CHEST

Anterior Mediastinal Mass

(Germ Cell Neoplasm)
• DDx
– Thymic lesion: thymoma, thymic hyperplasia,
carcinoid, carcinoma, cyst, lymphoma, thymolipoma
– Teratoma and other germ cell neoplasm
– Lymphoma
– Thyroid goiter/mass
– Vascular abnormalities
Seminoma
Thymic Cyst
Thymolipoma
Thymolipoma
• Germ cell neoplasm
– Anterior mediastinum is MC extragonadal site
– 70% are benign teratomas or dermoids
– Malignant tumors include seminoma, chorioCA,
embryonal cell CA, yolk sac tumor
– Teratomas/dermoid appear as heterogeneous
predominantly cystic masses with well-defined
margins, frequently with Ca+
• Fat or fat/fluid levels very helpful
Mature Teratoma
Mature Teratoma
Nonseminomatous Germ Cell Tumor
• Thymoma
– Majority of anterior mediastinal masses in adults
– Assoc w/myasthenia gravis, red cell aplasia,
hypogammaglobulinemia
– 40% of thymoma pts have myasthenia, 15% of myasthenics
have thymomas
– 20% have Ca+ which is usually curvilinear
– 30% are invasive, extending beyond fibrous capsule
• Spreads locally, usually to pleura
Thymoma
Invasive Thymoma
• Lymphoma
– Usually Hodgkin
– Findings: single soft tissue mass or large lobulated
mass of node conglomerates
– Nodes in other compartments or outside the thorax
helpful
– NO Ca+ if untreated
Hodgkin Lymphoma
Lymphoma
• Thyroid
– Behind the great vessels while others are in front
– Most are goiters, rest are adenomas and neoplasms
– Most asymptomatic but can compress trachea or esophagus
– XR: tracheal deviation to right side
– Features favoring thyroid origin: continuity with thyroid, foci
of high attenuation on NCCT, foci of heterogeneous
attenuation, intense and prolonged enhancement on CECT
Goiter
Goiter
Goiter
 Bronchogenic Carcinoma
• Case findings: RUL atelectasis with endobronchial/hilar
mass
• Reverse S sign of Golden: central endobronchial lesion
causing RUL collapse
• Other appearances of lung CA include hilar or perihilar
mass, adenopathy, parenchymal SPN
• 4 types: small cell, large cell, adenoCA (MC), squamous
– AdenoCA and large cell tend to be peripheral, small cell and
squamous central
 Staging
• T0: no evidence of a primary tumor
• Tis: in situ
• T1: < 3 cm (T1a: < 2 cm; T1b: 2-3 cm)
• T2: 3-7 cm (T2a: 3-5 cm; T2b: 5-7 cm), involves main bronchus >
2 cm from carina, invasion of visceral pleura, lobar atelectasis
• T3: > 7 cm; chest wall, diaphragm, mediastinal pleura, or
pericardium invasion; < 2 cm from carina; whole lung atelectasis;
satellite nodules in ipsilateral tumor lobe
• T4: heart, great vessel, trachea, esophagus, vertebral body, or
carina invasion; tumor nodules in different lobe of ipsilateral lung
• N0: no nodes
• N1: ispilateral hilar nodes
• N2: ipsilateral mediastinal nodes; includes subcarinal and midline
nodes
• N3: contralateral mediastinal, ipsilateral or contralateral scalene or
supraclavicular

