CHEST RADIOLOGY

HRCT part I : Basic

Interpretation 1
HRCT part II: ILD
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Mediastinal Lymph Node
Stations 54
Mediastinal Masses
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Non-Small Cell Lungcancer
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Solitary pulmonary nodule
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Chest X-Ray - Heart Failure
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HRCT part I : Basic Interpretation

Robin Smithuis, Otto van Delden and Cornelia Schaefer-Prokop
Radiology Department of the Rijnland Hospital, Leiderdorp and the Academical Medical Centre, Amsterdam, the Netherlands
 Secondary lobule
 Reticular pattern back to overview print
 Nodular pattern Publicationdate 24-12-
 Algorithm for nodular pattern : 2006
In this article a practical approach is given for the interpretation of HRCT
 Tree-in-bud
examinations
 High Attenuation pattern
 Ground-glass opacity
We will discuss the following subjects:
 Mosaic attenuation
 Anatomy of the secondary lobule
 Crazy Paving
 Basic HRCT patterns
 Consolidation
 Distribution of abnormalities
 Low Attenuation pattern
 Differential diagnosis of interstitial lung diseases
 Emphysema
 Cystic lung disease
 Honeycombing In HRCT part II the most common HR-diagnoses will be discussed.
 Distribution within the lung
 Additional findings
 Differential diagnosis of interstitial lung diseases

Secondary lobule
 Secondary lobule
Knowledge of the lung anatomy is essential for understanding HRCT.
The secondary lobule is the basic anatomic unit of pulmonary structure
and function.
Interpretation of interstitial lung diseases is based on the type of
involvement of the secondary lobule.
It is the smallest lung unit that is surrounded by connective tissue septa.
It measures about 1-2 cm and is made up of 5-15 pulmonary acini, that
contain the alveoli for gas exchange.
The secondary lobule is supplied by a small bronchiole (terminal
bronchiole) in the center, that is parallelled by the centrilobular artery.
Pulmonary veins and lymphatics run in the periphery of the lobule within
the interlobular septa.
Under normal conditions only a few of these very thin septa will be seen.
Secundary lobules. The terminal bronchiole in the center divides into There are two lymphatic systems: a central network, that runs along the
respiratory bronchioli with acini that contain alveoli. bronchovascular bundle towards the centre of the lobule and a peripheral
Lymphatics and veins run within the interlobular septa network, that is located within the interlobular septa and along the pleural
linings.
Centrilobular area is the central part of the secundary lobule.
It is usually the site of diseases, that enter the lung through the airways
( i.e. hypersensitivity pneumonitis, respiratory bronchiolitis, centrilobular
emphysema ).

Perilymphatic areais the peripheral part of the secundary lobule.

It is usually the site of diseases, that are located in the lymphatics of in the
interlobular septa ( i.e. sarcoid, lymphangitic carcinomatosis, pulmonary
edema).
These diseases are usually also located in the central network of
lymphatics that surround the bronchovascular bundle.

Centrilobular area in blue (left) and perilymphatic area in yellow (right)

Basic Interpretation
A structured approach to interpretation of HRCT involves the following
questions:

 What is the dominant HR-pattern:

o reticular
o nodular
o high attenuation (ground-glass, consolidation)
o low attenuation (emphysema, cystic)
 Where is it located within the secondary lobule (centrilobular, perilymphat
or random)
 Is there an upper versus lower zone or a central versus peripheral
predominance
 Are there additional findings (pleural fluid, lymphadenopathy, traction
bronchiectasis).
 These morphologic findings have to be combined with the history of the
patient and important clinical findings.
When we study patients with HRCT, we have to realize that we are
looking at a selected group of patients.
Common diseases like pneumonias, pulmonary emboli, cardiogenic
edema and lungcarcinoma are already ruled out.
So uncommon diseases like Sarcoidosis, Hypersensitivity pneumonitis,
Langerhans cell histiocytosis, Lymphangitic carcinomatosis, Usual
Interstitial Pneumonitis (UIP) and many others become regular HRCT
diagnoses and can be real Aunt Minnies.

Typical UIP with honeycombing and traction bronchiectasis in a patient

with idiopathic pulmonary fibrosis (IPF)

Reticular pattern
In the reticular pattern there are too many lines, either as a result of
thickening of the interlobular septa or as a result of fibrosis as in
honeycombing.
Septal thickening
Thickening of the lung interstitium by fluid, fibrous tissue, or infiltration by
cells results in a pattern of reticular opacities due to thickening of the
interlobular septa.
Although thickening of the interlobular septa is relatively common in
patients with interstitial lung disease, it is uncommon as a predominant
finding and has a limited differential diagnosis (Table).

Smooth septal thickening is usually seen in interstitial pulmonary edema

(Kerley B lines on chest film); lymphangitic spread of carcinoma or
lymphoma and alveolar proteinosis.

Nodular or irregular septal thickening occurs in lymphangitic spread of

carcinoma or lymphoma; sarcoidosis and silicosis.
 On the left we see focal irregular septal thickening in the right upper lobe
in a patient with a known malignancy.
This finding is typical for lymphangitic carcinomatosis.
There are also additional findings, that support this diagnosis like
mediastinal lymph nodes and a nodular lesion in the left lung, that
probably represents a metastasis.

Pulmonary lymphangitic carcinomatosis (PLC)

In 50% of patients the septal thickening is focal or unilateral.
This finding is helpful in distinguishing PLC from other causes of
interlobular septal thickening like Sarcoidosis or cardiogenic pulmonary
edema.
Hilar lymphadenopathy is visible in 50% and usually there is a history of
(adeno)carcinoma.
Focal septal thickening in lymphangitic carcinomatosis Identical findings can be seen in patients with Lymphoma and in children
with HIV infection, who develop Lymphocytic interstitial pneumonitis
(LIP), a rare benign infiltrative lymphocytic disease.
On the left a patient who had a CT to rule out pulmonary embolism.
There is a combination of smooth septal thickening and ground-glass
opacity with a gravitational distribution.
The diagnosis based on this CT was cardiogenic pulmonary edema.

Cardiogenic pulmonary edema generally results in a combination of

septal thickening and ground-glass opacity.
There is a tendency for hydrostatic edema to show a perihilar and
gravitational distribution.
Thickening of the peribronchovascular interstitium, which is called
peribronchial cuffing, and fissural thickening are also common.
Common additional findings are an enlarged heart and pleural fluid.
Usually these patient are not imaged with HRCT as the diagnosis is readily
Septal thickening and ground-glass opacity with a gravitational made based on clinical and radiographic findings, but sometimes
distribution in a patient with cardiogenic pulmonary edema. unsuspected hydrostatic pulmonary edema is found.
On the left a patient with both septal thickening and ground glass opacity
in a patchy distribution.
Some lobules are affected and others are not.
This combination of findings is called 'crazy paving'.
Crazy paving was thought to be specific for alveolar proteinosis, but is also
seen in many other diseases such as pneumocystis carinii pneumonia,
bronchoalveolar carcinoma, sarcoidosis, nonspecific interstitial pneumonia
(NSIP), organizing pneumonia (COP), adult respiratory distress syndrome
and pulmonary hemorrhage.

Alveolar proteinosis is a rare diffuse lung disease of unknown etiology

characterized by alveolar and interstitial accumulation of a periodic acid-
Schiff (PAS) stain-positive phospholipoprotein derived from surfactant.
Alveolar proteinosis
 Honeycombing represents the second reticular pattern recognizable on
HRCT.
Because of the cystic appearance, honeycombing is also discussed in the
chapter discussing the low attenuation pattern.
Pathologically, honeycombing is defined by the presence of small cystic
spaces lined by bronchiolar epithelium with thickened walls composed of
dense fibrous tissue.
Honeycombing is the typical feature of usual interstitial pneumonia (UIP).

Honeycombing in a patient with UIP

Nodular pattern
The distribution of nodules shown on HRCT is the most important factor in
making an accurate diagnosis in the nodular pattern.
In most cases small nodules can be placed into one of three categories:
perilymphatic, centrilobular or random distribution.
Random refers to no preference for a specific location in the secondary
lobule.

Perilymphatic distribution
In patients with a perilymphatic distribution, nodules are seen in relation
to pleural surfaces, interlobular septa and the peribronchovascular
interstitium.
Nodules are almost always visible in a subpleural location, particularly in
relation to the fissures.

Centrilobular distribution
In certain diseases, nodules are limited to the centrilobular region.
Unlike perilymphatic and random nodules, centrilobular nodules spare the
pleural surfaces.
The most peripheral nodules are centered 5-10mm from fissures or the
pleural surface.

Random distribution
Nodules are randomly distributed relative to structures of the lung and
secondary lobule.
Nodules can usually be seen to involve the pleural surfaces and fissures,
but lack the subpleural predominance often seen in patients with a
perilymphatic distribution.
 Algorithm for nodular pattern
The algorithm to distinguish perilymphatic, random and centrilobular
nodules is the following:

 Look for the presence of pleural nodules.

These are often easiest to see along the fissures.
If pleural nodules are absent or few in number, the distribution is likely
centrilobular.
 If pleural nodules are visible, the pattern is either random (miliary) or
perilymphatic.
 If there are pleural nodules and also nodules along the central
bronchovascular interstitium and along interlobular septa, you are dealing
with a periplymphatic distribution.
 If the nodules are diffuse and uniformly distributed, it is likely a random
distribution.

Perilymphatic distribution
Perilymphatic nodules are most commonly seen in sarcoidosis.
They also occur in silicosis, coal-worker's pneumoconiosis and
lymphangitic spread of carcinoma.
Notice the overlap in differential diagnosis of perilymphatic nodules and
the nodular septal thickening in the reticular pattern.
Sometimes the term reticulonodular is used.

On the left a typical case of perilymphatic distribution of nodules in a

patient with sarcoidosis.
Notice the nodules along the fissures indicating a perilymphatic
distribution (red arrows).
Always look carefully for these nodules in the subpleural region and along
the fissures, because this finding is very specific for sarcoidosis.
Typically in sarcoidosis is an upper lobe and perihilar predominance and in
this case we see the majority of nodules located along the
bronchovascular bundle (yellow arrow).

Sarcoidosis
 On the left another typical case of sarcoidosis.
In addition to the perilymphatic nodules, there are multiple enlarged
lymph nodes, which is also typical for sarcoidosis.
In end stage sarcoidosis we will see fibrosis, which is also predominantly
located in the upper lobes and perihilar.

Sarcoidosis
Centrilobular distribution
Centrilobular nodules are seen in:

 Hypersensitivity pneumonitis
 Respiratory bronchiolitis in smokers
 infectious airways diseases (endobronchial spread of tuberculosis or
nontuberculous mycobacteria, bronchopneumonia)
 Uncommon in bronchioloalveolar carcinoma, pulmonary edema, vasculitis

In many cases centrilobular nodules are of ground glass density and ill
defined (figure).
They are called acinair nodules.

Ill defined centrilobular nodules of ground glass density in a patient

with hypersensitivity pneumonitis
Tree-in-bud
In centrilobular nodules the recognition of 'tree-in-bud' is of value for
narrowing the differential diagnosis.
Tree-in-bud describes the appearance of an irregular and often nodular
branching structure, most easily identified in the lung periphery.
It represents dilated and impacted (mucus or pus-filled) centrilobular
bronchioles.

Tree-in-bud almost always indicates the presence of:

 Endobronchial spread of infection (TB, MAC, any bacterial

bronchopneumonia)
 Airway disease associated with infection (cystic fibrosis, bronchiectasis)
 less often, an airway disease associated primarily with mucus retention
(allergic bronchopulmonary aspergillosis, asthma).
 On the left a tree-in-bud is seen.
In the proper clinical setting suspect active endobronchial spread of TB.

In most patients with active tuberculosis, the HRCT shows evidence of

bronchogenic spread of disease even before bacteriologic results are
available (6).

Typical Tree-in-bud appearance in a patient with active TB.

