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PLEURAL EFFUSION n TYPES
PNEUMOTHORAX
PLEURAL THICKENING
PLEURAL CALCIFICATION
PLEURAL TUMORS
Is the commonest abn of pleura
Pathogenesis off pleural effusion
1. Inc cap HP – CHF
2. Dec cap OP - hypoalbuminemia.
3. Inc cap perm- inflammation.
4. Obst lymphatics - tumor.
5. Movement of fluid from extrathoracic site
• less of protein
◦ Clear, watery fluids
◦ imbalance b/w HP n
OP
◦ Usual b/l
TRANSUDATES VS EXUDATES
•excess protein
•Amber, cloudy
fluid clots on
standing to
frank pus
•Usual u/l
except
PE, RA,SLE,
dressler,myx,
Lymphoma
R sided – liver, ascites, CHF
L sided – eso , panc, aorta, pericard
Massive – T n inf
DRUGS – pt also
Uremia – pericarditis
CAPD – sweet hydrothorax
 Massive effusion may cause complete
radiolucency of thorax – c/l med shift
 No shift – collapse , ext pleural ca
 Diaphragmatic inv – esp left
SUPINE --Hazziness of hemithorax with
preserved vascular shadows
 Lamellar effusion
◦ Reprents interstitial pulm fluid and are not true
pleural effusions
◦ Remains fixed with postural change
 Subpulmonic effusion
◦ Increased separation between stomach gas and
apparent hemidiaphragm (>2cm)
Adhesions
b/w Vp – Pp , fissures location
TRANSUDATES --anechoic
 Exudates
1. Echoes
2. Septa
3. Strands
4. Pt ( > 1cm)
5. Diaphragmatic nodule - CA
Densely echogenic fluid VS mass–
1. Fibrin strands
2. Components move wid respi
PLEURALEFFUSION VS PLEURALTHICKENING
1. USG - colour doppler ( eff gives colour) ( pt little or
no)
2. CT – d/t IV contrast in late venous phase -- pleura
dilineated
3. MRI – T2 ---- EPF (white) , pt ( black), pleural fluid
(white)
 Pleural effusion on CT is seen as homogeneous
crescenteric opacity in most dependent part of
pleural cavity
 On CT pleural effusion shows low attenuation
than pleural thickening or consolidated or
fibrotic lung
 Cant diff bw transudate or exudate ( a/w pt)
 Loculated – lenticular – smooth margins- non
dep part
PLEURALFLUID VS ASCITES
Displacedcrussign:
DiaphragM sign:
Interfacesign:
Bare areasign
Low SI - T1W images and high SI - T2 W (
trans)
Can diff btw transudate n exudate
TRIPLE ECHO PULSE SEQUENCE –
Highest SI – complicated exudate ( pus)
High - exudate
Low – transudate
 Milky effusions ---TG/CM
 rupture of thoracic duct and seepage of
collaterals
 neoplastic, traumatic developmental
anomalies
 X ray and CT no diff from non chylous
 MRI : high SI
 Pseudochylothorax --milky effusion cholesterol or
lecithin globulin complexes rather than
chylomicrons
◦ Occurs in pleural disease of many years
◦ Seen in TB, rheumatoid disease
 CXR – usual – on clot –loculation , fib strand
 CT – hyperdense
 MRI – subacute /chronic - inc SI T1 , T2 – (
concentric ring sign)
 Trauma , AA rupture , coagulopathies ,
traumatic pneumo
 Purulent pleural effusion -infection of
pleural space
 Empyema has a strong tendency to loculate
 Malignant neoplasms may arise in the walls
of chronic long standing empyema cavities
 CXR = usual / loculated
CT
• Lenticular shaped collection with an obtuse angle at
the interface with chest wall.
• Thick uniform soft tissue density wall (Vp , Pp)
• Smooth inner and outer edge
• k/a split pleura sign
• Enhancement of pleura is seen after contrast
• Septa, LAP ( Subcarinal , paratracheal i/l)
• Inc attenuation of EPF (>50HU)
• Air bubbles +
•Exudate
btw them
I/P ABSCESS
Spherical
Thick walled
Abrupt vessel cut off
at margin
Bronchi seen at lung
abscess interface
 The most common cause of primary
spontaneous pneumothorax is rupture of an
apical subpleural bleb.