• M0: no distant mets

• M1a: spread to contralateral lung, malignant pleural effusion,
malignant pericardial effusion
• M1b: spread to distant organs or lymph nodes
• Stage 0: Tis, N0, M0
• Stage 1
– 1A: T1, N0, M0
– 1B: T2a, N0, M0
• Stage 2
– 2A: T1, N1, M0 or T2a, N1, M0 or T2b, N0, M0
– 2B: T2b, N1, M0 or T3, N0, M0
• Stage 3
– 3A: T1 to T3, N2, M0 or T3, N1, M0 or T4, N0 to N1, M0
– 3B: Any T, N3, M0 or T4, N2, M0
• Stage 4: M1a or M1b
• Tx
– Stage 3B and 4, unresectable
– Stage 3A and below, surgery
 Aortic Dissection
• Separation of intima from media
• Almost all arise either in ascending aorta 1 cm above
sinotubular ridge or in descending aorta just beyond
aortic isthmus
• Most progress distally
– Some proximal  pericardial tamponade, aortic insufficiency,
coronary occlusion
• 2 classifications: Stanford and Debakey
– Debakey 1 = ascending + descending, 2 = ascending only, 3 =
descending only
– Stanford A = any dissection involving ascending, B =
descending only
• Tx: ascending = surgical repair, descending = BP control
• Criteria for surgical/endovascular tx in type B
dissection
– Persistent symptoms despite medical treatment
– Aortic diameter > 5-6 cm, growth > 1 cm/y
– Impending or frank rupture
– Major-organ malperfusion (renovascular HTN,
pulseless extremities, visceral ischemia)
– Uncontrollable HTN
• XR: wide mediastinum, separation of Ca+ from wall of
the arch, double knob sign, prominent knob, left apical
cap, displacement of trachea and esophagus, pleural
effusion
• CT: linear filling defect representing intimal flap,
complications: hemopericardium and hemothorax
• MR: intimal flap with black blood or white blood
techniques
• Angio: double barrel aorta with interposed flap, left renal
artery frequently fed by false lumen, left iliac > right,
aortic insufficiency and coronary involvement
 Atrial Septal Defect
• Most not detected in infancy (look for older child or
adult XR), whereas most VSDs are (neonate XR)
• Most are of ostium secundum type
– Defect in central portion of fossa ovalis
• XR: shunt vascularity, enlarged pulmonary arteries,
RA/RV
• Eisenmenger syndrome: chronic right-sided pressure
elevation w/reversal of shunt from right to left
– Heart decreases in size, pulmonary arteries are aneurysmal and
calcified
• MR: incomplete atrial septum, enlarged pulmonary
arteries, RA/RV
• Ostium secundum ASD (MC)
– Occurs in center of atrial septum
• Ostium primum ASD
– Next MC type
– Located in lower portion of atrial septum
• Sinus venosus ASD
– Least common type
– Located in upper portion of atrial septum
– Often assoc w/partial anomalous pulmonary venous
return
• DDx convex main PA
– PA HTN: pruning/rapid tapering of peripheral
vasculature
– Pulmonic stenosis: usu no shunt vascularity, enlarged
main and left PA but NOT the right, RV mildly dilated
and RA WNL
– Left-to-right shunt
• VSD: similar to ASD, w/shunt vascularity, ↑ PAs, sometimes
Eisenmenger; should have LA dilation
• PDA: shunt vascularity, cardiomegaly w/enlarged LA/LV/Ao
• ASD
– Pulmonary artery aneurysm
DDx: Pulmonary Artery Aneurysm
DDx: Pulmonary Artery Aneurysm
Mycotic Pulmonary Artery Aneurysm
 Pulmonary Arterial Hypertension
• Systolic PAP > 30, mean PAP > 18
• Findings: enlarged central PAs, enlarged RV, PA calcification
(chronic)
• Causes
– Pre-capillary: obstruction from thromboembolism, tumor
– Capillary: ↑ capillary resistance from interstitial lung disease, COPD,
widespread airspace disease, primary pulmonary HTN, Eisenmenger/left-
to-right shunts
– Post-capillary: obstruction to venous drainage from LV failure, restrictive
cardiomyopathy, mitral stenosis, hypoplastic left heart, pulmonary veno-
occlusive disease, fibrosing mediastinitis
 Miliary Nodules
• DDx micronodules (< 5 mm)
– Mets: thyroid, melanoma
– Infection: TB, fungal, healed varicella (calcified)
– Sarcoid, silicosis/coal worker’s lung (upper lobes,
eggshell Ca+ nodes)
– Subacute hypersensitivity pneumonitis (acute: lower
lobe consolidation; subacute: upper lobe centrilobular
nodules; chronic: upper lobe interstitial fibrosis)
Miliary Tuberculosis
Miliary Tuberculosis
Metastatic Thyroid Carcinoma
Miliary Sarcoidosis
Healed Varicella
• DDx macronodules (> 5 mm)
– Tumor: mets, lymphoma, primary lung CA, BAC
– Infection: fungal, TB, viral, bacterial, parasites
– Collagen vascular: Wegener and RA
– Vascular: septic emboli, infarcts, AVMs (Osler-
Weber-Rendu)
– Miscellaneous: amyloid, sarcoid, PMF
Cannonball Metastases (RCC)
Osteosarcoma Mets w/PTX
Osteosarcoma Mets w/PTX
Osteosarcoma Mets w/PTX
Lymphoma
Amyloidosis (Parenchymal Nodular)
 Pulmonary Nodules
• HRCT anatomic distribution
– Perilymphatic: subpleural, peribronchovascular, septal nodules
• DDx: sarcoidosis (classic), lymphangitic spread (less common) > silicosis/CWP >
amyloidosis, LIP
– Random
• DDx: miliary TB/fungal, hematogenous mets, sarcoidosis (uncommon)
– Centrilobular: occur in relation to centrilobular artery or bronchiole, centered
5-10 mm from pleura
• DDx: bronchiolitis (infectious, inflammatory), endobronchial spread of TB/MAC,
bronchopneumonia, hypersensitivity pneumonitis, endobronchial spread of tumor
(BAC), pneumoconiosis (silicosis), organizing pneumonia, histiocytosis (rare),
edema or vasculitis (uncommon)
• Tree-in-bud DDx: endobronchial spread of TB/MAC, bronchopneumonia,
bronchiectasis or bronchitis, cystic fibrosis, panbronchiolitis (rare), aspiration
(rare), ABPA or asthma (rare), BAC (rare)
Perilymphatic (Sarcoidosis)
 Perilymphatic
(Amyloidosis, Alveolar Septal)
 Random
(Miliary Coccidioidomycosis)
 Centrilobular
(Subacute Hypersensitivity Pneumonitis)
 Pulmonary Edema
• Causes
– Cardiogenic (MC): LV failure, mitral valve disease, pulmonary venous
occlusion, pericardial disease
– Noncardiogenic: increased hydrostatic pressure (renal failure, excessive IV
fluids, neurogenic), decreased oncotic pressure (hypoproteinemia, lung re-
expansion), increased capillary permeability (aspiraton, near drowning,
trauma, radiation, drugs, anaphylaxis)
• Permeability causes usually in peripheral distribution rather than
perihilar, and usually do not have associated effusions
• Noncardiogenic causes usually have a normal-sized heart
• XR
– Cephalization of vessels on erect XR
– Vascular indistinctness and peribronchial thickening
– Kerley lines and pleural effusions
– Alveolar edema: symmetric perihilar alveolar
opacities
Noncardiogenic Pulmonary Edema
 Primary Tuberculosis
• Pts usually asymptomatic
• Findings
– Consolidation in any lobe, favors lower lobes
– Usually does NOT cavitate
– Hilar or mediastinal adenopathy
– Pleural effusion
• On CT, nodes often have low density necrotic centers
• Ghon focus: calcified tuberculoma
• Ranke complex: Ca+ lung focus + lymph node
TB Adenopathy
TB Adenopathy
• Causes of mediastinal lymphadenopathy
– Metastasis: lung, breast, esophagus, renal, testis, H&N
– Lymphoma
– TB/MAC
– Sarcoidosis
– AIDS-related lymphadenopathy
• DDx low density lymph nodes
– TB/MAC
– Metastasis (necrosis: SCC or adenoCA)
• DDx hypervascular lymph nodes
– Castleman disease
– Kaposi sarcoma
Castleman Disease
 Reactivation Tuberculosis
• Usually in apical and posterior segments of upper lobes and superior
segment of lower lobes
• Cavitary nodules are classic finding, but can also just be patchy
consolidation
• Upper lobe nodules w/volume loss, hilar retraction, pleural
thickening
• Upper lobe bronchiectasis
• Bronchogenic spread results when cavitary lesion erodes into
bronchus
– Ill-defined nodules 5-6 mm in diameter, numerous and bilateral
– On CT, produces tree-in-bud appearance: centrilobular nodules and
centrilobular branching linear opacities
• DDx: sarcoid, radiation, ankylosing spondylitis
• Miliary TB
– Hematogenous dissemination
– XR: multiple 1-2 mm tiny interstitial nodules
– CT detects it earlier
 Lymphangitic Carcinomatosis
• Unilateral (MC lung) or bilateral
• Lung, breast, stomach, colon
• XR
– Diffuse reticular or reticulonodular opacities
– Thickened septal lines
– Hilar, mediastinal adenopathy (helpful differential feature)