Random distribution
On the left a patient with random nodules as a result of miliary TB.
The random distribution is a result of the hematogenous spread of the
infection.
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)

Sarcoidosis usually has a perilymphatic distribution, but when it is very

Random distribution of nodules in miliary tuberculosis extensive, it spreads along the bronchovascular bundle to the periphery of
the lung and may reache the centrilobular area.
Langerhans cell histiocytosis is an uncommon disease characterised by
multiple cysts in patients with nicotine abuse.
In a very early stage, these patients show only nodules, that later on
cavitate and become cysts (figure).
As in all smoking related diseases, there is an upper lobe predominance.

Langerhans cell histiocytosis: early nodular stage before the typical

cysts appear.

High Attenuation pattern

 Increased lung attenuation is called ground-glass-opacity (GGO) if there is
a hazy increase in lung opacity without obscuration of underlying vessels
and is called consolidation if the increase in lung opacity obscures the
vessels.

In both ground glass and consolidation the increase in lung density is the
result of replacement of air in the alveoli by fluid, cells or fibrosis.
In GGO the density of the intrabronchial air appears darker as the air in
the surrounding alveoli.
This is called the 'dark bronchus' sign
In consolidation, there is exclusively air left intrabronchial.
Dark bronchus sign in ground glass opacity. Complete obscuration of This is called the 'air bronchogram'.
vessels in consolidation.
Ground-glass opacity
Ground-glass opacity (GGO) represents:

 Filling of the alveolar spaces with pus, edema, hemorrhage, inflammation

tumor cells.
 Thickening of the interstitium or alveolar walls below the spatial resolution
the HRCT as seen in fibrosis.

So ground-glass opacification may either be the result of air space disease

(filling of the alveoli) or interstitial lung disease (i.e. fibrosis).

The location of the abnormalities in ground glass pattern can be helpfull:

 Upper zone predominance: Respiratory bronchiolitis, PCP.

 Lower zone predominance: UIP, NSIP, DIP.
 Centrilobular distribution: Hypersensitivity pneumonitis, Respiratory
bronchiolitis
Thus ground glass in itself is very unspecific.
Not suprisingly, there is a big overlap in the causes of ground-glass
opacity and consolidation and some diseases may present with both
areas of ground-glass and consolidation.
On the left we see consolidation and ground-glass opacity in a patient with
persistent chest abnormalities and weight loss without signs of infection.
This suggested a chronic disease.
There is no honeycombing or traction bronchiectasis, so we can rule out
fibrosis.
The weight loss is suggestive of a malignant disease.
Histology revealed broncho-alveolar cell carcinoma

Broncho-alveolar cell carcinoma with ground-glass opacity and Broncho-alveolar cell carcinoma (BAC) may present as:
consolidation
1. solitary nodule or mass (40% of patients)
2. focal or diffuse consolidation (30%) as in this case.
3. diffuse ill-defined centrilobular nodules (30%) due to endobronchial
spread.
 Treatable or not treatable?
Ground-glass opacity is nonspecific, but highly significant finding since 60-
80% of patients with ground-glass opacity on HRCT have an active and
potentially treatable lung disease.
In the other 20-40% of the cases the lung disease is not treatable and the
ground-glass pattern is the result of fibrosis.
In those cases there are usually associated HRCT findings of fibrosis, such
as traction bronchiectasis and honeycombing.
On the left two cases with GGO, one without fibrosis and potentially
treatable and the other with traction bronchiectasis indicating fibrosis.
LEFT: No fibrosis, so potentially treatable lung disease.
RIGHT: Fibrosis, so no treatable lung disease.
On the left a patient with GGO as dominant pattern.
In addition there is traction bronchiectasis indicating the presence of
fibrosis.
This case is one of the possible patterns of nonspecific interstitial
pneumonia (NSIP).

NSIP is characterized histologically by a relatively uniform pattern of

cellular interstitial inflammation associated with variable degrees of
fibrosis.
As in UIP (usual interstitial pneumonia) it mainly involves the dependent
regions of the lower lobes, but NSIP lacks the extensive fibrosis with
honeycombing.
NSIP may be idiopathic or associated with collagen vascular diseases or
exposure to drugs or chemicals.
Non specific interstitial pneumonitis (NSIP). Notice lower lobe
NSIP has a relative good prognosis and the majority of patients respond
predominance.
to treatment with corticosteroids. This outcome is quite different from that
seen in UIP, which has a poor prognosis.
Mosaic attenuation
The term 'mosaic attenuation' is used to describe density differences
between affected and non-affected lung areas.
There are patchy areas of black and white lung.
The role of the radiologist is to determine which part is abnormal: the
black or the white lung.
When ground glass opacity presents as mosaic attenuation consider:

 Infiltrative process adjacent to normal lung

 Normal lung appearing relatively dense adjacent to lung with air-trapping
 Hyperperfused lung adjacent to oligemic lung due to chronic
thromboembolic disease
It can be difficult to distinguish these three entities.

There are two diagnostic hints for further differentiation:

 Look at expiratory scans for air trapping

 Look at the vessels

If the vesses are difficult to see in the 'black' lung as compared to the
'white' lung, than it is likely that the 'black' lung is abnormal.
Then there are two possibilities: obstructive bronchiolitis or chronic
Three different causes of mosaic attenuation pulmonary embolism.
 Sometimes these can be differentiated with an expiratory scan.

If the vessels are the same in the 'black' lung and 'white' lung, then you
are looking at a patient with infiltrative lung disease, like the one on the
right with the pulmonary hemmorrhage.

Temporary bronchiolitis with air trapping is seen in:

 (post) infection
 Inhalation of toxin
 Rheumatoid arthritis, Sjögren
 Post transplant
 Drug reaction (penicillamine)
On the left a patient with ground glass pattern in a mosaic distribution.
Some lobules are involved and others are not.
The differential diagnosis is hypersensitivity pneumonitis, bronchiolitis or
thromboembolic disease.
The history was typical for hypersensitivity pneumonitis.
Hypersensitivity pneumonitis usually presents with centrilobular nodules
of ground glass density (acinar nodules).
When they are confluent, HRCT shows diffuse ground glass.

Hypersensitivity pneumonitis (HP) is an allergic lung disease caused

by the inhalation of antigens contained in a variety of organic dusts.
Farmer's lung is the best-known HP syndrome and results from the
Mosaic pattern in a patient with hypersensitivity pneumonitis inhalation of fungal organisms that grow in moist hay or exposure to birds
as pets (1).
HP usually presents in two forms either as ground glass in a mosaic
distribution as in this case or as centrilobular nodules of ground glass
density (acinar nodules).
On the left a patient with ground glass pattern in a mosaic distribution.
The clue here is the enlargement of pulmonary arteries (arrow) in the
areas of ground glass.
The ground glass appearance is the result of hyperperfused lung adjacent
to oligemic lung with reduced vessel caliber due to chronic
thromboembolic disease.

Mosaic pattern in a patient with chronic thromboemboli

On the left another patient with ground glass pattern in a mosaic
distribution.
Again the ground glass appearance is the result of hyperperfused lung
with large vessels adjacent to oligemic lung with small vessels due to
chronic thromboembolic disease.
Emboli adherent to the wall and intravascular septa are typical for chronic
thromboemboli in which partial recanalization took place.
 Crazy Paving
Crazy Paving is a combination of ground glass opacity with superimposed
septal thickening (5).
It was first thought to be specific for alveolar proteinosis, but later was
also seen in other diseases.

Crazy Pavin can also be seen in:

 Alveolar proteinosis
 Sarcoid
 NSIP
 Organizing pneumonia (COP/BOOP)
 Infection (PCP, viral, Mycoplasma, bacterial)
 Neoplasm (Bronchoalveolarca (BAC)
Crazy Pavin in a patient with Alveolar proteinosis.  Pulmonary hemorrhage
 Edema (heart failure, ARDS, AIP)
Consolidation
Consolidation is synonymous with airspace disease.
When you think of the causes of consolidation, think of 'what is replacing
the air in the alveoli'?
Is it pus, edema, blood or tumor cells (Table on the left).
Even fibrosis as in UIP, NSIP and long standing sarcoidosis can replace the
air in the alveoli and cause consolidation.

Acute consolidation is seen in:

 Pneumonias (bacterial, mycoplasma, PCP)

 Pulmonary edema due to heart failure or ARDS
 Hemorrhage
 Acute eosinophilic pneumonia

Chronic consolidation is seen in:

 Organizing Pneumonia
 Chronic eosinophilic pneumonia
 Fibrosis in UIP and NSIP
 Bronchoalveolar carcinoma or lymphoma

Most patients who are evaluated with HRCT, will have chronic
consolidation, which limits the differential diagnosis.
 On the left two cases with chronic consolidation.
There are patchy non-segmental consolidations in a subpleural and
peripheral distribution.

The differential diagnosis is the same as the list above.

The final diagnosis was cryptogenic organizing pneumonia (COP).
In chronic eosinophilic pneumonia the HRCT findings will be the same, but
there will be eosinophilia.
In fibrosis there will be other signs of fibrosis like honeycombing or
traction bronchiectasis.
Bronchoalveolar carcinoma can also look like this.

Organizing pneumonia (OP)

Organizing pneumonia represents an inflammatory process in which the
healing process is characterized by organization and cicatrization of the
Two patients with chronic consolidations as a result of COP exudate rather than by resolution and resorption.
(cryptogenic organizing pneumonia) It is also described as 'unresolved pneumonia'.
If no cause can be identified it is called cryptogenic organizing pneumonia
(COP).
It was described in earlier years as Bronchiolitis-obliterans-organizing
pneumonia (BOOP).
Patients with COP typically present with a several-month history of
nonproductive cough.
Many cases are idiopathic, but OP may also be seen in patients with
pulmonary infection, drug reactions, collagen vascular disease, Wegener's
granulomatosis and after toxic-fume inhalation.
On the left a case of chronic eosinophilic pneumonia.
It was a patient with low-grade fever, progressive shortness of breath and
an abnormal chest radiograph.
There was a marked eosinophilia in the peripheral blood.
Like in COP we see patchy non-segmental consolidations in a subpleural
distribution.

Chronic eosinophilic pneumonia is an idiopathic condition

characterized by extensive filling of alveoli by an infiltrate consisting
primarily of eosinophils.
Chronic eosinophilic pneumonia is usually associated with an increased
number of eosinophils in the peripheral blood and patients respond
promptly to treatment with steroids.

Chronic eosinophilic granuloma

Low Attenuation pattern

 The fourth pattern includes abnormalities that result in decreased lung
attenuation or air-filled lesions.
These include:

 Emphysema
 Lung cysts (LAM, LIP, Langerhans cell histiocytosis)
 Bronchiectasis
 Honeycombing

Most diseases with a low attenuation pattern can be readily distinguished

on the basis of HRCT findings.

Emphysema
Emphysema typically presents as areas of low attenuation without visible
walls as a result of parenchymal destruction.

 Centrilobular emphysema
oMost common type
oIrreversible destruction of alveolar walls in the centrilobular portion of t
lobule
o Upper lobe predominance and uneven distribution
o Strongly associated with smoking.
 Panlobular emphysema
o Affects the whole secondary lobule
o Lower lobe predominance
o In alpha-1-antitrypsin deficiency, but also seen in smokers with advan
Centrilobular emphysema due to smoking. The periphery of the lung
is spared (blue arrows). Centrilobular artery (yellow arrows) is seen in emphysema
the center of the hypodense area.  Paraseptal emphysema
o Adjacent to the pleura and interlobar fissures
o Can be isolated phenomenon in young adults, or in older patients with
centrilobular emphysema
o In young adults often associated with spontaneous pneumothorax
Paraseptal emphysema
Paraseptal emphysema is localized near fissures and pleura and is
frequently associated with bullae formation (area of emphysema larger
than 1 cm in diameter).
Apical bullae may lead to spontaneous pneumothorax.
Giant bullae occasionally cause severe compression of adjacent lung
tissue.