 The etiology is obscure--- Difference in
alveolar pressure in upright human between
the base and the apex.
 Children --cystic fibrosis.
 More common in men (6:1). , smoker
 Typical patient is young, tall, thin man in late
adolescence and early adulthood.
 Secondary spontaneous pneumothorax
◦ predisposing lung disease
◦ COPD -commonest
◦ The most common sarcoma - osteosarcoma and
synovial sarcoma.
◦ Catamenial pneumothorax, -first three days of menses,
 Tension pneumothorax
◦ gross mediastinal shift.
◦ depression of i/l hemidiaphragm ( more reliable)
 avascular space ------
visceral pleural line.
 Expiratory film or decubitus
view with suspected side
uppermost
 subsequent collapse of
ipsilateral lung
 Tension pneumothorax
 White visceral pleura line
mimics
1. Skin folds ( wider)
 Deep sulcus sign
 I/l transradiancy
 DOUBLE DIAPHRAGM
SIGN
( ant CP recess)
Complications of pneumothorax
• Loculated or encysted pneumothorax
• Haemopneumothorax
• Pyopneumothorax
• Presence of pleural fluid- hydropneumothorax-
there is horizontal air fluid level
• Tension pnumothorax
• Adhesions
• Re expansion edema
 LUNG SLIDING SIGN –nt ( large probe – dec
depth)
 BARCODE ( M MODE)
 Lung point
 False positive – COPD
IOC
No false positive
Can diff btw pneumo n bullae
Connection btw airway and pleura
Persistent pneumo , hydropneumo despite
continuous drainage
Seen in necrotising infections ,partial or
complete lung resection
Pt ---
1. Benign – a) diffuse /fibrothorax
b) focal / plaques
2. Malignant --- a) primary / MPM
( can b diffuse) b) secondary /mets (MC)
Calcifications = // to chest wall, diaphragm,
cardiac border ( cxr)
CXR -- Soft tissue shadowing --dependent
lateral and posterior parts of chest
 USG -- homogeneous dense layer adjacent to
chest wall.
CT-layer of soft tisssue opacity at chest wall
and lung inteface/ INNER TO RIBS
MRI – use to see tumor ext
1. CIRCUMFERENTIAL THICKENING / RIND
PLEURAL THICKNESS (>1 cm) – in max
width
NODULAR / IRREG PLEURAL THICKENING
MEDIASTINAL PLEURAL INV
Cause = empyema, hemothorax, asbestos ,
TB,
 MPM , mets ( adenoCA) = malig pt,U/L
/asym
Can cause ventilatory restriction
Calcification inf>>>>>>>> asbestos
Hemo – a/w rib #
Empyema -- primary cause
Post talc sandwich = thick vp n pp with talc
in btw ( inc attenuation)
Asbestos ? b/l inv
CXR ---
soft tissue density along chest wall/ pleural
space ( extent > plaque) ( ¼ chest wall)
Blunting of CP angle -- common
CC =8cm
LATERALLY = 5cm
THICKNESS = 3mm
 Can occur in the cupula / apical cap
 Apical cap – TB n radiation, pancoast tumor ,
thoracic aorta injury , pt, age
 d/d on cxr - companion rib shadow ( scallop)
 EPF (u/l)
 Large = seen on cxr
Pleural plaques -- asbestos exposure ( MC)
 asymptomatic ( vs lung path = symp)
Marker of asbestos exposure
Multifocal , b/l
Always on parietal pleura ( may involve
fiss)
in posterolateral location along chest wall
and on diaphragmatic pleura ( never at
apex/ cp)
Calcify , ossify,
Inc risk of MPM n BAC
Can inc in size , thickness
In paravertertebral area – mimic I/C veins
If a/w interstitial lines k.a HAIRY PLAQUES
CLASSIFICATION
THICKNESS LENGTH
MINIMUM
(few )
< 1mm 1-3Cm
MODERATE
( multiple)
1 – 3 mm 3-5cm
SEVERE
( indent lung)
> 3 mm 8cm CC ,
> 5cm lat
PLEURAL PLAQUES ( ASBESTOS) / BENIGN CHR PT
↓
ROUND ATELECTESIS/ MASS ( LUNG)
↓
BVMCONVERGEFROMHILUMONTOMASS
↓
COMETTAIL SIGN
s/s +
Infiteration +
Inc in size with time
Pleural effusion