– Pleural effusions
– Check for clues: mastectomy
• HRCT: smooth or nodular axial interstitial thickening, septal
thickening, nodular (or smooth) thickening of fissures, NO
architectural distortion
Lymphangitic Carcinomatosis
Lymphangitic Carcinomatosis
 Usual Interstitial Pneumonitis
• DDx basilar lung disease
– IPF/UIP: honeycombing, traction bronchiectasis
– Asbestosis: pleural plaques (80%), occupational hx
– Scleroderma: dilated esophagus, UIP or NSIP pattern
– Rheumatoid arthritis: erosive arthritis, UIP or NSIP pattern
– Cryptogenic organizing pneumonia: patchy consolidation
– Drugs (bleomycin): often nodular, mimicking mets
– Hematogenous mets
– ARDS
Scleroderma
Asbestosis
 Organizing Pneumonia
• Findings: patchy air space disease (consolidation 80%,
GGO 60%), subpleural or peribronchiolar,
effusions/lymphadenopathy uncommon
• Idiopathic = cryptogenic organizing pneumonia
• Secondary causes
– Collagen vascular disease
– Infections
– Bone marrow transplantation (GVHD)
– Wegener
– Toxic inhalation
• DDx peripheral consolidation: organizing
pneumonia, chronic eosinophilic pneumonia,
pulmonary infarct, pulmonary contusion
Pulmonary Infarct
 Cystic Fibrosis
• DDx upper lung disease
– Silicosis/CWP: occupational hx
– Sarcoidosis: bronchovascular distribution
– EG: young smokers, nodules  bizarre cysts,
hyperinflation
– Hypersensitivity pneumonitis
– Reactivation TB/fungal: nodules, cavities, apical volume
loss, hilar retraction
– Ankylosing spondylitis: fibrocystic change, spine findings
– Cystic fibrosis: hyperinflation, bronchiectasis
Cystic Fibrosis
Ankylosing Spondylitis
 Eosinophilic Granuloma
• Young to middle-aged smokers (> 90%)
• XR
– Normal to increased lung volumes
– Reticulonodular opacities
– PTX (25%)
• HRCT
– Upper lobe nodules  bizarre cysts
– Costophrenic angles spared
 Lymphangioleiomyomatosis
• Premenopausal women
• PTX, chylous effusions
• Same findings may occur in tuberous sclerosis
• XR
– Fine reticular pattern
– Increased lung volumes
• HRCT
– Diffuse, uniform cysts that eventually replace lung
parenchyma
DDx: Lung Cysts
• DDx increased lung volumes
– Cystic lung disease: EG, LAM
– Airway disease: asthma, CF, BO, dysmotile cilia,
ABPA
– Obstructive/destructive lung disease: emphysema
 Coarctation of the Aorta
• See Peds
Aortic Pseudocoarctation
 Aortic Stenosis
• XR
– Dilated ascending aorta best seen on frontal, right of midline
– LVH or normal-sized heart
– Calcification of aortic valve on the lateral
– Normal pulmonary vascularity
• MR/Angio: look for bicuspid valve
• Cine MR: stenotic jet through aortic valve
• Infantile aortic stenosis
– Cardiomegaly and pulmonary edema
• Types
– Supravalvular (nearly always congenital)
• Isolated lesion or part of Williams syndrome
– Valvular (congenital or acquired)
• Bicuspid valve (MC congenital cause)
• Unicuspid valve (less common)
• Rheumatic disease
• Degnerative stenosis (MC cause in adults)
– Subvalvular (congenital)
• MC thin membrane situated w/in 1 cm beneath cusps
• Muscular stenosis caused by asymmetric HCM
Supravalvular Aortic Stenosis
 Pulmonary Embolism
• XR
– Westermark sign: oligemia distal to embolus
– Fleischner sign: enlargement of pulmonary artery
– Hampton hump: peripheral wedge-shaped density
representing a pulmonary infarct
– Atelectasis and pleural effusions are other nonspecific
findings
Pulmonary Embolism
DDx: Pulmonary Artery Sarcoma
 Mitral Stenosis
• XR
– LA appendage enlargement
– LA enlargement: displacement of left main stem bronchus
superiorly on frontal and posteriorly on lateral, splaying of
carina, posterior displacement of barium-filled esophagus,
double density along right side of spine
– Cephalization of upper lobe pulmonary vessels
– Calcification of mitral valve
– If severe, Ca+ LA  often atrial fib and atrial thrombus
• DDx: left atrial myxoma
 LUL Atelectasis
• Lobar atelectasis
– RUL
• Collapses superomedial creating a wedge opacity
• Minor fissure displaced upward on frontal
• Major fissure displaced anteriorly on lateral
• Right hemidiaphragm, hilum elevated
• If central mass, convex bulge in medial aspect of fissure
• Hyperaeration of RML and RLL is typical
– LUL
• Looks different than RUL b/c no minor fissure
• Hazy density silhouettes upper left heart border on frontal
• May be periaortic lucency due to compensatory hyperinflation of LLL
• Leftward tracheal shift and elevated left hemidiaphragm and hilum
• On lateral view, major fissure is shifted anteriorly parallel to sternum
• Lobar atelectasis (cont.)
– RML
• Best seen on lateral view
• Triangular opacity over heart with depression of minor fissure and elevation of
major fissure
• On frontal, hazy density silhouetting right heart border
• An apical lordotic view is helpful
– Lower lobes
• Similar on both sides
• Both collapse posteromedial and inferior
• On lateral, upper half of major fissure swings down and lower half swings back
• On frontal, silhouetting of medial hemidiaphragm and on lateral, silhouetting of
posterior hemidiaphragm
• Heart shifted toward collapsed side and hilum is depressed
• Causes of lobar collapse
– Tumor (extrinsic compression, intrinsic):
bronchogenic carcinoma, carcinoid
– Mucous plugging
– Foreign body
– Broncholith (TB)
– RML syndrome
– Compressive atelectasis
RLL Collapse
RML/RLL Collapse
LLL Collapse
 Asbestos-related Pleural Disease
• Pleural plaques
– MC manifestation of asbestos exposure
– Asymptomatic
– Usually bilateral, more prominent in lower lobes
– Veil-like opacities when seen en face
– Calcification common
– Apices and CP angles spared
• Diffuse pleural thickening
– Smooth and does involve CP angles
– Involves visceral pleura and lung parenchyma
– Must measure 8 cm craniocaudal, 5 cm wide, and 3 mm thick
• Rounded atelectasis
– Round sharply-marginated lung mass abutting pleura
– Volume loss, ipsilateral pleural disease (plaque, thickening, effusion), broad area of
pleural contact, comet tail sign (swirling vessels)
– Usually at bases
– Need follow up CT to exclude CA
Calcified Pleural Plaques
Rounded Atelectasis
Rounded Atelectasis
 Transposition of the Great Vessels
• D-type
– Ao arises from RV and PA from LV
– Must have shunt (ASD > PDA, VSD) to survive
– Cyanotic
– XR
• Narrow mediastinum due to thymic involution and abnormal
relationship of aorta and pulmonary artery
• Large heart, predominantly right-sided
• Above findings produce egg-on-a-string appearance
• Increased pulmonary blood flow
– Angio
• Right-sided injection fills aorta
• Left-sided injection fills PA
– Tx: Jatene procedure, an arterial switch with reimplantation of
coronaries
• L- type
– Congenitally corrected transposition
– Morphologic (smooth) LV on right side serving as RV
– Morphologic RV (trabeculated) on left, serving as LV
– Assoc w/complex congenital heart disease
– XR
• Absence of normal ascending Ao contour b/c the relationship of PA to
Ao is abnormal, with Ao lying anterior and to left of PA
• See ascending Ao along the left heart border
– Angio
• Smooth ventricle supplies pulmonary artery
• Trabeculated ventricle supplies Ao
 Posterior Mediastinal Mass
(Ganglioneuroma)
• Clues to posterior mediastinal location
– Displacement of paraspinal lines, azygoesophageal line
– Does not obscure heart border, hilum
– Rib spreading or posterior rib erosion
– On lateral, projects over vertebral bodies and may be difficult to see
• DDx posterior mediastinal mass
– Neurogenic (MC): sympathetic chain (ganglioneuroma,
ganglioneuroblastoma, neuroblastoma), peripheral nerves (schwannoma,
neurofibroma), paraganglia
– Vertebral body-related: trauma, infection, tumor
– Vascular
– Esophageal (can be posterior or middle)
– Lymph nodes
– Neurenteric cyst
– Bochdalek hernia
– Extramedullary hematopoiesis
Extramedullary Hematopoiesis
Extramedullary Hematopoiesis
• Neurogenic tumors
– Usually vertical, fusiform paravertebral masses +/-
vertebral body erosion and paraspinal extension
– MR: slightly higher than muscle on T1, very bright on
T2, homogeneous enhancement
Neurofibroma
Neurofibroma
Neurofibroma
 Bronchogenic Cyst
