blue (left) and perilymphatic area in yellow (right)
  • 69.
  • 70.
  • 71.
    ARE NODULES INCONTACT WITH PLEURA NO CENTRILOBULAR YES PERILYMPHATIC RANDOM
  • 73.
    Size, Distribution, Appearance Nodulesand 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
  • 74.
    Interstitial nodules Air space opacity Miliarytuberculosis sarcoidosis in a lung transplant patient with bronchopneumonia
  • 75.
    RANDOM: no consistentrelationship to any structures PERILYMPHATIC: corresponds to distribution of lymphatic CENTRILOBULAR: related to centrilobular structuresDistribution 75
  • 76.
    Disseminated histoplasmosis andnodular ILD. CT scan shows multiple bilateral round circumscribed pulmonary nodules.
  • 77.
    Notice the nodulesalong the fissures indicating a perilymphatic distribution (red arrows). The majority of nodules located along the bronchovascular bundle (yellow arrow).
  • 78.
    Sarcoidosis The majority ofnodules located along the bronchovascular bundle (yellow arrow).
  • 79.
    PERILYMPHATIC NODULES Perilymphatic andRandom distribution of nodules , seen in sarcoidosis.
  • 80.
    Centrilobular distribution Hypersensitivity pneumonitis Respiratorybronchiolitis in smokers infectious airways diseases (endobronchial spread of tuberculosis or nontuberculous mycobacteria, bronchopneumonia) Uncommon in bronchioloalveolar carcinoma, pulmonary edema, vasculitis
  • 81.
    Random distribution Small randomnodules are seen in:  Hematogenous metastases  Miliary tuberculosis  Miliary fungal infections  Sarcoidosis may mimick this pattern, when very extensive  Langerhans cell histiocytosis (early nodular stage)
  • 82.
    Langerhans cell histiocytosis:early nodular stage before the typical cysts appear.
  • 83.
    Differential diagnosis ofa nodular pattern of interstitial lung disease SHRIMP Sarcoidosis Histiocytosis (Langerhan cell histiocytosis) Hypersensitivity pneumonitis Rheumatoid nodules Infection (mycobacterial, fungal, viral) Metastases, Miliary TB Microlithiasis, alveolar Pneumoconioses (silicosis, coal worker's, berylliosis)
  • 84.
    Cystic Lung Lesions By GamalRabie Agmy , MD , FCCP Professor of Chest Diseases ,Assiut University
  • 85.
  • 86.
    Lung Cysts Pulmonary fibrosis(Honeycombing) Lymphangiomyomatosis Langerhanscell histiocytosis Lymphocytic Interstitial Pneumonia (LIP) Differential Diagnosis
  • 87.
    Rough Reticular FineReticular Traction Bronchiectasis and Interface sign Honey combing UIP UIP or NSIP
  • 88.
    Usual Interstitial PneumoniaUIP HRCT Findings Reticular opacities, thickened intra- and interlobular septa Irregular interfaces Honey combing and parenchymal distorsion Ground glass opacities (never prominent) Basal and subpleural predominance
  • 89.
    Basal and subpleuraldistribution UIP
  • 90.
    Inconsistent with UIP pattern(any one of seven features Possible UIP pattern (all three features) UIP pattern (all four features) •Upper or mid lung predominance subpleural basal predominance •subpleural basal predominance •peribronchovascular predominance reticular abnormality•reticular abnormality •extensive ground glass abnormality (extent > reticular abnormality) •honeycombing with or without traction bronchiectasis •profuse micronodules (bilateral, predominantly upper lobes Absence of features listed as inconsistent with UIP pattern Absence of features listed as inconsistent with UIP pattern •discrete cysts (multiple bilateral, away from areas of honeycombing) •diffuse mosaic attenuation/air trapping (bilateral in three or more lobes) •consolidation in broncho- pulmonary segment(s)/lobe(s) Radiological features of idiopathic pulmonary fibrosis: 2011
  • 91.
    Lymphangioleiomyomatosis (LAM) HRCT Morphology Thin-walledcysts (2mm - 5cm) Uniform in size / rarely confluent Homogeneous distribution Chylous pleural effusion Lymphadenopathy in young women
  • 94.
  • 95.
  • 96.
    Langerhans Cell Histiocytosis HRCTFindings Small peribronchiolar nodules (1-5mm) Thin-walled cysts (< 1cm), Bizarre and confluent Ground glass opacities Late signs: irreversible / parenchymal fibrosis Honey comb lung, septal thickening, bronchiectasis
  • 97.
    1 year later PeribronchiolarNodulesCavitating nodules and cysts Langerhans Cell Histiocytosis
  • 98.
  • 99.
    Langerhans Cell Histiozytosis KeyFeatures Upper lobe predominance Combination of cysts and noduli Characteristic stages Increased Lung volume Sparing of costophrenic angle S M O K I N G
  • 100.
  • 101.
    Langerhans Cell Histiocytosis DifferentialDiagnosis Only small nodules Sarkoidosis, Silikosis Only cysts idiopathic Fibrosis LAM Destruktive emphysema
  • 102.
    Benign lymphoproliferative disorder Diffuse interstitialinfiltration of mononuclear cells Not limited to the air ways as in follicular Bronchiolitis LIP = Lymphocytic Interstitial Pneumonia
  • 103.
  • 104.
    LIP = Lymphocytic InterstitialPneumonia Rarely idiopathic In association with: Sjögren’s syndrome Immune deficiency syndromes, AIDS Primary biliary cirrhosis Multicentric Castlemean’s disease
  • 105.