Seen in post lower lobe , middle , lingula
MRI dec SI T1 , inc SI T2
Same causes as pleural thickening
Ul/
• Empyema,
• hemorhorax
• Pleurisy
Bilateral
• Asbestos exposure (plaque>>> diffuse)
 Are relatively uncommon
 Can be localised or diffuse
 Localised
• Localised fibrous tumor
• Lipoma
• Extrathoracic mets
• submesenchymal cells of vp – origin
• MC , Asymtomatic ( benign)
• 6-7 decade , f>m
• Etiology ? Asbestos n radiation exposure
• Complication = hypertrophic osteoarthropathy /
hypoglycemia
• Calcify +
• Pleural effusion ±
• 1/3 malignant , 2/3 benign
• CXR =
• well defined ,,
• rounded or slightly lobulated mass –
• -variable size ----
• obtuse angle with chest wall
• Mobile with posture n resp
CT
Pleural mass ---- Size can be diff --- small and large
SMALL (<10 cm) LARGE (>10cm)
asymptomatic s/s + - cough, pain
,dysp,pneumo
Homogeneous enhancement heterogeneous ( d/t areas
of necrosis)
Pleural eff +
Atelectasis +
Mediastinal inv +
Invasion of chest wall+
benign malignant
Low to int SI on T1 , T2, proton density
If a/w necrosis , h’age – inc SI on T2
Gd – intense homogeneous enhancement
LIPOMA v/s LIPOSARCOMA
benign
Origin = fat tissue
Asymptomatic
Incidental finding
•CXR = pleural mass
•CT = uniform , pleural
mass , fat density ( < 50
HU)
•MRI = Inc SI on T1 , T2 (
T1>> T2)
Malignant
s/s +
Large
Infilterates surr
tissue
•CT = fat density +
soft ts. Density
•MRI = dec SI T1 ,
inc SI T2 d/t
myxoid
degeneration
Pleural mets’
• Are commonest cause of localised pleural mass with
rib destruction
• Seen in adeno CA ( breast, lung, GIT, ovary)
• Multiple
• Often a/w pleural effusion
Diffuse malignant mesothelioma
• Highly malignant progressive neoplasm
• Asbestos exposure ( chrysolite)
• Males
• 40-70 years
Irregular , nodular opacity ( peripherally)
Pleural effusion ± → + l/t c/l shift
Vol loss on affected side
Pt ±
CT` ( main for staging)
•Nodular soft ts mass with hypodens area ( necrosis)
•Pt = malignant esp in lower zones and diaphragmatic
surface
•effusion + = u/l , vol loss on i/l side
•Calcification may occur
•Fissural inv + / interlobar fissure thickening
•Chest wall inv + = rib displacement , bone destruction
•
•Loss of extrapleural fat and I/C muscles invasion
•ABSENCE OF PT does not rule out a neoplastic process
Can extend into chest wall via needle biopsy
tracks , surgical scars, chest tube tracts
VASCULAR invasion – obliteration of surr fat
planes, encasing >50% Circumference
TRANSDIAPHRAGMATIC INV – soft tissue
mass that encases hemidiaphragm
PULMONARY METS = nodules or masses
Min inc SI T1
Moderately Inc SI T2
Helpful to determine the soft tissue /chest
wall invasion/ diaphragm/ ETF
Uptake seen in both malignancy and
inflamm
Uptake malig>>> inflam
Used in staging and preop assessment
Detect occult extrathoracic mets
Predict prog (uptake i.p prog)
 always Used as adjunct with ct
• D/d
 Metastatic pleural deposits ( diff to diff) ( hilar LAP
more)
 Breast Ca
 Malignant thymoma ( drop mets in ant med mass)
 Lymphoma- deposits are more discrete and localised
 TB pleural thickenin
 Empyema- smooth , does not usually extend to
mediastinal pleura
RSNA, 2004
AJR 1990
RSNA 1999
RSNA 2012
RSNA 2002
RSNA 2007
GRAINGER
HAAGA
Diseases of pleura

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Diseases of pleura

  • 1.
  • 2. PLEURAL EFFUSION n TYPES PNEUMOTHORAX PLEURAL THICKENING PLEURAL CALCIFICATION PLEURAL TUMORS
  • 3.