• Clues to middle mediastinal location
– On frontal, mass effect on trachea, widened paratracheal stripe,
silhouetting of pulmonary artery
– On lateral overlies heart and great vessels
• DDx middle mediastinal mass
– Lymph nodes (MC): lymphoma, mets, sarcoid
– Vascular
– Pericardial cyst
– Bronchogenic cyst
– Tracheobronchial tumors
Vascular: Brachiocephalic Artery
Aneurysm
• Bronchogenic cyst
– Arise from primitive foregut
– Usually asymptomatic, although may compress structures or
become secondarily infected
– Classic location is subcarinal (next, right paratracheal)
– Usually smooth, round, homogeneous with very thin wall
– Air-fluid level when infected
– CT: fluid density, but often higher due to protein, hemorrhage,
mucin
– MR: T1 dark or bright for same reason, bright on T2
– Ca+ uncommon, but can occur in the wall
Pulmonary Bronchogenic Cyst
 Constrictive Pericarditis
• Thickening of pericardium which restricts
diastolic filling
• Causes: infection (TB), uremia, prior heart
surgery, radiation, hemorrhage
• DDx: restrictive cardiomyopathy (no Ca+ or
pericardial thickening)
• XR
– Eggshell Ca+ around margin of heart, spares LA b/c
pericardium does not extend posteriorly
– Tends to spare apex (distinguish from Ca+ aneurysm)
– Dilation of pulmonary veins and SVC/IVC, pulmonary edema,
with cephalization
– Left and right atria may both be enlarged
• MR
– Pericardial thickening > 4 mm
– Biatrial enlargement and distension of veins
Constrictive Pericarditis
Constrictive Pericarditis
 Ventricular Aneurysm (True)
• True aneurysms
– Usually post transmural MI
– May throw emboli, but rarely rupture
– XR
• Smooth bulge along left heart border on frontal +/- curvilinear rim
Ca+
• On lateral, bulge usually projects over heart (not behind it) b/c
they are anterolaterally located
– Angio: filling of aneurysm, dyskinesis
– CT: may show Ca+ aneurysm +/- thrombus
– MR: myocardial thinning, dyskinesis
• False aneurysms
– LV ruptures contained by pericardium or extracardiac
tissues  risk of rupture
– Usually posterolateral or at diaphragmatic wall
– XR: left retrocardiac double density, and on lateral
involves the posterior surface
– Angio: neck usually smaller than true aneurysm, often
delayed filling, delayed emptying
– MR: may have abnormal signal due to slow flow or
thrombus
False Ventricular Aneurysm
False Ventricular Aneurysm
False Ventricular Aneurysm
 Wegener Granulomatosis
• Lung involvement in 85%
• Findings
– Nodules, nodules w/cavitation, diffuse opacity
– Airway stenosis
• c-ANCA Ab positive in > 90%
• DDx cavitary lung lesion(s)
– Neoplastic: primary SCC, adenoCA, BAC, mets esp
from SCC
– Infectious: TB, fungus, bacterial from gram negatives
or staph, parasitic, papillomatosis
– Collagen vascular: Wegener
– Vascular: septic emboli, infarct
– Trauma
• Cavity wall thickness (thickest part)
– < 5 mm: 92% benign
– 5-15 mm: indeterminate (51% benign, 49%
malignant)
– > 15 mm: 95% malignant
Mycobacterial Infection
Squamous Cell CA
Septic Emboli
Papillomatosis, SCC
 Pneumothorax, Supine
• Most supine pts do not have visible visceral pleural line
• May just have hyperlucency of hemithorax, deep sulcus sign
• Air commonly accumulates medially  sharpening of mediastinal
borders and improved visualization of cardiac margin and aortic
knob
• Air may accumulate subpulmonic  sharply outlined
hemidiaphragm
• Air rarely collects posteromedially  medial lucent triangle
• Double diaphragm: lung outlines dome and air outlines the
anterior costophrenic sulcus
• Decubitus or upright XR to confirm
 Malpositioned
Lines/Tubes/Catheters
• Range from variant anatomy to true medical
screw ups
• Examples
– Swan-Ganz in left SVC: left SVC  coronary sinus
 RA  RV  PA
– Ao balloon pump tip perforation
– Malpositioned pacemaker leads
– Mediastinal hematoma from malpositioned line
Aortic Balloon Pump w/Dissection
 Pulmonic Valvular Stenosis
• Mostly congenital, rarely acquired in carcinoid
syndrome
• Findings
– Dilated main and left PA, normal-sized right PA
– NO shunt vascularity
– RV usually mildly enlarged
Pulmonic Stenosis
 Ascending Aortic Aneurysm
• DDx dilated ascending aorta on XR
– Aneurysm, dissection, poststenotic dilation related to aortic stenosis, and proximal
to a coarctation or other cause of aortic narrowing
• Aneurysm causes: Marfan, syphilis, Takayasu, atherosclerotic, trauma
• Marfan: sinotubular ectasia with tulip bulb appearance, related to cystic medial
necrosis
• Syphilis: saccular (like most infectious aneurysms), spares aortic root
• Takayasu: aneurysm + stenoses
• Atherosclerotic: fusiform +/- thrombus
• Tx: surgery when > 5.5 cm, enlarging > 1 cm/y, or symptomatic (> 5 cm in
Marfan)
 Solitary Pulmonary Nodule
• Well-defined round or oval lesion < 3 cm
• 50% lung CA, 40% benign, 10% solitary mets
• Get old films  stable for 2 y = benign
• If no priors, get CT to look for fat or Ca+
– Fat = hamartoma
– CT can also evaluate AVM, mycetoma, round atelectasis,
mucoid impaction
• Benign Ca+ patterns: diffuse, central, laminar, popcorn
• Indeterminate: no Ca+, stippled or eccentric Ca+
– Requires further workup  PET  bx
• Ca+ pitfalls
– Carcinoid tumors often calcify
– Metastatic sarcomas (particularly osteogenic) may
calcify densely
– If significant noncalcified soft tissue component
present (> 90%), SPN cannot be assumed benign
Pulmonary Hamartoma
Giant Pulmonary Hamartoma
Management of SPN
• Biopsy
– Central endobronchial: bronchoscopic
– Most others: percutaneous CT-guided
– FNA sensitivity for primary/metastatic CA > 90%
– Core bx may be needed for dx of thymoma,
lymphoma
– Complications: PTX (25%; of pts w/PTX, 25%
require chest tube), minor hemoptysis (common), air
embolism, significant pulmonary hemorrhage (rare)
 Descending TAA
• Causes: atherosclerotic (MC; fusiform +/- thrombus &
Ca+), trauma (pseudoaneurysm), mycotic (saccular),
dissection
• Degenerative thoracic aneurysms have a low risk of
rupture if < 5 cm, with risk increasing after 5 cm
• Usually repaired if > 6.5 cm (risk of rupture > surgical
risk), enlarging > 1 cm/y, or symptomatic (> 6 cm in
Marfan)
• Rupture on CT produces mediastinal hematoma +/-
contrast extravasation
• Impending rupture produces high density crescent sign
within aortic thrombus or between thrombus and aortic
wall
Impending AAA Rupture
 Atrial Myxoma
• DDx intracardiac mass
– Thrombus (MC in adults)
– Benign tumors: myxoma, lipoma, rhabdomyoma,
papillary fibroelastoma
– Metastatic disease (second MC in adults)
– Malignant primary tumors: angiosarcoma,
mesothelioma, fibrosarcoma, leiomyosarcoma
• Benign tumors tend to be well circumscribed
whereas malignant are large and infiltrative, with
broad attachment and pericardial effusion, and
intense enhancement
• Atrial myxoma
– Benign mass arising in atria, left > right
– Usually from interatrial septum, attached by narrow pedicle
– Dumbell myxoma: grows through fossa ovalis to other atrium
– 10% calcified
– MR: iso or slightly hyperintense on T1 and T2 to myocardium
– Enhance with contrast
– Sxs of mitral stenosis or fever, anemia, elevated ESR
– May embolize and cause strokes
• Thrombus: brighter on T1, dark on T2, GRE, no enhancement
• Lipoma: fat on all sequences, fat saturation helpful, right atrium >
left
 Mitral Regurgitation
• Similar appearance to mitral stenosis, with
cephalized pulmonary vessels, and enlarged left
atrium and atrial appendage
• Also LV enlargement
• Causes: MI with papillary muscle rupture, mitral
valve prolapse, rheumatic heart disease
 Pulmonary Hemorrhage
(Goodpasture Syndrome)
• DDx consolidation
– Acute: edema/ARDS, hemorrhage, PNA/aspiration
– Chronic
• Tumors: BAC, lymphoma
• Inflammation: TB/fungus, chronic eosinophilic PNA, COP,
alveolar sarcoid
• Alveolar proteinosis
• Lipoid PNA
• Chronic aspiration
BAC
Lipoid Pneumonia
 Tetralogy of Fallot
• Cyanotic, ↓ pulmonary flow, normal to mildly large heart
• 4 features: VSD, pulmonary infundibular stenosis, RV
hypertrophy, overriding aorta
• XR
– Concave main PA and upturned cardiac apex (from RVH)  boot-shaped
heart
– ↓ Pulmonary vascularity