Paraseptal emphysema with small bullae

 Panlobularl emphysema
On the left a typical case of panlobular emphysema.
There is uniform destruction of the underlying architecture of the
secondary pulmonary lobules, leading to widespread areas of abnormally
low attenuation.
Pulmonary vessels in the affected lung appear fewer and smaller than
normal.
Panlobular emphysema is diffuse and is most severe in the lower lobes.
In severe panlobular emphysema, the characteristic appearance of
extensive lung destruction and the associated paucity of vascular
markings are easily distinguishable from normal lung parenchyma.
On the other hand, mild and even moderately severe panlobular
Panlobular emphysema emphysema can be very subtle and difficult to detect on HRCT(1).
Cystic lung disease
Lung cysts are defined as radiolucent areas with a wall thickness of less
than 4mm.
Cystic lung diseases as listed in the table on the left.

Cavities are defined as radiolucent areas with a wall thickness of more

than 4mm and are seen in infection (TB, Staph, fungal, hydatid), septic
emboli, squamous cell carcinoma and Wegener's disease.
On the left a case with multiple round and bizarre shaped cysts.
There was an upper lobe predominance.
The patient had a long history of smoking.
This combination of findings is typical for Langerhans cell histiocytosis.

Langerhans cell histiocytosis (LCH) is an idiopathic disease

characterized in its early stages by granulomatous nodules containing
Langerhans histiocytes and eosinophils.
In its later stages, the granulomas are replaced by fibrosis and the
formation of cysts.
It is an uncommon condition.
The majority of patients are young or middle-aged adults presenting with
nonspecific symptoms of cough and dyspnea. Up to 20% of patients
Langerhans cell histiocytosis present with pneumothorax and over 90% of patients are smokers.
Most cysts appear round, but can also have bizarre shapes (bilobed or
clover-leaf shaped).
An upper lobe predominance in the size and number of cysts is common.
On the left a case with multiple cysts that are evenly distributed througout
the lung ( in contrast to LCH).
Notice the pneumothorax.
There was no history of smoking and this was a 40 year old female.
This combination of findings is typical for Lymphangiomyomatosis (LAM).

Lymphangiomyomatosis is a rare disease characterized by

progressive proliferation of spindle cells, resembling smooth muscle.
Proliferation of these cells along the bronchioles leads to air trapping and
the development of thin-walled lung cysts.
Rupture of these cysts can result in pneumothorax.
Other features of LAM include adenopathy and pleural effusion.

Lymphangiomyomatosis occurs only in women, usually of child-bearing

Lymphangiomyomatosis complicated by pneumothorax age, between 17 and 50 years. Identical clinical, radiologic, and pathologic
pulmonary changes are seen in about 1% of patients with tuberous
sclerosis.
Most patients die within 10 years of the onset of symptoms.
Bronchiectasis
Bronchiectasis is defined as localized bronchial dilatation.
The diagnosis of bronchiectasis is usually based on a combination of the
following findings:

 bronchial dilatation (signet-ring sign)

 bronchial wall thickening
 lack of normal tapering with visibility of airways in the peripheral lung
 mucus retention in the broncial lumen
 associated atelectasis and sometimes air trapping
A signet-ring sign represents an axial cut of a dilated bronchus (ring) with
its accompanying small artery (signet).
The most common cause of bronchiectasis is prior infection, usually viral,
at an early age.
It also occurs in patients with chronic bronchitis, COPD and cystic fibrosis.
Bronchiectasis may mimic cystic lung disease and bullous emphysema.
Bronchiectasis caused by primary airway disease should be differentiated
from tracion bronchiectasis as a result of fibrosis.
On the left we see a chest film with a typical finger-in-glove shadow.
The HRCT shows focal bronchiectasis with extensive mucoid impaction,
which is in the appropriate clinical setting (asthma and serum
eosinophilia) typical for Allergic bronchopulmonary aspergillosis (ABPA).

Allergic bronchopulmonary aspergillosis is a lung disease occurring

in patients with asthma or cystic fibrosis, triggered by a hypersensitivity
reaction to the presence of Aspergillus fumigatus in the airways.
It characteristically presents with the findings of central bronchiectasis,
mucoid impaction and atelectasis.

ABPA: glove-finger shadow due to mucoid impaction in central

bronchiectasis in a patient with asthma.
Honeycombing
Honeycombing is defined by the presence of small cystic spaces with
irregularly thickened walls composed of fibrous tissue.
Honeycomb cysts often predominate in the peripheral and subpleural lung
regions regardless of their cause.
Subpleural honeycomb cysts typically occur in several contiguous layers.
This finding can allow honeycombing to be distinguished from paraseptal
emphysema in which subpleural cysts usually occur in a single layer.
 The case on the left shows subpleural honeycomb cysts in several
contiguous layers.
There is also a lower lobe predominance and widespread traction
bronchiectasis.
These findings are typical for Usual Interstitial Pneumonia (UIP).

UIP or 'end-stage lung' is a pathology diagnosis and usually shown at

lungbiopsy, when honeycombing is visible.
Idiopathic pulmonary fibrosis (IPF), accounts for more than 60% of the
cases of UIP.
UIP with lung fibrosis is also a common pattern of auto-immune disease
and drug-related lung injury.
A long list of drugs have been implicated, but this pattern is most
commonly the result of cytotoxic chemotherapeutic agents such as
bleomycin, busulfan, vincristine, methotrexate, adriamycin, and
Honeycombing and traction bronchiectasis in UIP. carmustine (BCNU).

On the left another case of UIP.

The lower zone predominance is demonstrated when you scroll through
the images.
Notice the ground glass opacity in the left lower lobe as a result of fibrous
tissue replacing the air in the alveoli.

View more images: 1/2

UIP in a patient with progressive shortness of breath. Scroll through
the images.

Distribution within the lung

Upper lung zone preference is seen in:

 Inhaled particles: pneumoconiosis (silica or coal)

 Smoking related diseases (centrilobular emphysema
 Respiratory bronchiolitis (RB-ILD)
 Langerhans cell histiocytosis
 Hypersensitivity pneumonitis
 Sarcoidosis

Lower zone preference is seen in:

 UIP
 Aspiration
 Pulmonary edema
Central distribution is seen in sarcoidosis and cardiogenic pulmonary
edema.

Peripheral distribution is mainly seen in cryptogenic organizing

pneumonia (COP), chronic eosinophilic pneumonia and UIP.

Additional findings
Pleural effusion is seen in:

1. Pulmonary edema
2. Lymphangitic spread of carcinoma - often unilateral
3. Tuberculosis
4. Lymphangiomyomatosis (LAM)
5. Asbestosis

Hilar and mediastinal lymphadenopathy

In sarcoidosis the common pattern is right paratracheal and bilateral hilar
adenopathy ('1-2-3-sign').
In lung carcinoma and lymphangitic carcinomatosis adenopathy is usually
unilateral.
'Eggshell calcification' in lymph nodes commonly occurs in patients with
silicosis and coal-worker's pneumoconiosis and is sometimes seen in
sarcoidosis, postirradiation Hodgkin disease, blastomycosis and
scleroderma .

Differential diagnosis of interstitial lung

diseases
Reticular pattern

1. Lymphangitic carcinomatosis: irregular septal thickening, usually foc

or unilateral 50% adenopathy', known carcinoma.

2. Cardiogenic pulmonary edema: incidental finding in HRCT, smooth

septal thickening with basal predominance (Kerley B lines), ground-
glass opacity with a gravitational and perihilar distribution, thickening
of the peribronchovascular interstitium (peribronchial cuffing)

3. Lymphangitic carcinomatosis.

4. Lymphangitic carcinomatosis with hilar adenopathy.

5. Alveolar proteinosis: ground glass attenuation with septal thickening

(crazy paving).

6. Cardiogenic pulmonary edema.

Nodular pattern

1. Hypersensitivity pneumonitis: ill defined centrilobular nodules.

2. Miliary TB: random nodules

3. Sarcoidosis: nodules with perilymphatic distribution, along fissures,

adenopathy.

4. Hypersensitivity pneumonitis: centrilobular nodules, notice sparing o

the area next to pleura and fissure.
Nodular pattern(2)

1. Sarcoidosis: nodules with perilymphatic distribution, along fissures,

adenopathy.

2. TB: Tree-in-bud appearance in a patient with active TB.

3. Langerhans cell histiocytosis: early nodular stage before the typical

cysts appear.

4. Respiratory bronchiolitis in infection.

High Attenuation pattern

1. Chronic eosinophilic pneumonia with peripheral areas of ground glas

opacity.

2. Sarcoid end-stage with massive fibrosis in upper lobes presenting as

areas of consolidation. Notice lymphadenopathy.

3. Chronic eosinophilic pneumonia with peripheral areas of consolidatio

4. Broncho-alveolar cell carcinoma with both areas of ground glass

opacity and consolidation
High Attenuation pattern (2)

1. Non specific interstitial pneumonitis (NSIP): ground glass with tractio

bronchiectasis, no honeycombing.

2. Cryptogenic organizing pneumonia (COP).

3. Sarcoidosis end-stage: consolidation as a result of massive fibrosis

perihilar and in upper lobes.

4. COP.

Low Attenuation pattern

1. Lymphangiomyomatosis (LAM): uniform cysts in woman of child-

bearing age; no history of smoking; adenopathy and pleural effusion
sometimes pneumothorax.

2. LCH: multiple round and bizarre shaped cysts; smoking history.

3. Honeycombing

4. Centrilobular emphysema: low attenuation areas without walls.

 Low Attenuation pattern (2)

1. Centrilobular emphysema: low attenuation areas without walls. Not

the centrilobular artery in the center.

2. Langerhans cell histiocytosis (LCH): multiple thick walled cysts;

smoking history.

3. Honeycombing.

4. Lymphangiomyomatosis (LAM): regular cysts in woman of child-

bearing age.

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References
1. HIGH RESOLUTION LUNG CT UCSF Interactive Radiology Series on CD-ROM
This browser-based learning file based on Dr. Webb's HRCT text.
It offers a wide variety of cases dealing with common HRCT patterns of disease, diffuse lung diseases and their
significance, and clinical characteristics.
It is one of the best educational CD's ever made.
2. Practical Approach to HRCT
a spoken lecture given by Jud W. Gurney for www.chestx-ray
3. HRCT Diagnostic Picker
by Shanoe Cutts and Craig Johnson
4. Self-tutorial for HRCT interpretation
This web site is intended as a self-tutorial for residents and medical students to learn to interpret high-resolution
chest CT's with confidence.
by Spencer B. Gay, MD, Juan Olazagasti, MD, Christopher Ho, MD, and Richard Webb, MD, University of Virginia
Health Sciences Center Department of Radiology
5. 'Crazy-Pavin' Pattern at Thin-Section CT of the Lungs: Radiologic-Pathologic Overview
Santiago E. Rossi, MD et al
Radiographics. 2003;23:1509-1519
6. Role of HRCT in diagnosing active pulmonary Tuberculosis
M. Bakhshayesh Karam MD et al.
 HRCT part II: Key findings in Interstitial Lung Diseases
Robin Smithuis, Otto van Delden and Cornelia Schaefer-Prokop
Radiology Department of the Rijnland Hospital, Leiderdorp and the Academical Medical Centre, Amsterdam, the Netherlands
 Introduction
 Sarcoidosis back to overview print
 Silicosis / Coal worker pneumoconiosis Publicationdate 20-12-
 Lymphangitic Carcinomatosis : 2007
In this review we present the key findings in the most common interstitial lung
 Cardiogenic pulmonary edema
diseases.
 Hypersensitivity Pneumonitis
There are numerous interstitial lung diseases, but in clinical practice only about
 Tuberculosis
ten diseases account for approximately 90% of cases.
 Chronic eosinophilic pneumonia Knowledge of both, the radiological and clinical appearance of these more
 Pneumocystis carinii pneumonia common interstitial lung diseases, is therefore important for recognizing them i
 ARDS the daily practice and including them in the differential diagnosis.
 Idiopathic interstitial pneumonias Some less common interstitial lung diseases will also be presented because the
 UIP HRCT presentation may be very typical, allowing for a 'spot diagnosis' in selecte
 NSIP cases.
 COP
 RB-ILD and DIP In 'HRCT part I : basic interpretation' the terminology is introduced and a pract
 AIP approach is given for the interpretation of HRCT examinations.
 LIP
 Drug-induced lung disease A simple mouse click on an item on the left will bring you directly to this subjec
 Uncommon interstitial lung diseases
 Lymphangiomyomatosis
 Langerhans cell histiocytosis
 Alveolar proteinosis

Introduction
More than 100 entities manifest as diffuse lung disease.
Fortunately only about 10 of these account for about 90% of all diffuse lung
diseases, that are assessed by open lung biopsy.
Knowing the common and also uncommon HRCT-presentations of these
frequently encountered diffuse lung diseases is extremely important.