  • 4.
  • 5. Is the commonest abn of pleura Pathogenesis off pleural effusion 1. Inc cap HP – CHF 2. Dec cap OP - hypoalbuminemia. 3. Inc cap perm- inflammation. 4. Obst lymphatics - tumor. 5. Movement of fluid from extrathoracic site
  • 6. • less of protein ◦ Clear, watery fluids ◦ imbalance b/w HP n OP ◦ Usual b/l TRANSUDATES VS EXUDATES •excess protein •Amber, cloudy fluid clots on standing to frank pus •Usual u/l except PE, RA,SLE, dressler,myx, Lymphoma
  • 7. R sided – liver, ascites, CHF L sided – eso , panc, aorta, pericard Massive – T n inf DRUGS – pt also Uremia – pericarditis CAPD – sweet hydrothorax
  • 8.  Massive effusion may cause complete radiolucency of thorax – c/l med shift  No shift – collapse , ext pleural ca  Diaphragmatic inv – esp left SUPINE --Hazziness of hemithorax with preserved vascular shadows
  • 9.  Lamellar effusion ◦ Reprents interstitial pulm fluid and are not true pleural effusions ◦ Remains fixed with postural change  Subpulmonic effusion ◦ Increased separation between stomach gas and apparent hemidiaphragm (>2cm)
  • 10. Adhesions b/w Vp – Pp , fissures location
  • 11.
  • 12.
  • 13. TRANSUDATES --anechoic  Exudates 1. Echoes 2. Septa 3. Strands 4. Pt ( > 1cm) 5. Diaphragmatic nodule - CA
  • 14.
  • 15. Densely echogenic fluid VS mass– 1. Fibrin strands 2. Components move wid respi PLEURALEFFUSION VS PLEURALTHICKENING 1. USG - colour doppler ( eff gives colour) ( pt little or no) 2. CT – d/t IV contrast in late venous phase -- pleura dilineated 3. MRI – T2 ---- EPF (white) , pt ( black), pleural fluid (white)
  • 16.  Pleural effusion on CT is seen as homogeneous crescenteric opacity in most dependent part of pleural cavity  On CT pleural effusion shows low attenuation than pleural thickening or consolidated or fibrotic lung  Cant diff bw transudate or exudate ( a/w pt)  Loculated – lenticular – smooth margins- non dep part
  • 17.
  • 18. PLEURALFLUID VS ASCITES Displacedcrussign: DiaphragM sign: Interfacesign: Bare areasign
  • 19.
  • 20. Low SI - T1W images and high SI - T2 W ( trans) Can diff btw transudate n exudate TRIPLE ECHO PULSE SEQUENCE – Highest SI – complicated exudate ( pus) High - exudate Low – transudate
  • 21.  Milky effusions ---TG/CM  rupture of thoracic duct and seepage of collaterals  neoplastic, traumatic developmental anomalies  X ray and CT no diff from non chylous  MRI : high SI  Pseudochylothorax --milky effusion cholesterol or lecithin globulin complexes rather than chylomicrons ◦ Occurs in pleural disease of many years ◦ Seen in TB, rheumatoid disease
  • 22.  CXR – usual – on clot –loculation , fib strand  CT – hyperdense  MRI – subacute /chronic - inc SI T1 , T2 – ( concentric ring sign)  Trauma , AA rupture , coagulopathies , traumatic pneumo
  • 23.  Purulent pleural effusion -infection of pleural space  Empyema has a strong tendency to loculate  Malignant neoplasms may arise in the walls of chronic long standing empyema cavities  CXR = usual / loculated
  • 24. CT • Lenticular shaped collection with an obtuse angle at the interface with chest wall. • Thick uniform soft tissue density wall (Vp , Pp) • Smooth inner and outer edge • k/a split pleura sign • Enhancement of pleura is seen after contrast • Septa, LAP ( Subcarinal , paratracheal i/l) • Inc attenuation of EPF (>50HU) • Air bubbles +
  • 26.
  • 27. I/P ABSCESS Spherical Thick walled Abrupt vessel cut off at margin Bronchi seen at lung abscess interface
  • 28.  The most common cause of primary spontaneous pneumothorax is rupture of an apical subpleural bleb.  The etiology is obscure--- Difference in alveolar pressure in upright human between the base and the apex.  Children --cystic fibrosis.  More common in men (6:1). , smoker  Typical patient is young, tall, thin man in late adolescence and early adulthood.