– Frequently right aortic arch (deviates trachea toward left)
• MC type of right arch in TOF is mirror image branching
• Isolated left subclavian type (LSA arises from left PA) highest assoc w/TOF
• Tx: VSD closure, widening RVOT (temporary fix is the Blalock-
Taussig shunt to get blood to the lungs)
 Superior Sulcus (Pancoast) Tumor
• Bronchogenic CA at extreme lung apex
• Lung cancers that invade chest wall = T3
– Invasion of vertebral body or neural foramen = T4
– Subclavian artery, brachial plexus, vertebral body involvement
= unresectable
• Pain in shoulder or arm, weakness and atrophy of
muscles of the hand, Horner syndrome, bone destruction
• XR: apical cap, apical mass, or bone destruction
• MR: best for staging
Pancoast Tumor
Pancoast Tumor
Pancoast Tumor
 RML + RLL Atelectasis
• Occurs w/obstruction of bronchus intermedius
• Findings
– Major and minor fissures displaced downward and backward
– On frontal, obliteration of right hemidiaphragm as well as right
heart border
– Opacity is triangular, sharply marginated superiorly by
depressed minor fissure
– Ipsilateral cardiac and mediastinal shift is common
 Aspergilloma (Mycetoma)
• 4 forms of aspergillosis: aspergilloma, semi-invasive aspergillosis,
invasive aspergillosis, allergic bronchopulmonary aspergillosis
• Aspergilloma
– Normal immune status
– Fungus ball in a pre-existing cavity, cyst, or bulla
– Seen in assoc w/TB, sarcoid, CF  upper lobes
– XR: round opacity within a cyst or cavity, often a crescent of air b/w
fungus ball and cavity (Monad sign)
– Fungus ball usually mobile, shifting with changes in body position
– DDx: cavitating squamous cell CA or abscess
– Tx: considered when symptomatic (usu hemoptysis)
• Surgical resection, oral (or intracavitary) antifungal, bronchial artery
embolization
Semi-Invasive Aspergillosis
• Semi-invasive
– Occurs in mildly immune suppressed such as
alcoholism, diabetes, chronic illness
– Starts as focal consolidation in apex
– Progresses to a cavity, initially thick-walled, later
thin-walled with fungus ball inside
– XR: can look like aspergilloma, upper lobe
consolidation, or thick-walled cavity
– Often has extensive associated pleural thickening
Invasive Aspergillosis
Invasive Aspergillosis
• Invasive
– Occurs in truly immune compromised such as AIDS,
transplant, steroids
– Invasive necrotizing pneumonia due to invasion of blood
vessels with accompanying pulmonary infarction
– XR: multiple nodular areas of peripheral subpleural
consolidation which frequently cavitate and may form air
crescents or masses with surrounding ground glass opacity due
to hemorrhage (“CT halo” sign)
ABPA
ABPA
ABPA (High Attenuation Mucoid Impaction)
• ABPA
– Occurs only in asthmatics
– Blood eosinophilia and elevated IgE
– XR: mucoid impaction in central and upper lobe
bronchi (finger-in-glove pattern)
– As mucus plugs clear, residual central bronchiectasis
– Tx: steroids
 Bronchiectasis (Cystic Fibrosis)
• Abnormal permanent dilation of bronchi
• 3 types: cylindrical, varicose, cystic
• HRCT: key feature is bronchial diameter > accompanying artery
(signet ring)
• Causes
– Infection (MC): TB, viral, or chronic bacterial, or recurrent aspiration
– Cystic fibrosis (hyperinflation, upper lobe bronchiectasis, mucous
plugging, prominent hila)
– ABPA
– Immune deficiency in agammaglobulinemia or CGD of childhood
– Williams-Campbell, Mounier-Kuhn
– Dysmotile cilia or Kartagener (sinusitis, bronchiectasis, situs inversus)
– Pulmonary fibrosis from sarcoid, radiation, UIP (traction bronchiectasis)
Mounier-Kuhn
Kartagener
Morgagni Hernia
• DDx cardiophrenic angle mass (“LMNoP”)
– Lipoma/fat pad
– Morgagni hernia
– Nodes
– Pericardial cyst
• Pericardial cyst
– Attached to parietal pericardium, do not communicate w/pericardial space
– Smooth, well-defined oval or round
– R > L cardiophrenic angle
– CT: usually fluid density
– MR: bright T2, variable T1 depending on contents
• Lipoma and pericardial fat pad
– Similar appearance on XR
– Usually more lucent than pericardial cyst
– CT is diagnostic showing fat
• Morgagni hernia
– Appearance varies depending on hernia contents (omentum, liver, colon)
• Epicardial nodes
– Enlarged nodes almost always malignant, due to lymphoma or mets
– Common site of recurrence in Hodgkin following radiation
 Congenital Heart Disease
Nomenclature (van Praagh)
• Levoposition/levocardia: heart positioned in left hemithorax/apex left
• Dextroposition/dextrocardia: heart in right hemithorax/apex right
• Mesoposition/mesocardia: heart midline/apex midline
• Visceroatrial situs: SVC/IVC connection to atrium
– Solitus (S): morphologic RA on R connected to R-sided SVC/IVC, morphologic LA
on L, stomach/spleen on L, R liver > L liver, appendix on R, R lung trilobed, L lung
bilobed
– Inversus (I): stomach/spleen on R, L liver > R liver, appendix on L, L lung trilobed,
morphologic R atrium on L, SVC/IVC on L
– Ambiguous (A): lack of visceral sidedness, liver often midline, R/L isomerism
• Ventricular looping
– D (normal): morphologic RV to R and anterior to LV
– L: morphologic RV posterior and to L of LV
• Ventriculoarterial connections
– S (normal): LV  aorta, Ao valve posterior and R of PV
– D-TGV: Ao valve anterior and R of PV, RV  aorta, LV  PA
– L-TGV: Ao valve anterior and L of PV, RV  aorta, LV  PA
• Normal heart = [S,D,S]
 Nomenclature (Anderson)
• Atrioventricular connection types
– Concordant: morphologic RA to RV
– Discordant: morphologic RA to LV
– Ambiguous: atrial isomerism or situs ambiguous
– Double inlet: both atria connect to one ventricle
– Absent right connection or absent left connection: describe situation when
one AV connection is absent
• Ventriculoarterial connection
– Concordant: RV to PA, LV to Ao
– Discordant (i.e., transposition)
– Double outlet: both great arteries arise predominantly from a single
ventricle
– Single outlet: only one great artery is connected to the ventricle
• Single outlet-common arterial trunk
• Single outlet-solitary aortic trunk with pulmonary atresia
• Single outlet-solitary pulmonary trunk with aortic atresia
• Single outlet-solitary arterial trunk
 Pericardial Effusion
• Frontal XR: “water bottle”
• Lateral XR: sometimes nl pericardium visible
b/w epicardial and pericardial fat as a thin linear
opacity in retrosternal region
– If opacity > 4 mm  pericardial effusion
 Endotracheal Mass (SCC)
• In adults, 90% of primary tracheal tumors are malignant, 90%
benign in peds
• Benign tumors
– Tend to be focal, well defined, smooth, or lobulated
– No mediastinal invasion or adenopathy
– Ex: hemangioma, papilloma, hamartoma, lipoma, chondroma, fibroma,
granular cell myoblastoma
• Malignant tumors
– Intraluminal mass or circumferential tracheal wall thickening with direct
invasion of mediastinum and adenopathy
– Ex: squamous cell CA, adenoid cystic CA, secondary involvement by
esophageal or thyroid CA, mucoepidermoid CA, carcinoid, adenoCA,
lymphoma, small cell CA, mets (melanoma, breast, RCC)
Papillomatosis
Adenoid Cystic Carcinoma
Adenoid Cystic Carcinoma
Carcinoid
 Endobronchial Mass
• Recurrent or persistent atelectasis in an adult is
suspicious
• Similar DDx as endotracheal mass
Mucoepidermoid Carcinoma
Endobronchial Metastasis
 Ventricular Septal Defect
• Findings
– Pulmonary arteries enlarged with shunt vascularity
– LA enlargement (double density on frontal and
prominent posterior heart border on lateral)
– Biventricular enlargement (large left heart border on
frontal and filling of retrosternal space on lateral)
 Ebstein Anomaly
• Malposition of septal and posterior leaflets of tricuspid valve
 severe tricuspid insufficiency
• Large portion of RV lies above the valve, within the RA
(“atrialized”)
• XR: decreased pulmonary blood flow (severe TR and R to L
shunt via ASD), small PAs, huge heart due to enlarged RA/RV
• DDx cyanotic with decreased pulmonary flow
– Pulmonary atresia with intact septum (also cardiomegaly and
oligemia)
– TOF, pulmonary atresia with VSD (heart not as large)
Ebstein Anomaly
Ebstein Anomaly
 Partial Absence of the Pericardium