On the left you find three different lists of diagnoses.

Accounting for 80 - 90% of all diagnoses according to various literature
references.

In some of them the old names are used and in some the newer ones.
The 'mnemonic' for the first list is 'SHIT FACED' (alternative shaded fit).

Sarcoidosis
Sarcoidosis is a systemic disorder of unknown origin.
It is characterized by non-caseating granulomas in multiple organs, that
may resolve spontaneously or progress to fibrosis.
Pulmonary manifestations are present in 90% of patients.
Systemic symptoms such as fatigue, night sweats and weight loss are
common.
Löfgren's syndrome, an acute presentation of sarcoidosis, consists of
arthritis, erythema nodosum, bilateral hilar adenopathy and occurs in 9-
34% of patients.
Erythema nodosum is seen predominantly in women and arthritis is more
 common in men.

Two third of patients have a remission within ten years.

One third have continuing disease leading to clinically significant organ
impairment.
Less than 5% of patients die from sarcoidosis usually as a result of
pulmonary fibrosis.
Stages
Chest films in sarcoidosis have been classified into four stages:

1. Bilateral hilar lymphadenopathy

2. Bilateral hilar lymphadenopath + pulmonary disease
3. Only pulmonary disease
4. Irreversible fibrosis

These stages do not indicate disease chronicity or correlate with changes in

pulmonary function.
Sarcoidosis stage I: left and right hilar and paratracheal adenopathy
(1-2-3 sign) On the left a patient with stage I disease.
There is hilar and paratracheal adenopathy and no sign of pulmonary
involvement.
HRCT findings in Sarcoidosis.

 Common findings:
oSmall nodules in a perilymphatic distribution (i.e. along subpleural surfac
and fissures, along interlobular septa and the peribronchovascular bundle
o Upper and middle zone predominance.
o Lymphadenopathy in left hilus, right hilus and paratracheal (1-2-3 sign).
Often with calcifications.
 Uncommon findings:
o Conglomerate masses in a perihilar location.
o Larger nodules (> 1cm in diameter, in < 20%)
o Grouped nodules or coalescent nodlues surrounded by multiple satellite
nodules (Galaxi sign)
Sarcoidosis: typical presentation with nodules along the o Nodules so small and dense that they appear as ground glass or even as
bronchovascular bundle and fthe issures consolidations (alveolar sarcoidosis)
Notice the partially calcified node in the left hilum.
On the left a typical presentation of sarcoidosis with hilar lymphadenopathy
and small nodules along bronchovascular bundles (yellow arrow) and along
fissures (red arrows).
 On the left a detailed view with the typical HRCT-presentation with nodules
along bronchovascular bundle (red arrow) and fissures (yellow arrow).
This is the typical perilymphatic distribution of the noduless.

The HRCT appearance of pulmonary sarcoidosis varies greatly and is known

to mimic many other diffuse infiltrative lung diseases.
Approximately 60 to 70% of patients with sarcoidosis have characteristic
radiologic findings.
In 25 to 30% of cases the radiologic findings are atypical.
In 5 to 10% of patients the chest radiograph is normal.

On the left another typical presentation of sarcoidosis with mediastinal

lymphadenopathy and small nodules in a perilymphatic distribution along
bronchovascular bundles and along fissures (yellow arrows).
Always look for small nodules along the fissures, because this is a very
specific and typical sign of sarcoidosis.

Sarcoidosis: typical presentation

Fibrosis in Sarcoidosis.
Progressive fibrosis in sarcoidosis may lead to peribronchovascular
(perihilar) conglomerate masses of fibrous tissue.
The typical location is posteriorly in the upper lobes, leading to volume loss
of the upper lobes with displacement of the interlobar fissure.

Other diseases that commonly result in this appearance are:

1. Silicosis
2. Tuberculosis
3. Talcosis

Sarcoidosis with conglomerate masses of fibrous tissue

 On the left a typical chest film of long standing sarcoidosis (stage IV) with
fibrosis in the upper zones and volume loss of the upper lobes resulting in
hilar elevation.
Fibrosis results in obliteration of pulmonary vessels, which can lead to
pulmonary hypertension.

Sarcoidosis with fibrosis in the upper lobes. Typical chest film.

On the left another case of stage IV sarcoidosis.&#8232;
Notice the distribution of the conglomerate masses of fibrosis in the
posterior part of the lungs.
In addition there are multiple small well-defined nodules.
Some of these nodules have the typical subpleural distribution.

Sarcoidosis with fibrosis in the upper lobes. Typical HRCT findings.

Alveolar Sarcoidosis.

On the left a case of alveolar sarcoidosis.

Scroll through the images.

In this case the appearance resembles a ground glass attenuation, but with
a close look you may appreciate that the increased attenuation is the result
of many tiny grouped nodules.
Also notice the hilar lymphadenopathy.

View more images: 1/3

 Alveolar Sarcoidosis (2)
On the left a 47-year old female patient with a dry cough, slightly breathless
and a normal blood analysis.
A chest film was taken and she was treated with antibiotics.
A follow up film was made, because she did not improve.

The first chest film shows bilateral consolidations in the lower lobes (arrow),
initially interpreted as infection.
After two weeks of treatment with antibiotics, there is no improvement.
The differential diagnosis now includes tumor (bronchoalveolar carcinoma or
lymphoma), eosinophilic pneumonia , organizing pneumonia, Wegener's
disease or an uncommon presentation of sarcoidosis.
47-year old female patient treated for possible infection Now continue with the HRCT.
Scroll through the images on the left .
There are multiple areas of consolidation.
Ancillary findings are hilar and mediastinal lymphadenopathy.

The differental diagnosis of the CT-images is basically the same as of the

chest film.
Histology revealed alveolar sarcoid.
There is only one clue to the diagnosis and that is the presence of small
nodules that can be identified in image 3, but these are difficult to see.
This case nicely demonstrates that sarcoidosis truely is 'the great mimicker'.
Sarcoidosis should be therefore in our differential diagnostic list!.&#8232;

View more images: 1/4

On the left a case of fibrosing sarcoidosis, showing fibrosis, traction
bronchiectases and crowding of the involved bronchi, predominantly in the
perihilar region and upper lobes.
Nodular abnormalities are absent, but the appearance and the location of
the fibrosis are very suggestive of the diagnosis of sarcoidosis.
 Differential diagnosis of Sarcoidosis.

 Lymphadenopathy:
oPrimary TB: asymmetrical adenopathy
oHistoplasmosis
oLymphoma
oSmall cell lung cancer with nodal metastases
 Nodular pattern:
o Silicosis / Pneumoconiosis: predominantly centrilobular and subpleural
nodules.
o Miliary TB: random nodules.
 Fibrotic pattern:
o Usual Interstitial Pneumonia (UIP): basal and peripheral fibrosis,
honeycombing.
o Chronic Hypersensitivity Pneumonitis: mid zone fibrosis with mosaic
pattern.
o Tuberculosis (more unilateral).

On the left some diseases with a nodular pattern.

1. Hypersensitivity pneumonitis: ill defined centrilobular nodules.

2. Miliary TB: random nodules of the same size.
3. Sarcoidosis: nodules with perilymphatic distribution, along fissures,
adenopathy.
4. Hypersensitivity pneumonitis: centrilobular nodules, notice sparing of t
subpleural area.
5. Sarcoidosis: nodules with perilymphatic distribution, along fissures,
adenopathy.
6. TB: Tree-in-bud appearance in a patient with active TB.
7. Langerhans cell histiocytosis: early nodular stage before the typical cys
appear.
8. Respiratory bronchiolitis: ill defined centrilobular nodules of ground-gla
opacity.

Silicosis / Coal worker pneumoconiosis

Silicosis and Coal worker pneumoconiosis (CWP) are pathologically distinct
entities with differing histology, resulting from the inhalation of different
inorganic dusts.
The radiographic and HRCT appearances of these diseases, however, may
not be distinguishable from each other and may be similar to sarcoidosis.
It is important to realize that these diseases are rare compared to
sarcoidosis.&#8232;
Silicosis and CWP occur in a specific patient group (construction workers,
mining workers, workers exposed to sandblasting, glass blowing and
pottery).
 HRCT findings in Silicosis/CWP

 Small well-defined nodules of 2 to 5mm in diameter in both lungs.

 Upper lobe predominance
 Nodules may be calcified
 Centrilobular and subpleural distribution
 Sometimes random distribution
 Irregular conglomerate masses, known as progressive massive fibrosis
 Masses may cavitate due to ischemic necrosis.
 Often hilar and mediastinal lymphnodes.

On the left a case of silicosis showing nodules of varying sizes with a random
and subpleural distribution. One nodule contains calcification (arrow). Note
the absence of a lymphatic distribution pattern (peribronchovascular and
along fissures), which would be suggestive of sarcoidosis.
Differential diagnosis of Silicosis / Pneumoconiosis.

 Sarcoidosis : can be difficult to distinguish (look for distribution of nodules).

 Infection: miliairy TB, fungus.
 Hematogenous metastases: silicotic nodules in subpleural and peribronchiol
location up to the level of the secundary pulmonary lobule, may have a
seemingly random distribution and simulate metastases and miliary infectio
 Langerhans cell histiocytosis: can be difficult to distinguish from silicosis in th
early stage, when LCH is solely characterized by the presence of small
nodules. Look for nodules with cavitation.

Same patient with silicosis as previous images showing a

conglomerate mass in a perihilar location in the right upper lobe. The
left lobe shows multiple nodules of varying size.

Lymphangitic Carcinomatosis
Lymphangitic Carcinomatosis results from hematogenous spread to the
lung, with subsequent invasion of interstitium and lymphatics.&#8232;
The presenting symptoms are dyspnea and cough and can predate the
radiographic abnormalities.
In many cases however the patients are asymptomatic.
Lymphangitic Carcinomatosis is seen in carcinoma of the lung, breast,
stomach, pancreas, prostate, cervix, thyroid and metastatic
adenocarcinoma from an unknown primary.
 HRCT findings in Lymphangitic Carcinomatosis

 Interlobular septal thickening, thickening of fissures and thickening of the

peribronchovascular interstitium (bronchial cuffing).
 Depending on filling with fluid or with tumor cells, septal thickening is irregul
or smooth.
 Focal or unilateral abnormalities in 50% of patients.
 Hilar lymphadenopathy in 50% of patients.
 Pleural effusion due to pleuritic carcinomatosis ( > 50% of patients).

On the left a patient with Lymphangitic Carcinomatosis.

Notice the focal distribution.
This finding is helpful in distinguishing Lymphangitic Carcinomatosis from
other causes of interlobular septal thickening like pulmonary edema or
sarcoid.
There is also lymphadenopathy.

On the left another patient with Lymphangitic Carcinomatosis.

In this case there is distribution in both lungs.
Additional pleural fluid and lung metastases
Differential diagnosis of Lymphangitic Carcinomatosis.