  • 29.
  • 30.  Secondary spontaneous pneumothorax ◦ predisposing lung disease ◦ COPD -commonest ◦ The most common sarcoma - osteosarcoma and synovial sarcoma. ◦ Catamenial pneumothorax, -first three days of menses,  Tension pneumothorax ◦ gross mediastinal shift. ◦ depression of i/l hemidiaphragm ( more reliable)
  • 31.  avascular space ------ visceral pleural line.  Expiratory film or decubitus view with suspected side uppermost  subsequent collapse of ipsilateral lung  Tension pneumothorax  White visceral pleura line mimics 1. Skin folds ( wider)
  • 32.  Deep sulcus sign  I/l transradiancy  DOUBLE DIAPHRAGM SIGN ( ant CP recess)
  • 33.
  • 34. Complications of pneumothorax • Loculated or encysted pneumothorax • Haemopneumothorax • Pyopneumothorax • Presence of pleural fluid- hydropneumothorax- there is horizontal air fluid level • Tension pnumothorax • Adhesions • Re expansion edema
  • 35.  LUNG SLIDING SIGN –nt ( large probe – dec depth)  BARCODE ( M MODE)  Lung point  False positive – COPD
  • 36.
  • 37.
  • 38. IOC No false positive Can diff btw pneumo n bullae
  • 39.
  • 40. Connection btw airway and pleura Persistent pneumo , hydropneumo despite continuous drainage Seen in necrotising infections ,partial or complete lung resection
  • 41. Pt --- 1. Benign – a) diffuse /fibrothorax b) focal / plaques 2. Malignant --- a) primary / MPM ( can b diffuse) b) secondary /mets (MC) Calcifications = // to chest wall, diaphragm, cardiac border ( cxr)
  • 42. CXR -- Soft tissue shadowing --dependent lateral and posterior parts of chest  USG -- homogeneous dense layer adjacent to chest wall. CT-layer of soft tisssue opacity at chest wall and lung inteface/ INNER TO RIBS MRI – use to see tumor ext
  • 43. 1. CIRCUMFERENTIAL THICKENING / RIND PLEURAL THICKNESS (>1 cm) – in max width NODULAR / IRREG PLEURAL THICKENING MEDIASTINAL PLEURAL INV
  • 44.
  • 45.
  • 46. Cause = empyema, hemothorax, asbestos , TB,  MPM , mets ( adenoCA) = malig pt,U/L /asym Can cause ventilatory restriction Calcification inf>>>>>>>> asbestos Hemo – a/w rib # Empyema -- primary cause Post talc sandwich = thick vp n pp with talc in btw ( inc attenuation) Asbestos ? b/l inv
  • 47. CXR --- soft tissue density along chest wall/ pleural space ( extent > plaque) ( ¼ chest wall) Blunting of CP angle -- common
  • 48.
  • 49. CC =8cm LATERALLY = 5cm THICKNESS = 3mm
  • 50.  Can occur in the cupula / apical cap  Apical cap – TB n radiation, pancoast tumor , thoracic aorta injury , pt, age  d/d on cxr - companion rib shadow ( scallop)  EPF (u/l)  Large = seen on cxr
  • 51.
  • 52. Pleural plaques -- asbestos exposure ( MC)  asymptomatic ( vs lung path = symp) Marker of asbestos exposure Multifocal , b/l Always on parietal pleura ( may involve fiss) in posterolateral location along chest wall and on diaphragmatic pleura ( never at apex/ cp) Calcify , ossify, Inc risk of MPM n BAC
  • 53. Can inc in size , thickness In paravertertebral area – mimic I/C veins If a/w interstitial lines k.a HAIRY PLAQUES CLASSIFICATION THICKNESS LENGTH MINIMUM (few ) < 1mm 1-3Cm MODERATE ( multiple) 1 – 3 mm 3-5cm SEVERE ( indent lung) > 3 mm 8cm CC , > 5cm lat
  • 54.
  • 55.
  • 56. PLEURAL PLAQUES ( ASBESTOS) / BENIGN CHR PT ↓ ROUND ATELECTESIS/ MASS ( LUNG) ↓ BVMCONVERGEFROMHILUMONTOMASS ↓ COMETTAIL SIGN
  • 57.