• Most pericardial defects are partial and occur over

left atrial appendage and adjacent pulmonary artery
• 20% have assoc abnormalities (ASD, PDA, TOF,
bronchogenic cysts, sequestration)
• Risk of strangulation of portion of heart protruding
through defect
• XR: abnl convexity b/w PA and left atrial
appendage, concave AP window
Congenital Absence of the Pericardium
Congenital Absence of the Pericardium
 Sarcoidosis (Stage II)
• DDx bilateral hilar adenopathy
– Sarcoidosis: symmetric, bilateral hilar/paratracheal
– Lymphoma: asymmetric, other nodal stations
– Mets
– Infections: TB, fungal
– Castleman: enhance intensely on CECT
– Angioimmunoblastic lymphadenopathy: HSM, adenopathy
(hypervascular), skin rash, hemolytic anemia,
hypergammaglobulinemia
• Pts get lymphomas and PCP due to immunodeficiency
Sarcoidosis (Stage I)
Sarcoidosis (Stage III)
Sarcoidosis (Stage IV)
Sarcoidosis
Sarcoidosis
DDx: Berylliosis
 Complete Lung Atelectasis
• Findings
– Completely opaque hemithorax with ipsilateral shift
of heart and mediastinum
– Compensatory hyperinflation of contralateral side,
which crosses over midline, especially anteriorly,
producing large retrosternal space on lateral
• DDx: prior pneumonectomy, pulmonary agenesis
 Zenker Diverticulum
• XR
– Retroesophageal superior mediastinal mass containing
an air-fluid level (on upright)
– Best seen on lateral esophagram extending posteriorly
at the C5/6 level
– On frontal, it protrudes laterally (usually left) when it
is large
Zenker Diverticulum
 Neurofibromatosis, Type 1
• XR
– Multiple spherical paravertebral masses which may erode ribs,
widen rib spaces, and widen neuroforamina
– On lateral, look for posterior vertebral body scalloping and wide
neural foramina
– Can arise from intercostal nerves  multiple pleural-based
opacities with ribbon ribs
– Upper lobe cystic and bullous disease, lower lobe fibrosis
– Kyphoscoliosis
• NCCT: neurofibromas homogeneous or heterogeneous, with
punctate Ca+ in 10%
• MR: low to intermediate T1 and high T2
NF 1
NF 1
NF 1
 Pneumomediastinum
• Causes
– Lung: alveolar rupture, usually from asthma, but also from mechanical ventilation
or pneumothorax, with air dissecting into mediastinum via interstitium
– Trauma: tracheal or esophageal rupture, pneumothorax, iatrogenic (endoscopy,
surgery)
– Abdomen: pneumoperitoneum or pneumoretroperitoneum extending to
mediastinum
• XR
– Linear lucency extending from aortic knob down left heart border
– Continuous diaphragm sign underlying the cardiac silhouette
– Outlining of descending aorta and pulmonary arteries
– Subcutaneous emphysema
– Air may also outline SVC and great vessels
– Decubitus: pneumomediastinum does not change
• Esophageal perforation
– Air next to esophagus
– +/- Abscess
– Leak on water soluble esophagram
– Left effusion and mediastinal widening
• Tracheobronchial injury
– Persistent, severe pneumomediastinum, subcutaneous
emphysema and PTX
– Does not resolve with chest tube placement
– Fallen lung sign: lung falls inferolateral instead of the usual
medial collapse
– Ectopic ETT or balloon cuff
Pneumopericardium
Pneumocardia
Pneumoperitoneum
 SVC Syndrome
(Fibrosing Mediastinitis)
• Causes
– Malignancy, mediastinal fibrosis from histoplasmosis, catheter-related
thrombosis
• Facial & neck swelling, cyanosis, venous distension, SOB, HA,
and hoarseness
• May be life threatening if untreated due to laryngeal edema or
CNS congestion
• CT/MR: SVC stenosis, thrombosis, occlusion, cause (mass of
tumor or calcified nodes in histoplasmosis with fibrosing
mediastinitis)
• Angio: narrowing/luminal effacement, collateral flow
• Tx: emergent radiation or chemo (if due to malignancy),
percutaneous thrombolysis, balloon angioplasty, stent (large
wallstent, 16 mm)
 Mediastinitis
• Infection
• Fibrosing mediastinitis
– Deposition of fibrous tissue, collagen
– MC due to histoplasmosis
– Encases and obliterates vessels, airway, esophagus
– Infiltrative
– Frequently calcifies
 Pulmonary AVM
• Simple (80%; one feeding artery, one draining
vein) or complex (20%; 2 or more feeding
arteries, 2 or more draining veins)
• 70% have Osler-Weber-Rendu, a syndrome of
cutaneous and mucosal telangiectasias and
AVMs in other organs
• R to L shunt, which may lead to stroke, brain
abscess, cyanosis
• Favors lower lungs
• XR
– Single or multiple nodules, typically in medial third of
lung
– Feeding artery often seen as dilated vessel originating
in hilum, and draining vein heading toward left atrium
• CT: enhancing feeding and draining vessels
• Angio: feeding and draining veins and nidus
• Tx: coils (1-2 mm larger than artery being
embolized) placed proximal to nidus or glue
 Tuberculous Empyema, Fibrothorax
• Empyema
– XR: loculated lenticular collection, forms obtuse angles with chest wall,
does not change with pt positioning, air-fluid level if bronchopleural fistula
– CT: split pleura sign (enhancement of both visceral and parietal pleura
around loculated effusion), increased adjacent extrapleural fat
• Fibrothorax
– Circumferential pleural thickening causing decreased lung volume
– Causes: TB, hemorrhagic effusion, pyogenic empyema, asbestos,
malignancy (mesothelioma, metastatic adenoCA)
– When Ca+, TB is almost always the cause (NOT asbestos, the fibrothorax
of asbestos does not calcify)
– Malignancy is lumpy/nodular/masslike, circumferential, > 1 cm thick
Empyema
 Truncus Arteriosus
• 4 MC CHD with right arch: truncus arteriosus, TOF, transposition,
tricuspid atresia
– Of these, only truncus and transposition routinely have increased
pulmonary flow
– Tricuspid atresia can but it is variable
• Truncus arteriosus
– Single vessel arising from heart giving rise to systemic, pulmonary and
coronary circulation
– ALWAYS an associated VSD
– Subtypes based on origin of PA from truncus
– 1/3 have right sided arch
– XR: increased pulmonary flow, right arch, cardiomegaly (biventricular)
• Although pulmonary flow is increased, main pulmonary artery area is often
concave b/c PA is not arising in its normal location from the RVOT
Right Arch w/Mirror Image Branching
 Intracardiac Lipoma
• Findings
– Bright on T1 and bright on FSE T2, dark on FS and
no enhancement
– More common in the right atrium
Double Aortic Arch
 Pulmonary Contusion
• Usually evident on XR by 6 h post trauma
• Clears rapidly, within 72 h
• XR: usually nonsegmental, homogeneous
opacities, frequently peripheral in location, +/-
associated fractures
• If parenchymal opacity does not resolve post
trauma, consider pneumonia, ARDS, or
pulmonary edema
 Mitral Valve Replacement
• Indications: symptomatic CHF with mitral stenosis or insufficiency,
deteriorating LV function indices (EF) with mild or moderate symptoms
• Mechanical
– St Jude: bileaflet configuration
– Bjork-Shiley: tilting disk
– Starr-Edwards: caged ball
• Bioprosthetic
– Homograft from cadaver
– Porcine xenograft
• XR
– On lateral, valve projects posterior to line drawn connecting point where sternum
touches diaphragm anteriorly and tracheal bifurcation posteriorly
– On frontal, harder to distinguish different valves, but long axis of mitral valve will
parallel line drawn from right heart border through cardiac apex, whereas long axis
of an aortic valve is angled more toward the right neck
 Scimitar Syndrome
• AKA hypogenetic lung syndrome, congenital pulmonary
venolobar syndrome
• Hypoplasia of R lung, R PA, anomalous venous drainage of R
lung by single vein which runs inferiorly parallel to R heart border
to join IVC below diaphragm
• Usually systemic arterial supply to R lung off aorta
• XR
– Small R hemithorax with small R PA and decreased pulmonary vascularity
– Shift of heart and mediastinum to right
– Curvilinear opacity (scimitar vein) heading toward diaphragm
Scimitar Syndrome
 Pectus Excavatum
• Pectus deformities: excavatum and carinatum
• Excavatum
– Inward depression of sternum
– Assoc w/Marfan, Poland, OI, congenital scoliosis
– XR
• Leftward shift of heart and loss of right heart border
• Posterior ribs are horizontal and anterior ribs are vertical
• Lateral shows inward depression of sternum
• LV displaced posteriorly, even though heart is not enlarged
• Very narrow AP diameter of chest and loss of normal thoracic kyphosis
– CT
• Helps define deformity and effects on heart and mediastinal structures
• Carinatum
– Outward bowing
Pectus Carinatum
 RML Syndrome
• RML susceptible to chronic collapse secondary to prior
inflammatory episodes
• MC in children with a history of asthma or atopy
• XR: RML volume loss with tubular lucencies and tram tracking
• CT: RML bronchus patent but narrowed and bronchiectasis
present in collapsed RML
• May be asymptomatic or have recurrent pneumonias
• Chronic MAC infection produces similar findings
– Usually in elderly females with systemic symptoms such as weight loss,
and in pts with COPD, asthma, CF, steroid use, and AIDS
 Traumatic Diaphragmatic Rupture
• Assoc w/severe injury and high mortality due to assoc injuries
• Tear typically in central tendon or musculotendinous junction, and
70% are left-sided
• Delayed diagnosis  bowel strangulation and obstruction
• XR: NG tube coiled in hemithorax, apparent elevation of
hemidiaphragm with loss of normal contour, contralateral
mediastinal shift, pleural effusion
• UGI: can confirm, showing stomach above hemidiaphragm
• CT: can show abdominal contents above hemidiaphragm
• MR: better for localizing tear, especially sagittal images
 Unilateral Hyperlucent Lung
(Bronchogenic Cyst Compressing L Bronchus)

• DDx unilateral hyperlucent lung

– Poland
– Swyer-James
– Scimitar syndrome
– Bronchial atresia
– Congenital lobar emphysema
– Endobronchial foreign body
– Pulmonary artery agenesis
– Central masses
– Technical factors
Poland Syndrome
Swyer-James Syndrome
Bronchial Atresia
 Pleural Lipoma
• DDx: solitary fibrous tumor of pleura
• Get old films, and if not helpful, a CT
– Fat density = lipoma
– Soft tissue = probably biopsy or PET scan
 Solitary Fibrous Tumor of Pleura

• Circumscribed
• 1-40 cm
• Ca+ 7-26%
• Effusion 17-37%
• Usually enhances
• HPOA 1/3
• Hypoglycemia 5%
• MR: low T1, T2
• Malignant 7-60%
 Progressive Massive Fibrosis
• Occurs in complicated silicosis, endstage sarcoid
• Represents nodules that have become confluent, > 1 cm
• Appear in periphery of mid to upper lobes and migrate to hilum
– Leave emphysematous tissue between fibrotic tissue and pleural surface
• As masses become larger, there tends to be less nodules elsewhere
in the lung
• Ca+ nodes, especially eggshell, suggests silicosis and CWP
• Superimposed TB may occur (silicotuberculosis) (25%)
– Suggested by asymmetric nodules/consolidation, cavitation, rapid disease
progression
Silicosis
Silicotuberculosis
DDx: Sarcoidosis
 Paravertebral Abscess
• XR: posterior mediastinal mass, vertebral body lytic
changes, widening of paravertebral stripe
• Unlike other posterior mediastinal masses, vertebral
body related ones (infection, trauma, tumors) often
produce bilateral fusiform findings
• Disk space narrowing and endplate irregularity
• Pott disease may show paraspinal abscesses in the psoas
 Malignant Mesothelioma
• Mostly males w/remote exposure to asbestos
• CT
– Nodular, circumferential pleural thickening, involves mediastinal pleura, > 1 cm
thick, thick fissures, pleural effusion, loss of volume, pleural Ca+, invasion of
chest wall
– Distant mets uncommon, may spread to hilar and mediastinal nodes
– Unresectability: direct chest wall/mediastinal invasion, spread to contralateral
nodes/thorax, spread through diaphragm to abdomen
• MR
– Better for determining resectability
– Slightly high on T1 and moderately high T2
• Tx: extrapleural pneumonectomy
• DDx: pleural mets from lung, breast, ovary, stomach, melanoma;
invasive thymoma; lymphoma
 Chest Wall Mass (Plasmacytoma)
• DDx chest wall mass
– Skin lesions: mole, wart, melanoma
– Osseous lesions: fibrous dysplasia, plasmacytoma, chondrosarcoma,
osteosarcoma
– Benign tumors: lipoma (MC), desmoid, hemangioma, neurogenic
(schwannoma, neurofibroma)
– Malignant tumors: MFH, fibrosarcoma, liposarcoma, mets, lung CA
invading chest wall; peds: PNET (Askin tumor),
rhabdomyosarcoma, extraosseous Ewing
– Infections: primary chest wall (Staph, TB), lung infections invading
chest wall (TB, actinomycosis, nocardia)
– Trauma with hematoma
Actinomycosis
 Bronchopulmonary Sequestration