On the left multiple diseases showing septal thickening:

1. Lymphangitic carcinomatosis: irregular septal thickening, usually focal

unilateral, in 50% adenopathy, known carcinoma.
2. Cardiogenic pulmonary edema: bilateral abnormalities, filling of alveoli
enlarged heart, rapid response to diuretics, ground-glass opacity due t
filling of alveoli with fluid, gravitational distribution of the alveolar fluid.
3. Lymphangitic carcinomatosis.
4. Lymphangitic carcinomatosis with hilar adenopathy and thickening of
central bronchovascular interstitium.
5. Alveolar proteinosis: sharply demarcated secondary lobeles with groun
glass attenuation as opposed to secondary lobules with normal aeratio
superimposed inter and intralobular septal thickening (crazy paving).
6. Cardiogenic pulmonary edema.

Cardiogenic pulmonary edema

Patients with pulmonary edema are not imaged with HRCT as their
diagnosis is usually based on a combination of clinical and chest radiographic
findings.
However sometimes the diagnosis is not that straightforward and
knowledge of the HRCT appearance of pulmonary edema can be helpful in
avoiding misdiagnosis.
 HRCT findings in cardiogenic pulmonary edema

 Bilateral septal thickening and ground-glass opacity.

 Perihilar and gravitational distribution predominatly in the dependent lung.
 Cardiomegaly and pleural fluid.

On the left typical features of cardiogenic pulmonary edema

There is smooth septal thickening and some ground glass opacity in the
dependent part of the lungs.
In addition there is bilateral pleural fluid.
In a patient with a known malignancy lymphangitic carcinomatosis would be
high in the differential diagnostic list.

Cardiogenic pulmonary edema

Differential diagnosis of cardiogenic pulmonary edema.

 Lymphangitic carcinomatosis
 Interstitial pneumonia (viral, mycoplasma)
 ARDS
 Pulmonary hemorrhage
On the left another example of cardiogenic pulmonary edema.
This patient had a CT to rule out pulmonary emboli.
There is smooth septal thickening and ground glass opacity in a more
patchy distribution.
Cardiogenic pulmonary edema Note: edema can have a very unusual appearance and be distributed
very patchy: some areas are filled with fluid as opposed to other areas in
immediate vicinity which appear normal.

Hypersensitivity Pneumonitis
Hypersensitivity pneumonitis (HP) is also known as extrinsic allergic alveolitis
(EAA).
HP is an allergic lung disease caused by the inhalation of a variety of
antigens (farmer's lung, bird fancier's lung, 'hot tub' lung, humidifier lung).
The radiographic and pathologic abnormalities in patients can be classified
into acute, subacute, and chronic stages.
Mostly HRCT is performed in the subacute stage of HP, weeks to months
following the first exposure to the antigen or in the chronic phase.
Subacute hypersensitivity pneumonitis
The key findings in the subacute hypersensitivity pneumonitis are:

 ill-defined centrilobular nodules of ground-glass opacity (80% of cases) or

 mosaic pattern of a combination of patchy ground-glass opacity due to lung
infiltration and patchy lucency due to bronchiolitis with air trapping
On the left a case with subacute hypersensitivity pneumonitis with a
typical mosaic pattern and without any signs of septal thickening or
distorsion of the airways.

Subacute hypersensitivity pneumonitis with ill-defined centrilobular

nodules
 On the left a case of subacute hypersensitivity pneumonitis.
There is subtle opacity in the centre of the secondary lobules (arrows) with
sparing of the subpleural region.

The case on the left also demonstrates subtle centrilobular opacity in a

patient with subacute HP.
Notice how ill-defined these centrilobular nodules are.

Sometimes the centrilobular opacities are more nodular in appearance like

in the case on the left.

On the left another case of hypersensitivity pneumonitis.

Here we see the mosaic pattern.
Some secundary lobules demonstrate ground-glass opacity due to lung
infiltration, while others are more lucent due to bronchiolitis with air
trapping.

Subacute hypersensitivity pneumonitis with mosaic pattern

 On the left a patient who presented with acute dyspnoe and a normal chest
film (not shown).
The HRCT at presentation (left) shows lobular areas of ground glass
attenuation.
A control HRCT ten days later demonstrated, that the findings had resolved
without any treatment.
The findings were thought to be due to hypersensitivity pneumonitis.

LEFT: HRCT at presentation

RIGHT: HRCT ten days later
Chronic hypersensitivity pneumonitis
The key findings in chronic hypersensitivity pneumonitis are:

 Mosaic pattern with areas of ground-glass atenuation and areas of low

attenuation.
 Fibrosis and parenchymal distortion in a mid zone distribution.

On the left a patient with chronic hypersensitivity pneumonitis.

The HRCT shows a mosaic pattern with hyperaerated secondary nodules
and secondry nodules of increased attenuation.
Additionally there is septal and intralobular reticular thickening, indicating
Chronic hypersensitivity pneumonitis: Nonspecific chest film, typical already existing irreversible fibrosis.
HRCT-findings.
Differential diagnosis of Hypersensitivity Pneumonitis.

 Subacute stage:
oRB-ILD: seen in smokers, upper lobe predilection, usually associated with
centrilobular emphysema.
o Alveolar proteinosis.
 Chronic stage:
o UIP: may show very similar HRCT findings.
UIP has a strong lower zone distribution.
UIP with honeycombing (left) and chronic HP (right) In chronic HP fibrotic changes are typically seen throughout the whole lun
parenchyma from the periphery towards the centrum.
 Chronic hypersensitivity pneumonitis (2)
The case on the left shows an inspiratory and expiratory scan: the mosaic
pattern with areas of ground-glass attenuation and areas of low attenuation,
that become more evident on the expiratory scan, indicating air trapping.
Signs of fibrosis such as distorted vessels and bronchi as well as septal
thickening are more pronounced in the mid and lower lung zones, but not
limited to the subpleural area.

The images on the left suggest the diagnosis hypersensitivity pneumonitis.

Based on the imaging findigs alone, alveolar proteinosis and other diseases
with a mozaic pattern should be included in the differential diagnosis.

Tuberculosis
Primary TB: Initial infection with consolidation, adenopathy and pleural
effusion.
Secondary TB : Post-primary or reactivation TB.
This is the reactivation of the original infection.
Usually located in the apical segments of upper lobes with cavitation
Endobronchial spread: May occur in both primary and secondary TB,
when the infection is not contained.
Hematogenous spread (miliary TB): May occur in both primary and
secondary TB, when the infection is not contained.
HRCT findings in TB

 Primary TB:
o Consolidation anywhere, lymphadenopathy and pleural effusion. Usually
regresses to calcified lung nodule and calcified ipsilateral lymph node.
 Secondary TB:
o Consolidation in apical segments of upper lobes or superior segments of
lower lobes.
o Cavitation
 Endobronchial spread:
o Tree in bud appearance
 Miliary TB:
o 2-3 mm nodules with random disrtibution.
TB: cavitating lesion and endobronchial spread On the left a patient with TB. There is a cavitating lesion and typical
tree-in-bud appearance. The blue arrow indicates the biopsy needle.
 Miliary TB
This represents a hematogenous dissemination of infection and may occur
in association with either primary or postprimary disease.
It is characterized by uniform small nodules with a random distribution.

Miliary TB
Cavitation in TB
The chest film on the left shows diffuse areas with nodular air space
opacifications.
&#8232;The HRCT demonstrates multiple nodules in peribronchial
distribution, partially confluent, and a cavitation, strongly suggestive for
tuberculosis.&#8232;
Other diseases in the differential are Wegener granulomatosis or
malignancy (both show no tree-in-bud).

TB with cavitation
Endobronchial spread of TB
This can occur with primary or postprimary infection.
In most subjects, the primary infection is localized and clinically inapparent.
However, in 5 to 10% of patients with primary TB, the infection is poorly
contained and dissemination occurs.
This is termed progressive primary tuberculosis.
Extensive cavitation of the tuberculous pneumonia lead to endobronchial
spread of the infection.
Rupture of necrotic lymph nodes into the bronchi can also result in
endobronchial dissemination.

Tree-in-bud appearance is typical for active endobronchial spread of

infection.
It occurs in acute tuberculosis but also in any other bacterial infection.
Endobronchial spread of TB with tree-in-bud
 Differential diagnosis of TB.

 Primary TB: Acute bacterial pneumonia

 Secondary TB: Sarcoidosis, Silicosis, Pneumoconiosis
 Endobronchial spread of TB: Bronchopneumonia, Hypersensitivity pneumon
 Miliary TB: metastases of medullary thyroid ca, chorionca and melanoma.
In both miliary TB and metastases the nodules have a random
distribution.
In miliary TB the nodules are more uniform in size.

LEFT: miliary TB
RIGHT: metastases

Chronic eosinophilic pneumonia

Chronic eosinophilic pneumonia is an idiopathic condition characterized by
filling of the alveoli with eosinophils.
It is associated with an increased number of eosinophils in the peripheral
blood and patients present with fever, cough, weight loss, malaise, and
shortness of breath.
The symptoms are often severe and last three months or more.
Patients respond promptly to treatment with steroids.
HRCT findings in Chronic eosinophilic pneumonia

 Peripheral consolidations with upper lobe predominance (photo negative of

pulmonary edema).
On the left a contrast enhanced CT in a patient with chronic eosinophilic
pneumonia.
Notice peripheral distribution of the consolidations.

Chronic eosinophilic pneumonia

Differential diagnosis of Chronic eosinophilic pneumonia

 Organizing pneumonia (COP)

 Löffler syndrome (eosinophilia and vanishing peripheral consolidations)
 Churg-Strauss syndrome (also serum eosinophilia, asthma, systemic vascu
affecting multiple organs: renal insufficiency, arthralgia and myocarditis and
pericarditis)
 Pulmonary infarcts
The images on the left show the similarities between chronic eosinophilic
pneumonia and organizing pneumonia.
Differentiation has to be made on the basis of clinical and laboratory
Chronic eosinophilic pneumonia (left) versus Organizing pneumonia findings.
(right)

Pneumocystis carinii pneumonia

Pneumocystis carinii pneumonia (PCP) or pneumocystis jiroveci as it is
currently named, is an opportumistic infection in immunocompromised
patients.
PCP used to affect most HIV-infected patients at some point during the
course of their disease, but with the new anti-viral drugs it has become less
common.
Nowadays PCP is seen more in immunosuppressed patients, i.e. transplant
recipients and patients on chemotherapy.
HRCT findings in PCP

 Perihilar or diffuse ground-glass opacification.

 Sometimes thickened septal lines in association with areas of ground-glass
 Later cysts (or pneumatoceles) in 10-35% of patients, typically involving
upper lobes
 Cysts may have bizarre shapes and thick walls
 Following therapy these lesions eventually regress, resulting either in comple
disappearance, or residual nodules or scars
 Pneumothorax in 35% of patients with cysts
On the left an immunocompromised patient with PCP.
The CT findings are diffuse ground-glass opacification.
The findings are not specific for PCP, but in this clinical setting PCP is the
most likely diagnosis.

PCP with diffuse ground-glass opacification

On the left another patient with PCP.
Scroll through the images.

View more images: 1/5

PCP: Scroll through the images

ARDS
 Acute respiratory distress syndrome (ARDS) is a sudden, life-threatening
lung failure requiring mechanical ventilation.
ARDS represents the result of increased permeability often in combination
with injury to the respiratory epithelium.
A variety of underlying conditions, from infections to major trauma, can
cause ARDS.

Primary pulmonary risk factors include aspiration, pneumonia, toxic

inhalation and pulmonary contusion.
Extrapulmonary risk factors are sepsis, pancreatitis, multiple blood
transfusions, trauma and the use of drugs such as heroin.

Mild forms of ARDS may resolve completely, while severe forms result in
irreverible fibrosis.
Why some people develop ARDS and others do not is unknown.
Extra-pulmonary ARDS
On the left a patient who was involved in a traffic accident and within hours
developed ARDS.
The dominant pattern is ground glass opacity.
In the dependent parts of the lung there is also some consolidation, so there
is a gradient from front to back.
An important finding in extra-pulmonary ARDS is the symmetry of the
abnormalities.