    Sjoegren disease Dry eyeand dry mouth Fibrosis, bronchitis and bronchiolitis LIP Overlap Sarcoid, DM/PM, MXCT SLE, RA (pleural effusion) Up to 40 x increased risk for lymphoma (mediastinal adenopathy) and 2 x times increased risk for neoplasma
  • 106.
    Young woman Drymouth Smoker LAM LIP Histiocytosis
  • 107.
  • 108.
  • 109.
  • 110.
    Honeycombing and tractionbronchiectasis in UIP.
  • 111.
    Typical UIP withhoneycombing and traction bronchiectasis in a patient with idiopathic pulmonary fibrosis (IPF)
  • 112.
  • 114.
    Reticular Pattern Gamal RabieAgmy, MD, FCCP Professor of chest Diseases, Assiut university
  • 115.
    Linear Pattern A linearpattern is seen when there is thickening of the interlobular septa, producing Kerley lines. Kerley B lines Kerley A lines The interlobular septa contain pulmonary veins and lymphatics. The most common cause of interlobular septal thickening, producing Kerley A and B lines, is pulmonary edema, as a result of pulmonary venous hypertension and distension of the lymphatics. Kerley B lines Kerley A lines
  • 116.
    DD of KerlyLines: Pulmonary edema is the most common cause Mitral stenosis Lymphangitic carcinomatosis Malignant lymphoma Congenital lymphangiectasia Idiopathic pulmonary fibrosis Pneumoconiosis Sarcoidosis
  • 117.
    HRCT of thelung Reticular pattern – HRCT numerous, clearly visible interlobular septa outlining lobules of characteristic size and shape interlobular septal thickening very fine network of lines within visible lobules intralobular interstitial thickening several layers of air-filled cysts, 3-10 mm in diameter, with thick walls (1-3 mm) honeycombing
  • 118.
    Reticular pattern Interlobular septalthickening – dd smooth thickening pulm. edema pulm. hemorrhage lymphangitic carc. lymphoma nodular thickening lymphangitic carc. sarcoidosis amyloidosis irregular thickening fibrosis
  • 119.
    Reticular pattern Interlobular septalthickening – pulmonary edema  smooth septal thickening, isolated or in combination with ground-glass opacity  peribronchovascular and subpleural interstitial th.  perihilar and gravitational distribution, bilateral  findings of CHF
  • 120.
    Reticular pattern Interlobular septalth. – lymphangitic carcinomatosis  smooth or nodular septal thickening  smooth or nodular thickening of peribronchovascular interstitium and fissures  thickening of the intralobular axial interstitium  focal or asymmetric distribution
  • 121.
    Reticulation or notreticulation …… “crazy paving”
  • 122.
    Reticular pattern Honeycombing –significance air-containing cystic spaces having thick, fibrous walls lined by bronchiolar epithelium  fibrosis is present UIP is likely the histologic pattern IPF is very likely, in the absence of a known disease
  • 123.
    Reticular pattern Honeycombing –differential diagnosis basal distribution middle/upper distribution chronic HP sarcoidosis IPF collagen vasc. dis. asbestosis drugs
  • 124.
    Reticular pattern adapted from:Webb RW – HRCT of the lung, III ed; 2001 interlobular septal thickening irregular, lung distorsion nodularsmooth •fibrosis (sarcoidosis, asbestosis) •pulm. edema •linf. carc. •hemorrhage •sarcoidosis •linf. carc.
  • 125.
    Reticular pattern adapted from:Webb RW – HRCT of the lung, III ed; 2001 honeycombing •IPF (60%) •collagen vascular dis. •drug reaction •asbestosis (uncommon) subpleural, posterior LL predominance •sarcoidosis •chronic HP •radiation other distribution (UL; parahilar)
  • 126.
    Head cheese sign Itrefers to mixed densities which includes # consolidation # ground glass opacities # normal lung # Mosaic perfusion • Signifies mixed infiltrative and obstructive disease
  • 127.
    Head cheese sign Commoncause are : 1. Hypersensitive pneumonitis 2. Sarcoidosis 3. DIP 127
  • 128.
    Headcheese sign Headcheese signin hypersensitivity pneumonitis. HRCT scan shows lung with a geographic appearance, which represents a combination of patchy or lobular ground-glass opacity (small arrows) and mosaic perfusion (large arrows).
  • 129.
    Mosaic Patternitie By Gamal RabieAgmy , MD , FCCP Professor of Chest Diseases ,Assiut University
  • 130.
  • 131.
    Where is thepathology ??????? in the areas with increased density meaning there is ground glass in the areas with decreased density meaning there is air trapping
  • 132.
    Pathology in blackareas Airtrapping: Airway Disease Bronchiolitis obliterans (constrictive bronchiolitis) idiopathic, connective tissue diseases, drug reaction, after transplantation, after infection Hypersensitivity pneumonitis granulomatous inflammation of bronchiolar wall Sarcoidosis granulomatous inflammation of bronchiolar wall Asthma / Bronchiectasis / Airway diseases
  • 133.
  • 134.
    Pathology in whiteAreas Alveolitis / Pneumonitis Ground glass desquamative intertitial pneumoinia (DIP) nonspecific interstitial pneumonia (NSIP) organizing pneumonia In expiration both areas (white and black) decrease in volume and increase in density DECREASE IN CONTRAST DIFFERENCES
  • 135.
    Mosaic Perfusion Chronic pulmonaryembolism LOOK FOR Pulmonary hypertension idiopathic, cardiac disease, pulmonary disease
  • 136.