• Nonfunctioning lung segment

• Lung tissue lacks normal communication
w/tracheobronchial tree
• Systemic arterial supply
• MC left lower lobe
• Intralobar (MC): pulmonary venous return, contained
in visceral pleural of normal lung
• Extralobar: systemic venous return, own visceral
pleural envelope
Achalasia
 Azygous Continuation of the IVC

• XR: prominent azygous node/vein area (AKA

right tracheobronchial angle)
• CT: enlarged azygous vein, absence of
intrahepatic IVC
 Total Anomalous Pulmonary
Venous Return
• Type I: “snowman” heart on XR
• Type II: indistinguishable from ASD on XR
• Type III: small heart, reticular pattern in lungs (edema
on XR)
• Cardiomegaly (types I and II), small heart (type III)
• Shunt vascularity (types I and II), pulmonary edema
(type III)
• Wide mediastinum (type I, “snowman heart”), narrow
mediastinum (types II and III, thymic atrophy)
Supradiaphragmatic TAPVR
 Myocardial Infarction
• Delayed hyperenhancement on MR
• Always involves the subendocardium
– Most vulnerable because of distance from epicardial
coronary arteries
• Corresponds to coronary artery territories
Watershed Infarct
• Nonischemic causes of delayed
hyperenhancement
– Cardiomyopathies
• HCM: predominantly patchy rather than confluent, and
mainly localized to interventricular septum at sites of
attachment of right ventricle to left ventricle
• Dilated: patchy longitudinal mid wall or similar to ischemic
• ARVD: right ventricular wall
• Restrictive: idiopathic or secondary to radiation fibrosis,
amyloidosis, sarcoidosis, inborn errors of metabolism
– Trauma and post ablation
– Myocarditis
 Cardiac MR
• Single-shot double inversion fast spin-echo
– Double-IR FSE and HASTE (half-Fourier acquisition turbo spin-echo)
– Black blood
– Rapid morphologic imaging (breath hold not required)
– Standard orthogonal imaging planes (axial, sagittal, or coronal)
• Steady state free precession
– Bright blood
– Rapid acquisition (breath hold not required)
– Useful in evaluation of disorders producing intraluminal abnormalities
• Steady state free precession
– May be adapted for cine acquisition (multiple images obtained at a single slice location in rapid succession
during different phases of cardiac cycle)
– Allows evaluation of ventricular wall motion abnormalities, dynamic changes in wall thickness, and
measurement of chamber sizes
– Also allows assessment of valvular morphology and function
– Segmented (data from several heart beats combined to yield the image), retrospectively gated acquisition
• If arrhythmia  prospective gating
• If gating unsuccessful  real-time cine acquisition (single-shot rather than segmented)
• Perfusion imaging
– Saturation recovery gradient-recalled echo + gadolinium
– Most often used for detection of obstructive coronary artery disease, where
it is performed with pharmacological vasodilation (similar to nuclear
myocardial perfusion imaging)
• Viability imaging
– Contrast will washout of normal myocardium at a much more rapid rate than it will from infarcted or scarred myocardium
– Areas of prior infarction will have higher concentrations of contrast on delayed images (5 to 10 min after intravenous
administration)
– Segmented gradient echo read-out and an inversion prepulse (null normal myocardium)
– Approximately 8 to 12 s acquisition (breath hold required)
• If arrhythmia, difficulty breath holding  SSFP inversion recovery
– Assessment of myocardial infarction and viability, detection of viral myocarditis, identification of cardiac involvement by
sarcoidosis, and differentiation of ischemic from non-ischemic cardiomyopathy
• Flow-sensitive imaging
– Velocity-encoding sequences
– Sequential application of bipolar magnetic field gradients
• Opposed gradients produce a phase shift with the first pulse that will be reversed by the second pulse
• Stationary spins acquire equal and opposite phases in the two gradients, and have no net phase at the end of the sequence
• Flowing spins acquire a net phase change, which is dependent on their velocity in the direction of the flow-encoding gradients
– Maximum velocity encoded by the sequence is termed the Venc
– Used for quantification of gradients across stenotic valves, and for measurement of blood flow
• MR angiography
– Thin section T1-weighted spoiled gradient-echo image acquisitions during
the arterial passage of intravenously administered contrast
– Thin slices are obtained in a 3-D volumetric technique, and are then
assembled into maximum intensity projection images, as well as volume
rendered images
Left Atrial Appendage Thrombus
 Coronary Artery Aneurysm
• Kawasaki disease MC cause worldwide
• Atherosclerotic disease MC cause in US
• MC RCA followed by LAD
Coronary Artery Aneurysm
CABG Pseudoaneurysm
 Bronchopleural Fistula
• Complication of thoracic surgery
• Postpneumonectomy space normally fills 2 rib
spaces per day
• MC cause of death is aspiration pneumonia with
subsequent ARDS
• More common after R pneumonectomy
• Other causes: trauma, lung necrosis, airways
disease, malignancy
 Mediastinal Lipomatosis
• Causes: Cushing syndrome, exogenous steroids,
obesity
• Typically involves superior mediastinum
• XR: mediastinal widening
• CT: confirms fat
10-day follow up normal
 Simple Pulmonary Eosinophilia
(Loeffler Syndrome)
• Characterized by migrating, peripheral, nonsegmental
pulmonary opacities (consolidation), increased
peripheral blood eosinophils, minimal or no pulmonary
symptoms, and spontaneous resolution within 1 m
• Causes: idiopathic, parasites, ABPA, drugs
• DDx migratory pulmonary opacities: pulmonary
hemorrhage, vasculitis, COP, recurrent aspiration
Loeffler Syndrome
 Acute Eosinophilic Pneumonia
• Diagnostic criteria
– Acute febrile illness of < 5 d duration
– Hypoxemia
– Diffuse alveolar or mixed alveolar-interstitial opacities on CXR
– BAL fluid > 25% eosinophils
– Absence of parasitic, fungal, or other infection
– Prompt and complete response to corticosteroids
– No relapse after discontinuation of corticosteroids
• DDx: hydrostatic pulmonary edema, ARDS, AIP, atypical
bacterial or viral pneumonia
Acute Eosinophilic Pneumonia
 Chronic Eosinophilic Pneumonia