Extra-pulmonary ARDS with gravity dependent gradient

Pulmonary ARDS
On the left a patient who developed ARSD as a result of pneumonia (i.e.
pulmonary ARDS).
Note the patchy distribution of lung disease and the almost complete
distorsion more basal.
Patient is ventilated with PEEP (positive end expiratory pressure ) leading to
a barotrauma of the lung parenchyma: there are multiple subpleural cysts
and a bilateral pneumothorax.

Pulmonary ARDS with asymmetric patchy distribution of

consolidations.
Consolidations have a protecting effect on the lung parenchyma under PEEP
ventilation, while the ventrally located areas of more normal lung are most
prone to the effects of barotrauma.
As a result we find cystic destruction ventrally and residual fibrosis mostly in
the ventral lung areas.

LEFT: ARDS. RIGHT: Fibrosis in the anterior parts as a result of

damage related to barotraumas and PEEP ventilation

Idiopathic interstitial pneumonias

 The idiopathic interstitial pneumonias (IIPs) comprise a heterogenous group
of disorders.
They represent fundamental responses of the lung to injury and do not
represent 'diseases' per se.
Idiopathic indicates unknown cause and interstitial pneumonia refers to
involvement of the lung parenchyma by varying combinations of fibrosis
and inflammation.
IIPs include seven entities listed in the table on the left in order of relative
frequency.

These diseases have specific patterns of morphologic findings on HRCT and

histology.
Before we call these findings idiopathic or cryptogenic, we should realise,
that these patterns are also common findings in collagen vascular diseases
(e.g., sclerodermia, rheumatoid arthritis) and drug-related lung diseases.
For instance in patients with rheumatoid arthritis findings of NSIP, UIP, OP
and LIP have been reported.

UIP
Usual Interstitial Pneumonitis (UIP) is a histologic diagnosis.
UIP has distinctive HRCT findings and is usually shown at lungbiopsy, when
honeycombing is visible. If the UIP pattern is of unknown cause (i.e.
idiopathic), the disease is called Idiopathic pulmonary fibrosis (IPF).
IPF accounts for more than 60% of the cases of UIP.

In the presence of a surgical biopsy showing a UIP pattern the diagnosis of

IPF requires exclusion of other known causes of UIP including drug toxicities,
environmental exposures (asbest), and collagen vascular diseases like RA,
SLE, polyarteritis nodosa and sclerodermia.
A long list of drugs have been implicated, but this pattern is most commonly
the result of cytotoxic chemotherapeutic agents such as bleomycin,
busulfan, vincristine, methotrexate, adriamycin, and carmustine (BCNU).

The differentiation between NSIP and UIP has tremendous prognostic

implication for the patient.
UIP is more progressive and more than 50% of patients with UIP die within
3 years.
On the left a chest film of a patient with UIP due to IPF.
The findings on the chest film comprise volume loss and fibrotic changes in
the basal lung area.
The radiographic appearance of honeycombing comprises reticular densities
caused by the thick walls of the cysts.
Whenever you see a chest film with long standing reticulation with a lower
lobe and peripheral preference also think 'UIP'.

Chest film in a patient with UIP demonstrating the reticular pattern in

basal and subpleural distribution due to honeycombing.
 HRCT findings in UIP

 Honeycombing consisting of multilayered thick-walled cysts.

 Architectural distortion with traction bronchiectasis due to fibrosis.
 Predominance in basal and subpleural region.
 Mild mediastinal lymphadenopathy

Typical UIP
Differential diagnosis of UIP.

 Chronic Hypersensitivity Pneumonitis

 End stage Sarcoidosis
 NSIP

Chronic HP may be indistinguishable.

It is suspected if there is a mosaic pattern with sparing of the lung bases or
when there are centrilobular nodules.
Sarcoidosis is a more likely diagnosis if the fibrosis is located in the posterior
parts of the upper lobes or in the perihilar area and if there are also nodules
in a perilymphatic distribution or if there is extensive mediastinal
lymphadenopathy.

The presence of pleural plaques helps for the differentiation between IPF
and asbestosis.

View more images: 1/2

On the left a patient with UIP.
UIP: Lower lobe predominance
Notice the honeycombing and the preference of the subpleural and basal
lung areas.
It is usually easy to recognize the pattern of UIP on HRCT.
UIP: Typical case
NSIP
Nonspecific interstitial pneumonia (NSIP) is by some considered as a specific
entity, with specific histologic characteristics, but by others as a
'wastebasket' diagnosis, representing cases of idiopathic interstitial
pneumonia that cannot be classified as UIP, DIP, or OP.
NSIP is histologically characterized by a homogeneous, uniform pattern of
cellular interstitial inflammation associated with variable degrees of fibrosis.
In contrast, UIP is associated with extensive fibrosis which is temporally
inhomogeneous (i.e. various lesions are of different ages).

NSIP is a very inhomogeneous group.

NSIP ranges from type I which is a cellular pattern seen as ground glass
opacity on HRCT to type IV with a fibrotic pattern, which may be
indistinguishable from UIP.
On the left a patient with a NSIP.
This patient had a rash and muscle weakness.
Scroll through the images.

The predominant finding is ground glass opacity (GGO).

There is very subtle traction bronchiectasis, indicating that the GGO is the
result of fibrosis and therefore irreversible.
It is important to note that we do not see the classic distribution of UIP, from
which NSIP has to be differentiated.
The history of this patient is suggestive for the diagnosis dermatomyositis.
NSIP is by far the most common interstitial lung disease in patients with
connective tissue disease.

View more images: 1/3

Scroll through the images.
NSIP (2)
NSIP is not a diagnosis on it's own.
It is a pattern of lung damage.
For the pathologist the key feature is the uniformity of the abnormality
within the lung.
The role of the radiologist is more to &#8216;exclude UIP pattern&#8217;
rather than to make the diagnosis of NSIP.
The diagnosis of NSIP requires histological proof.
&#8232;In all patients with a NSIP pattern, the clinician should be advised
to look for connective tissue diseases, hypersensitivity pneumonitis or
drugs .

On the left two cases of NSIP.

Note the varying combination of GGO and fibrosis (traction bronchiectasis),
but the lack of honeycombing.
NSIP (3)
NSIP is the prevalent lung pattern in systemic sclerosis and
polymyosisits/dermatomyositis (more than 90%), but also may occur in RA
SLE, Sjögren's and MCTD.
In the images on your left you can appreciate again the spectrum of findings
seen in NSIP.
All three patients were suffering from connective tissue disease, all cases
were biopsy proven. &#8232;
The first (top left) shows a very subtle GGO.
Note the difference in the density of the air within the bronchus and
surrounding lungparenchyma (dark bronchus sign).
The second (top right) is a more obvious example of GGO with a
superimposed fine reticular densities as a result of thickening of the
intralobular septa.
The last image also shows GGO with a fine reticular pattern.
Notice the lack of honeycombing in all three cases, excluding UIP as
diagnosis.
NSIP (4)
The HRCT of this patient with scleroderma and NSIP shows a fine subpleura
reticular pattern in the upper lobes and more extensive abnormalities in the
lower lung zones.
There are also areas of ground-glass and traction bronchiectases, but
honeycombing is typically lacking.
Note also the mildly dilated esophagus, which is consistent with
scleroderma.

COP
Cryptogenic organizing pneumonia (COP) used to be described as
bronchiolitis obliterans with organizing pneumonia (BOOP) in an earlier
version of the classification of idiopathic interstitial pneumonias.
It is a inflammatory process in which the healing process is characterized by
organization of the exudate rather than by resorption ('unresolved
pneumonia').
Organizing pneumonia is mostly idiopathic and then called cryptogenic, but
is also seen in patients with pulmonary infection, drug reactions, collagen
vascular disease, Wegener's granulomatosis and after toxic-fume inhalation.
OP presents with a several-month history of nonproductive cough, low-
grade fever, malaise and shortness of breath.
There is a good response to corticosteroid therapy and a good prognosis.
 OP is again a great mimicker and can show a broad variety of HRCT
findings, which makes it a frequent differential diagnosis and actually
represents a diagnosis of exclusion.
Frequently biopsy is needed for final proof.

HRCT findings in OP

 Bilateral peripheral consolidations, sharply demarcated.

 Consolidations may be migratory.
 Lesions may show pleural tags or spiculae and give the impression of volum
loss and slight retraction of the surrounding parenchyma (DD bronchogenic
carcinoma).
 Bronchial wall thickening and dilatation are seen in most patients and are
usually restricted to areas of consolidation or ground glass opacifications.
 Additional findings are pleural thickening, small pleural effusions and
parenchymal bands.

On the left a patient with the typical bilateral peripheral consolidations of OP.
After exclusion of other diseases such as lymphoma, infection,
bronchoalveolar carcinoma, the diagnosis of cryptogenic organizing
pneumonia was made.
On the left a patient who complained of arthritic pain.&#8232;
There are multiple small bilateral peripheral consolidations.
The findings in this patient are not as specific as in the former case, but this
was also organizing pneumonia, but now related to collagen vascular
disease.

OP in a patient with collagen vascular disease

On the left a patient with rheumatoid arthritis and bilateral peripheral
consolidations as a result of organizing pneumonia.
Patients with OP associated with collagen vascular diseases respond less
well to therapy with steroids.

OP in rheumatoid arthritis
 Differential diagnosis of Organizing Pneumonia.

 Chronic eosinophilic pneumonia

 Bronchoalveolar cell carcinoma
 Aspiration pneumonia
 Pulmonary infarction
 Lymphoma

The images on the left show the similarities between chronic eosinophilic
pneumonia and organizing pneumonia.
Differentiation has to be made on the basis of clinical and laboratory
Chronic eosinophilic pneumonia (left) versus Organizing pneumonia findings.
(right)
RB-ILD and DIP
Respiratory bronchiolitis (RB), respiratory bronchiolitis-associated interstitial
lung disease (RB-ILD), and desquamative interstitial pneumonia (DIP)
represent different degrees of severity of small airway and parenchymal
reaction to cigarette smoke (8).

All smokers have various degrees of respiratory bronchiolitis, but it is usually

asymptomatic.&#8232;
However 5-10% of smokers have a clinically significant lung disease in
association with RB, presenting with symptoms, lung function tests and
auscultatory findings at clinical examination.
The term RB-ILD was proposed to describe the bronchocentric (or
centrilobular) lung disease in these patients and the term DIP was used to
describe the more diffuse disorder.
Radiologically however these diseases cannot be clearly separated because
of the overlap of CT findings.
HRCT findings in RB-ILD

 Centrilobular nodules of ground glass opacity with upper lobe predominance

 Bronchial wall thickening
 Secondary lobuli with decreased attenuation (air trapping)

On the left a patient with RB-ILD.

The dominant feature is ground glass opacification and there are some
thickened interlobular septa (arrow).
Usually these patients will also have smoking induced centrilobular
emphysema and there is some evidence that respiratory bronchiolitis is the
precursor of emphysema.
 RB-ILD (2)
On the left a smoker with RB-ILD with subtle HRCT-findings.
The dominant pattern is ground glass opacification.
Additional findings in this patient are paraseptal emphysema in the upper
lobes and some subtle septal thickening in the basal parts.

Based on these non-specific CT findings there is a broad differential

diagnosis and additional clinical information is mandatory for the interpretion
of the HRCT.
Since this patient is a smoker we first think RB-ILD.
In a immunocompromised patient PCP would be on top of the list.
If this patient was coughing up blood, this probably would be pulmonary
hemorrhage (although we would expect more pulmonary densities in these
patients).
If this patient was a bird-fancier we would first think hypersensitivity
pneumonitis, but mostly these patients do not smoke.
On the left two different patients with similarl HRCT findings.
The left one is a smoker with RB-ILD and the patient on the right has
hypersensitivity pneumonits. Note the difference in severity of ground glass
opacities and the well defined areas of airtrapping in HP.