  • 58. s/s + Infiteration + Inc in size with time Pleural effusion Seen in post lower lobe , middle , lingula MRI dec SI T1 , inc SI T2
  • 59. Same causes as pleural thickening Ul/ • Empyema, • hemorhorax • Pleurisy Bilateral • Asbestos exposure (plaque>>> diffuse)
  • 60.  Are relatively uncommon  Can be localised or diffuse  Localised • Localised fibrous tumor • Lipoma • Extrathoracic mets
  • 61. • submesenchymal cells of vp – origin • MC , Asymtomatic ( benign) • 6-7 decade , f>m • Etiology ? Asbestos n radiation exposure • Complication = hypertrophic osteoarthropathy / hypoglycemia • Calcify + • Pleural effusion ± • 1/3 malignant , 2/3 benign
  • 62. • CXR = • well defined ,, • rounded or slightly lobulated mass – • -variable size ---- • obtuse angle with chest wall • Mobile with posture n resp
  • 63. CT Pleural mass ---- Size can be diff --- small and large SMALL (<10 cm) LARGE (>10cm) asymptomatic s/s + - cough, pain ,dysp,pneumo Homogeneous enhancement heterogeneous ( d/t areas of necrosis) Pleural eff + Atelectasis + Mediastinal inv + Invasion of chest wall+ benign malignant
  • 64.
  • 65. Low to int SI on T1 , T2, proton density If a/w necrosis , h’age – inc SI on T2 Gd – intense homogeneous enhancement
  • 66. LIPOMA v/s LIPOSARCOMA benign Origin = fat tissue Asymptomatic Incidental finding •CXR = pleural mass •CT = uniform , pleural mass , fat density ( < 50 HU) •MRI = Inc SI on T1 , T2 ( T1>> T2) Malignant s/s + Large Infilterates surr tissue •CT = fat density + soft ts. Density •MRI = dec SI T1 , inc SI T2 d/t myxoid degeneration
  • 67. Pleural mets’ • Are commonest cause of localised pleural mass with rib destruction • Seen in adeno CA ( breast, lung, GIT, ovary) • Multiple • Often a/w pleural effusion
  • 68. Diffuse malignant mesothelioma • Highly malignant progressive neoplasm • Asbestos exposure ( chrysolite) • Males • 40-70 years
  • 69. Irregular , nodular opacity ( peripherally) Pleural effusion ± → + l/t c/l shift Vol loss on affected side Pt ±
  • 70. CT` ( main for staging) •Nodular soft ts mass with hypodens area ( necrosis) •Pt = malignant esp in lower zones and diaphragmatic surface •effusion + = u/l , vol loss on i/l side •Calcification may occur •Fissural inv + / interlobar fissure thickening •Chest wall inv + = rib displacement , bone destruction • •Loss of extrapleural fat and I/C muscles invasion •ABSENCE OF PT does not rule out a neoplastic process
  • 71.
  • 72. Can extend into chest wall via needle biopsy tracks , surgical scars, chest tube tracts VASCULAR invasion – obliteration of surr fat planes, encasing >50% Circumference TRANSDIAPHRAGMATIC INV – soft tissue mass that encases hemidiaphragm PULMONARY METS = nodules or masses
  • 73.
  • 74.
  • 75.
  • 76.
  • 77.
  • 78.
  • 79. Min inc SI T1 Moderately Inc SI T2 Helpful to determine the soft tissue /chest wall invasion/ diaphragm/ ETF
  • 80.
  • 81. Uptake seen in both malignancy and inflamm Uptake malig>>> inflam Used in staging and preop assessment Detect occult extrathoracic mets Predict prog (uptake i.p prog)  always Used as adjunct with ct
  • 82. • D/d  Metastatic pleural deposits ( diff to diff) ( hilar LAP more)  Breast Ca  Malignant thymoma ( drop mets in ant med mass)  Lymphoma- deposits are more discrete and localised  TB pleural thickenin  Empyema- smooth , does not usually extend to mediastinal pleura
  • 83. RSNA, 2004 AJR 1990 RSNA 1999 RSNA 2012 RSNA 2002 RSNA 2007 GRAINGER HAAGA