• Idiopathic condition
• Middle aged, ~50% have asthma
• Women > men
• XR
– Nonsegmental peripheral airspace consolidation (“photographic
negative of pulmonary edema”)
– Mainly upper lobes
• CT
– Nonsegmental areas of airspace consolidation with peripheral
predominance
– Pleural effusion in < 10%
• DDx: COP, Churg-Strauss syndrome, Loeffler
syndrome
Chronic Eosinophilic Pneumonia
Chronic Eosinophilic Pneumonia
 Pulmonary Alveolar Proteinosis
• Air spaces and septa fill with phospholipoprotein derived from
surfactant
• May be assoc w/myeloproliferative disorders
• Similar syndrome caused by inhalation of silica dust
• Tx: bronchoalveolar lavage
• DDx crazy paving pattern
– Pulmonary edema
– Pneumonia (lipoid)
– Alveolar hemorrhage
– Diffuse alveolar damage
– Lymphangitic carcinomatosis
Lipoid Pneumonia
 Bronchioloalveolar Carcinoma
• Subtype of adenocarcinoma
• Characterized by growth along preexisting
bronchiolar and alveolar walls (“lepidic growth”)
without invasion or distortion
• Localized: solitary pulmonary nodule or focal area
of ground-glass opacity on CT
• Diffuse (multifocal or transbronchial spread):
airspace opacification simulating pneumonia or
diffuse bilateral nodular airspace opacities
Diffuse BAC
BAC
BAC
BAC
 MAI (Nonclassic;
Lady Windermere Syndrome)
• Nontuberculous mycobacteria
• Variable findings: consolidation, cavitation, fibrosis, nodules,
bronchiectasis, adenopathy
• Five distinct clinicoradiologic manifestations
– Classic infection: similar to active TB
– Nonclassic infection: bronchiectasis, centrilobular nodules in lingula, RML
– Nodules in asymptomatic pts
– Infection in pts with achalasia: confluent consolidation, resembles
aspiration
– Infection in immunocompromised pts: mediastinal/hilar adenopathy
 Kaposi Sarcoma
• AIDS-related
• Chronic cough, dyspnea, fever, hemoptysis
• XR
– Middle to lower lung reticular opacities and
parenchymal nodules w/bronchovascular distribution
– May progress to consolidation, peribronchial cuffing,
Kerley B lines, pleural collections, hilar or
mediastinal adenopathy
• CT
– Bilateral and symmetric ill-defined nodules in a
peribronchovascular distribution (flame-shaped lesions),
usually exceeding 1 cm in diameter
– Ground-glass opacities may be seen surrounding the
nodules (“halo sign”)
– Peribronchovascular and interlobular septal thickening,
fissural nodularity, adenopathy, pleural effusions
– Less common: asymmetric distribution of nodules,
larger masses
Kaposi Sarcoma
Kaposi Sarcoma
 Apical Lung Herniation
• Most are right-sided
• DDx: pharyngocele, laryngocele, tracheal or
esophageal diverticulum
Tracheal Diverticulum
 Tracheal Stenosis
• DDx focal tracheal/bronchial stenosis
– Intubation, tracheostomy
– Wegener (focal or diffuse)
– Sarcoidosis (subglottic, thick-walled)
– TB/fungal, broncholith
– Compression by tumor
Histoplasmosis
• DDx longer segment tracheal/bronchial stenosis
– Relapsing polychondritis (wall thickening)
– Tracheobronchial amyloidosis (diffuse or multifocal)
– Tracheobronchopathia osteochondroplastica
Relapsing Polychondritis
Amyloidosis (Tracheobronchial)
Tracheobronchopathia
Osteochondroplastica
Acute
Subacute
Subacute
Chronic
 Hypersensitivity Pneumonitis
• Acute, subacute, and chronic forms
• Secondary to inhalation and sensitization to
chemical antigens
• DDx acute: hemorrhage, edema, pneumonia
• DDx subacute: RB-ILD
• DDx chronic: sarcoid
DDx: RB-ILD
 Pneumocystis Pneumonia
• Opportunistic fungal infection often affecting individuals with T-
cell immunodeficiency
• Findings
– Ground-glass opacities that are perihilar or diffuse
– If untreated, evolves into consolidative appearance
– Concurrent upper lobe cysts, usually located in periphery in 30% of AIDS
pts
• Malaise, fever, dyspnea gradually worsening over 2-6 w
• Hypoxia on room air very common
• At risk for other immunosuppression-related infections or
neoplasms
Pneumocystis Pneumonia
Pneumocystis Pneumonia
Pneumocystis Pneumonia
 Radiation-induced Lung Disease

• Typical timeline (rule of 4’s)

– 4 w to deliver therapy of 40 Gy
– 4 w after end of tx is earliest radiation pneumonitis:
indistinct vessel margins
– 4 m after end of tx is peak radiation pneumonitis:
consolidation
– 12 (4 x 3) m after end of tx: after peak pneumonitis,
consolidation gradually clears & evolves into scar
(cicatricial atelectasis)
– Scarring produces progressive volume loss
 Emphysema
• Centrilobular
– Common, associated with smoking
– HRCT: centrilobular or spotty lucencies, walls not usually visible
– Upper lobe predominance
• Panlobular
– Uncommon
– Alpha-1-antitrypsin deficiency, smokers, IV methylphenidate
(Ritalin)
– HRCT: large lung volumes, low attenuation, small pulmonary
vessels, focal lucencies usually absent, diffuse or lower lobe
predominance
• Paraseptal
– Common, isolated or assoc w/centrilobular
– Spontaneous PTX
– HRCT: subpleural lucencies, marginated by
interlobular septa, bulla (> 1 cm)
– Upper lobe predominance
Alpha-1-Antitrypsin Deficiency
Panlobular Emphysema
Panlobular Emphysema
Panlobular Emphysema
w/Left Lung Transplant
IV Ritalin
IV Ritalin
Paraseptal Emphysema
Inspiration

Expiration
Mosaic Attenuation (Postinfectious
Bronchiolitis)
• HRCT
• DDx
– Small airways disease (air trapping: lucent areas
accentuated on expiration)
• Bronchiolitis obliterans, asthma, hypersensitivity
pneumonitis
– Vascular disease (attenuated vessels in lucent areas,
no air trapping)
Chronic PE
• Causes of bronchiolitis obliterans
– Post-infectious
– Post-inhalational
– Collagen vascular disease
– GVHD
– Chronic lung transplant rejection
Bronchiolitis Obliterans
Lung Transplant Complications
 Pseudotumor
• Pleural collections
– Loculated, “pseudotumor”
– Exudative effusion
• Empyema, malignancy, asbestos
• Thickened, enhancing pleura
– Chylothorax
• Lymphoma, trauma, LAM
– Hemothorax
• Trauma, iatrogenic, tumor
Hemothorax
 Alveolar Microlithiasis
• Radiologic-clinical dissociation
• Etiology unknown
• Any age: predominates 20-50 y
• Findings: Ca+ micronodules (< 1 mm), reticular
pattern (“sandstorm”), black pleural line
(extrapleural fat and/or subpleural cysts)
• DDx: pulmonary ossification, metastatic Ca+,
amyloidosis
DDx: Pulmonary Ossification
(= Chronic Mitral Stenosis)
DDx: Metastatic Calcification
(Hypercalcemia, CRF)
 DDx: Amyloidosis
(Parenchymal Nodular)
 Patent Ductus Arteriosus
• Failure to close > 48 h
• 2 distinct presentations
– Premature infants: postnatal low O2 tension from
immature lungs  prevents ductus closure
– Term infants at 3 m
• F > M, 2:1
• XR: LAE, LVH, enlarged PA and aorta
• Tx: indomethacin, ligation (may need to keep open
with PGE in CHD)
 Arrhythmogenic RV Dysplasia
• Disease of fibrofatty replacement of RV, and
occasionally LV as well
• Ventricular arrhythmias and sudden death
• Tx: implantable cardioverter-defibrillator
• Findings
– RV dilatation and dysfunction, global and/or regional
– Fatty infiltration of the RV free wall (T1W spin-echo imaging
and fat-suppression techniques)
– Late Gd enhancement of RV myocardium may be seen
 Coronary Artery Anomalies
(Anomalous Origin of RCA)
• Anomalies of origin, course, and termination
• Anomalous origin of LCA or RCA from pulmonary
artery typically show symptoms early in infancy or
during early childhood
• Left and right coronary arteries can arise from
noncoronary sinus or opposite sinus
– 4 courses: retroaortic, prepulmonic, septal (beneath
RVOT), or interarterial (b/w aorta and pulmonary artery)
– Interarterial  high risk for sudden cardiac death
Anomalous Origin of LCA
 Acute Chest Syndrome
• Leading cause of death among pts with sickle cell
disease
• Chest pain, fever, prostration, pulmonary opacities
• Pneumonia and infarction implicated in the
pathogenesis
• Findings
– Patchy airspace disease in a segmental, lobar, or
multilobar distribution
 Amiodarone Toxicity
• Commonly used to treat refractory ventricular
tachyarrhythmias
• Pulmonary toxicity occurs in 5-10%
• Usually within months of starting therapy
• Risk increased if daily maintenance dose > 400
mg and if pt is elderly
• Prognosis is good, w/most improving after
discontinuation of therapy
• NSIP is MC manifestation
• A distinctive feature is occurrence of focal,
homogeneous pulmonary opacities
– Typically peripheral and of high attenuation
• Combination of high-attenuation abnormalities
within lung, liver, or spleen is characteristic
 Takotsubo Cardiomyopathy
• Mimics acute MI at clinical presentation
– Acute chest pain, dyspnea, ST elevation on EKG
• Cardiac catheterization: characteristic left ventricular wall-
motion pattern w/o obstructive atherosclerotic coronary
disease
• Left ventricle resembles an octopus-fishing pot (takotsubo)
at end-systolic ventriculography
• Most cases in postmenopausal women
• Acute emotional or physiological stressors generally
precede symptoms