 If a patient is a smoker, think RB-ILD and look for additional smoking

related features.
 If a patient is a non-smoker, think HP, and look at the expiratory CT scans.
LEFT: RB-ILD in smoker. RIGHT: Hypersensitivity pneumonitis in
non-smoker Somehow smoking seems to protect against HP.
This is not a 100% specific criterium but is quite helpful for differential
diagnosis.
RB-ILD (3)
On the left a patient with DIP.
The HRCT shows diffuse areas of ground-glass density in the lower lobes
and some mosaic pattern as the sole abnormality.
Reticular abnormalities and signs of fibrosis are typically absent.
These abnormalities are usually reversible and will disappear upon cessation
of smoking.

AIP
Acute interstitial pneumonia (AIP, earlier named Hamman Rich
Pneumonitis) is a rare idiopathic lung disease characterized by diffuse
alveolar damage with subsequent fibrosis.
It has a fatal outcome in many cases.
The histologic pattern aswell as the HRCT findings in AIP are
indistinguishable from acute respiratory distress syndrome (ARDS).

The HRCT characteristics are diffuse or patchy consolidation, often with a

crazy paving appearance like in the case on the left.
There are areas of consolidation and extensive areas of ground-glass
AIP density with a crazy-paving appearance.
These abnormalities developed in several days and this rapid progression of
 disease combined with these imaging findings are very suggestive of the
diagnosis AIP.
LIP
Lymphocytic interstitial pneumonitis or LIP is uncommon, being seen mainly
in patients with autoimmune disease, particularly Sjögren's syndrome, and
in patients with AIDS.
Symptoms are nonspecific and often those of the patient's underlying
disease

HRCT findings are usually nonspecific.

On the left a patient with Sjogren's syndrome with LIP.

On the left three different patients with lung cysts.

From left to right: Lymphangiomyomatosis, LIP and Langerhans cell
histiocytosis.

Lymphangiomyomatosis, LIP and Langerhans cell histiocytosis

Drug-induced lung disease

Drug-induced lung disease is a major source of iatrogenic lung injury.
The major diagnostic problem is, that it may present with a large variety of
radiologic patterns.
It may present as organizing pneumonia, eosinophilic pneumonia, fibrosis,
hypersensitivity pneumonitis or even as ARDS.
The diagnosis of drug-induced pulmonary disease is usually one of
exclusion.
 On the left a patient who is treated with cytotoxic drugs for a hematologic
malignancy.

The radiographic findings are areas of ground glass opacity, some traction
bronchiectasis and subtle honeycombing in the left lower lobe.
This could be the result of an idiopathic form of fibrosis like idiopathic
pulmonary fibrosis and non-specific interstitial pneumonitis or fibrosis in
chronic hypersensitivity pneumonitis and longstanding sarcoid.
However it is not one of the typical forms of fibrosis, that we commonly
encounter in patients with a UIP pattern or NSIP pattern seen in
collagenvascular diseases.
When there is fibrosis, that does not fit into any of the common diseases
with fibrosis always consider drug-related lung disease in the differential.

Drug-induced interstitial lung fibrosis

Drug-induced organizing pneumonia is commonly caused by Bleomycin and
Cyclophosphamide and other drugs like Methotrexate, Amiodarone,
Nitrofurantoin and Penicillamine (9).
The HRCT findings are the same as in cryptogenic organizing pneumonia.

Drug-induced organizing pneumonia

Drug-induced non-specific interstitial pneumonita (NSIP) occurs most
commonly as a manifestation of carmustine toxicity or of toxicity from
noncytotoxic drugs such as amiodarone.
The radiologic findings are the same as in other forms of NSIP.

Uncommon interstitial lung diseases

Lymphangiomyomatosis
 Rare disease, that occurs only in premenopausal women
 Characterized by progressive proliferation of atypical muscle cells along the
bronchioles leading to air trapping and the development of thin-walled cysts
that replace normal lung parenchyma.
 Identical pulmonary changes seen in 1% of patients with tuberous sclerosis
(predominant involvement of young men).

Clinical findings:

 Majority of patients present with dyspnea.

 Chylous pleural effusions (40%), Pneumothorax (40%), hemoptysis (40%)
 Patients die within 10 years of the onset of symptoms.
 Pregnancy may exacerbate disease.
 Key findings in Lymphangiomyomatosis:

 Numerous thin-walled cysts, surrounded by normal parenchyma.

 Cysts range from 2mm to 5cm in diameter, are round in shape and more o
less uniform.
 Cysts are distributed diffusely throughout the lungs and upper and lower lob
are involved to a similar degree.
 Wall thickness of the cysts ranges from barely perceptible to 4 mm.
 Mediastinal or hilar adenopathy and pleural effusions (40%).
 Recurrent pneumothorax (40%).

On the left a typical case of LAM with multiple evenly spread thin walled
cysts complicated by a pneumothorax.

Differential diagnosis of Lymphangiomyomatosis:

 Langerhans cell histiocytosis: > 90% are smokers, cysts have irregular shap
and the basal costophrenic angles are spared.
 Centrilobular emphysema: characterized by airspaces that have no percepti
wall, centrilobular artery seen as dot in the centre.
 Lymphoid interstitial pneumonitis: seen in patients with HIV and Sjögren
syndrome.
On the left another typical case of LAM.

.
Langerhans cell histiocytosis
Langerhans cell histiocytosis is also known as pulmonary histiocytosis X or
eosinophilic granuloma.
LCH is probably an allergic reaction to cigarette smoke since more than
90% of patients are active smokers.
In the early nodular stage it is characterized by a centrilobular
granulomatous reaction by Langerhans histiocytes.
In the cystic stage bronchiolar obliteration causes alveolar wall fibrosis and
cyst formation.
HRCT findings in Langerhans cell histiocytosis:

 Early stage:
o Small irregular or stellate nodules in centrilobular location.
 Late stage (more commonly seen)
o Cystic airspaces < 10 mm in diameter with walls that range from barely
perceptible to several millimeters thick.
o Cysts have bizarre shapes, they may coalesce and than become larger.
o Upper and mid lobe predominance.
Early stage Langerhans cell histiocytosis with small nodules o Recurrent pneumothorax.

On the left early stage Langerhans cell histiocytosis with small nodules.
There are no cysts visible.
 In a later stage the nodules start to cavitate and become cysts.
These cysts start as round structures but finally coalesce to become the
typical bizarre shaped cysts of LCH.
In patients with LCH 95% have a smoking history.

Late stage Langerhans' cell histiocytosis. Cysts progress to typical

bizarre shaped cysts.
On the left radiological pathological correlation of Langerhans cell
histiocytosis in respectively nodular stage and early and late cystic stage.

Specimen of Langerhans cell histiocytosis in three different stages

On the left a chest film of a 19 year old patient with Langerhans cell
histiocytosis.
The dominant findig on the chest film is a reticular patern and that's about
as far as you can go.
There is also hyperinflation.
No way you would have recognized that this pattern was caused by multiple
cysts.

This is late stage Langerhans cell histiocytosis.

The most challenging differential diagnosis in this patient is centrilobular

emphysema.
Emphysema however is defined as airspaces without definable walls.
Usually we can identify the central dot sign.
The upper lobe predominance is not helpfull in the differential as we can
appreciate this in many inhalational diseases and also in emphysema.

Langerhans' cell histiocytosis

 On the left another case of Langerhans' cell histiocytosis.
It started as small noduli, which progressed over time to cavitating nodules.
In the end this will progress to bizarre shaped cysts, that replace normal
lung tissue.

Langerhans cell histiosytosis: early phase and late phase

Differential diagnosis of Langerhans cell histiocytosis.

 Nodular LCH:
oSarcoidosis: perilymphatic distribution.
oMetastases: random distribution.
 Cystic LCH:
o LAM: round cysts, evenly distribution in women in the child-bearing age
o Cystic bronchiectasis: 'signet ring sign'.
o Centrilobular emphysema: no walls, central dot.
o LIP

Emphysema, when it is severe, can mimick Langerhans cell histiosytosis.

When it extends beyond the centrilobular area to the edge of the secondary
lobule, it may look as if it is cystic with walls.
In patients with LCH, the pathologist may find LCH, but also areas of
emphysema, respiratory bronchiolitis and even fibrosis.
So these smoking-related diseases do not represent discrete entities.

Emphysema mimicking Langerhans cell histiocytosis

 Alveolar proteinosis
Alveolar proteinosis is a rare disease characterized by filling of the alveolar
spaces with PAS positive material due to an abnormality in surfactant
metabolism.
The diagnosis is based on the suggestive HRCT pattern (crazy paving) and
the characteristic features of BAL fluid (Broncho Alveolar Lavage)

 Usually between 30 and 50 years old.

 Nonproductive cough, fever, and mild dyspnea.
 Prognosis has improved since the advent of treatment using bronchoalveola
lavage.

Alveolar proteinosis with crazy paving pattern

Key findings in alveolar proteinosis

 Crazy paving pattern: reticular pattern superimposed on ground glass

opacification.
 Opacifications range from ground glass to consolidation.
On the left a typical case of alveolar proteinosis with extensive thickening
of interlobular and intra-lobular septa.
This is caused by the fact that the proteinacious material, which is
removed from the alveolar space by macrophages is transported to the
interstitium and thus leads to thickening of septa.

The crazy paving pattern is a rather non-specific finding.

Many other diseases may present with this finding and are listed in the
differential diagnosis.

Differential diagnosis of alveolar proteinosis

 Non cardiogenic edema: ARDS, Acute Interstitial Pneumonia.

 Pneumonia:
o Infection (PCP and CMV).
o OP (organizing pneumonia).
o Chronic eosinophilic pneumonia.
 Hemorrhage.
 Bronchoalveolar ca.

Special Thanks
The authors like to thank Dr. Sujal Desai of the King's College Hospital in
London for his inspiring lectures.
Some of the images used in this overview were provide by him.
We would also like to thank Dr. Richard Webb who produced such a
fabulous educational CD (1).
References
1. High resolution CT of interstitial lung disease: key findings in common disorders
by Schaefer-Prokop, C, Prokop M, Fleischmann D, Herold CJ.
European Radiology 2001;11: 373-392
 2. High Resolution Lung CT, UCSF Interactive Radiology Series on CD-ROM
This browser-based learning file is based on Dr. Webb's HRCT text.
It offers a wide variety of cases dealing with common HRCT patterns of disease, diffuse lung diseases and their
significance, and clinical characteristics.
It is one of the best educational CD's ever made.
3. High resolution CT of diffuse lung disease: value and limitations
by Hansell DM.
Radiol Clin North Am 2001:39: 1115-35
4. HRCT of the lung (3rd edition) Lipincott 2001
by Webb, Mueller and Naidich.
5. High Resolution CT in Diagnosis of Diffuse Infiltrative Lung Disease
by Zampatori M, Sverzellati N, Poletti V et al.
Semin Ultrasound CT MR 2005;20(3): 176-85
6. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification
of the Idiopathic Interstitial Pneumonias
This Joint Statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was
adopted by the ATS Board of Directors, June 2001 and by The ERS Executive Committee, June 2001
7. What Every Radiologist Should Know about Idiopathic Interstitial Pneumonias
by Christina Mueller-Mang, MD, Claudia Grosse, MD, Katharina Schmid, MD, Leopold Stiebellehner, MD, and
Alexander A. Bankier, MD
RadioGraphics 2007;27:595-615
8. Respiratory bronchiolitis, respiratory bronchiolitis-associated interstitial lung disease, and desquamative
interstitial pneumonia: different entities or part of the spectrum of the same disease process?
by LE Heyneman, S Ward, DA Lynch, M Remy-Jardin, T Johkoh and NL Muller
American Journal of Roentgenology, Vol 173, 1617-1622
9. Pulmonary Drug Toxicity: Radiologic and Pathologic Manifestations
by Santiago E. Rossi, MD, Jeremy J. Erasmus, MD, H. Page McAdams, MD, Thomas A. Sporn, MD and Philip C.
Goodman, MD.
Radiographics. 2000;20:1245-1259

Mediastinal Lymph Node Stations

Robin Smithuis
Radiology department of the Rijnland Hospital in Leiderdorp, the Netherlands
 Regional Lymph Node Classification
 Axial CT of Lymph Nodes back to overview print
 Mediastinoscopy and EUS Publicationdate 15-6-
 Conventional mediastinoscopy : 2007
Accurate assessment of the mediastinal lymph nodes is essential in selecting
 Extended mediastinoscopy
the best treatment and prognosis in patients with Non Small Cell Lung Cance
 EUS-FNA
Illustrations and CT-images are provided for a better understanding of the
 Specific Mediastinal Lymph Nodes
mediastinal lymph node stations.

Regional Lymph Node Classification

 Superior Mediastinal Nodes (1-4)

 1. Highest Mediastinal: above the left brachiocephalic vein.

 2. Upper Paratracheal: above the aortic arch, but below the left
brachiocephalic vein.
 3. Pre-vascular or Pre-vertebral: these nodes are not adjacent to the trach
like the nodes in station 2. They are either anterior to the vessels (3A) or
behind the esophagus, which is prevertebral (3P).
 4. Lower Paratracheal (including Azygos Nodes): below upper margin of
aortic arch down to level of main bronchus.

Aortic Nodes (5-6)

 5. Subaortic (A-P window): nodes lateral to ligamentum arteriosum. Thes

nodes are not located between the aorta and the pulmonary trunk, but
lateral to these vessels.
 6. Para-aortic (ascending aorta or phrenic): nodes lying anterior and later
to the ascending aorta and the aortic arch.

Inferior Mediastinal Nodes (7-9)

Click to enlarge  7. Subcarinal.

Regional lymph node classification for lung cancer staging adapted  8. Paraesophageal (below carina).
from the American Thoracic Society mapping scheme  9. Pulmonary Ligament: nodes lying within the pulmonary ligaments.

Hilar, Interlobar, Lobar, Segmental and Subsegmental Nodes

(10-14)

 10-14: these are located outside of the mediastinum.

They are all N1-nodes.

Axial CT of Lymph Nodes

Scroll through the images on the left.

 1. Highest Mediastinal: above left brachiocephalic vein.

 2. Upper Paratracheal: below left brachiocephalic vein and above aortic ar
 3. Pre-vascular and Retrotracheal : anterior to the vessels (3A) or
prevertebral (3P).
 4. Lower Paratracheal : below upper margin of aortic arch down to level o
main bronchus.
 5. Subaortic (A-P window): nodes lateral to ligamentum arteriosum or
lateral to aorta or left pulmonary artery.
 6. Para-aortic: nodes lying anterior and lateral to the ascending aorta and
the aortic arch beneath the upper margin of the aortic arch.
 7. Subcarinal.
 8. Paraesophageal (below carina).
 9. Pulmonary Ligament: nodes lying within the pulmonary ligament.
 10-14: these nodes are outside of the mediastinum.
View more images: 1/8

Mediastinoscopy and EUS

Conventional mediastinoscopy
The following nodal stations can be biopsied by cervical mediastinoscopy:
the left and right upper paratracheal nodes (station 2L and 2R), left and
right lower paratracheal nodes (station 4L and 4R) and the subcarinal
nodes (station 7).
Station 1 nodes are located above the suprasternal notch and are not
routinely accessed by cervical mediastinoscopy.

Extended mediastinoscopy
Left upper lobe tumors may metastasize to the subaortic lymph nodes
(station 5) and paraaortic nodes (station 6).
These nodes can not be biopsied through routine cervical
mediastinoscopy.
Extended mediastinoscopy is an alternative for the anterior-second
interspace mediastinotomy which is more commonly used for exploration
of mediastinal nodal stations.
This procedure is far less easy and therefore less routinely performed than
conventional mediastinoscopy.

EUS-FNA
Endoscopic Ultrasound with Fine Needle Aspiration can be performed of al
the mediastinal nodes that that can be assessed from the oesophagus.
In addition the left adrenal gland and the left liver lobe can be visualized.
EUS particularly provides access to nodes in the lower mediastinum
(station 7,8 and 9)
 Specific Mediastinal Lymph Nodes
1. Highest Mediastinal
Nodes located above a horizontal line running along the upper rim of the
left brachiocephalic vein, where it crosses in front of the trachea.

1. Highest Mediastinal nodes

On the left a station 1 node.
The brachiocephalic vein is still to the left of the midline.
Therefore this node is above the line where the left brachiocephalic
crosses in front of the trachea.

2. Upper Paratracheal
Upper Paratracheal nodes are located below the left brachiocephalic vein
and above the upper margin of the aortic arch.

On the left a station 2 node in front of the trachea.

There is also a small prevascular node, i.e. a station 3A node.
 3. Prevascular and Prevertabral nodes
Station 3 nodes are not adjacent to the trachea like station 2 nodes.
They are either anterior to the vessels (3A) or behind the esophagus,
which lies prevertebrally (3P).

Station 3 nodes are not accessible with mediastinoscopy, however 3P

nodes are accessible with endoscopic ultrasound (EUS).

3A and 3P nodes
On the left a 3A node in the prevascular space.
Notice also lower paratracheal nodes on the right, i.e. 4R nodes.

4. Lower Paratracheal
The lower paratracheal nodes lie below a horizontal line drawn
tangentially to the upper margin of the aortic arch.

4R nodes are lower paratracheal nodes that are located to the right of the
midline of the trachea.
They extend down to a horizontal line that runs across the right main
bronchus at the upper margin of the upper lobe bronchus.

4R. Lower Paratracheal nodes

 On the left we see 4R paratracheal nodes.
In addition there is an aortic node lateral to the aortic arch, i.e. station 6
node.

4L nodes are lower paratracheal nodes that are located to the left of the
tracheal midline, between a horizontal line drawn tangentially to the upper
margin of the aortic arch and a line extending across the left main
bronchus at the level of the upper margin of the left upper lobe bronchus.
These include paratracheal nodes that are located medially to the
ligamentum arteriosum.
Station 5 (AP-window) nodes are located laterally to the ligamentum
arteriosum.

4L. Lower paratracheal nodes

On the left an image just above the level of the pulmonary trunk
demonstrating lower paratracheal nodes on the left and on the right.
In addition there are also station 3 and 5 nodes.
On the left an image at the level of the lower trachea just above the
carina.
To the left of the trachea 4L nodes.
Notice that these 4L nodes are between the pulmonary trunk and the
aorta, but are not located in the AP-window, because they lie medially to
the ligamentum arteriosum.
The node lateral to the pulmonary trunk is a station 5 node.

5. Subaortic nodes
Subaortic or aorto-pulmonary window nodes are lateral to the
ligamentum arteriosum or the aorta or left pulmonary artery and
proximal to the first branch of the left pulmonary artery and lie within the
mediastinal pleural envelope.

6. Para-aortic nodes
Para-aortic (ascending aorta or phrenic) nodes are located anteriorly and
laterally to the ascending aorta and the aortic arch, below the upper
margin of the aortic arch.
7. Subcarinal nodes
These nodes are located caudally to the carina of the trachea, but are not
associated with the lower lobe bronchi or arteries within the lung.

On the left a station 7 subcarinal node to the right of the esophagus.

 8 Paraesophageal nodes
These nodes are below the carina.
They lie adjacent to the esophageal wall and to the right or left of the
midline.
They do not include the subcarinal nodes.

On the left an image below the carina.

To the right of the esophagus a station 8 node.

.
On the left a PET image demonstrating FDG uptake in a station 8 node.
On the corresponding CT image the node is not enlarged (blue arrow).
The probability that this is a lymph node metastasis is extremely high
since the specificity of PET in unenlarged nodes is higher than in enlarged
nodes.

9. Pulmonary ligament nodes

Pulmonary ligament nodes are lying within the pulmonary ligament,
including those in the posterior wall and lower part of the inferior
pulmonary vein.
The pulmonary ligament is the inferior extension of the mediastinal pleura
reflections that surround the hila.

10 Hilar nodes
Hilar nodes are proximal lobar nodes, distal to the mediastinal pleural
reflection and nodes adjacent to the intermediate bronchus on the right.
Nodes in station 10 - 14 are all N1-nodes, since they are not located in the
mediastinum.

References
 1. Conventional mediastinoscopy
by Paul De Leyn and Toni Lerut.
in the Multimedia Manual of Cardiothoracic Surgery
2. Regional lymph node classification for lung cancer staging
by CF Mountain and CM Dresler
Chest, Vol 111, 1718-1723
3. Mediastinal Staging of Non Small-Cell Lung Cancer
by Christian Lloyd, MD, and Gerard A.Silvestri, MD, FCCP Christian Lloyd, MD, and Gerard A.Silvestri, MD, FCCP
Cancer Control, July/August 2001,Vol.8, No.4 Cancer Control 311
4. State of the art lecture: EUS and EBUS in pulmonary medicine
by J. T. Annema, and K. F. Rabe
Endoscopy 2006; 38: 118-122
5. Imaging of the Patient with Non Small Cell Lung Cancer, What the Clinician Wants to Know
by Reginald F. Munden, MD, DMD, Stephen S. Swisher, MD, Craig W. Stevens, MD, PhD and David J. Stewart,
MD
Radiology 2005;237:803-818

Mediastinal Masses : localize and characterize

Sanjeev Bhalla, Marieke Hazewinkel and Robin Smithuis
Cardiothoracic Imaging Section of the Mallinckrodt Institute of Radiology, St. Louis, USA and the Radiology department the Medical Centre Alkmaar and
the Rijnland Hospital, Leiderdorp, the Netherlands
Introduction
Localize to the mediastinum back to overview print
Localize within the mediastinum Publicationdate 5-6-
Anterior Mediastinum : 2007
This review is based on a presentation given by Sanjeev Bhalla and was adapted
 Obliterated retrosternal clear space
for the Radiology Assistant by Marieke Hazewinkel and Robin Smithuis.
 Hilum Overlay Sign
Sanjeev Bhalla is section chief of the Cardiothoracic Imaging Section of the
 Cystic masses
Mallinckrodt Institute of Radiology.
Middle Mediastinum
Posterior Mediastinum This review will focus on how to narrow down the differential diagnosis of
 Cervicothoracic sign mediastinal lesions by localizing and characterizing them.
More than one compartment
Characterize
 Fluid containing masses
 Fat containing masses
 Enhancing masses

Introduction
Whenever you see a mass on a chest x-ray that is possibly located within the
mediastinum, your goal is to determine the following:

 Is it a mediastinal mass?
 Is it in the anterior, middle or posterior mediastinum?
 Are you able to characterize the lesion by determining whether it has any fatt
fluid or vascular components?
 The table on the left is the overall table for mediastinal masses.
In the next paragraphs we will discuss each compartment separately.

Statistically, it is important to remember the following:

 Most masses (> 60%) are:

o Thymomas
o Neurogenic Tumors
o Benign Cysts
o Lymphadenopathy (LAD)

 In children the most common (> 80%) are:

o Neurogenic tumors
o Germ cell tumors
o Foregut cysts

 In adults the most common are:

o Lymphomas
o LAD
o Thymomas
o Thyroid masses

Localize to the mediastinum

The following characteristics indicate that a lesion originates within the
mediastinum:

 Unlike lung lesions, a mediastinal mass will not contain air bronchograms.
 The margins with the lung will be obtuse.
 Mediastinal lines (azygoesophageal recess, anterior and posterior junction line
will be disrupted.
 There can be associated spinal, costal or sternal abnormalities.

A lung mass abutts the mediastinal surface and creates acute angles with the
lung, while a mediastinal mass will sit under the surface creating obtuse
angles with the lung (Figure).

LEFT: A lung mass abutts the mediastinal surface and creates acute
angles with the lung.
RIGHT: A mediastinal mass will sit under the surface of the
mediastinum, creating obtuse angles with the lung.
On the left you see two different patients.
Describe the findings and continue.

On the x-ray on the left there is a lesion that has an acute border with the
mediastinum.
This must be a lung mass.
The chest radiograph on the right shows a lesion with an obtuse angle to the
mediastinum.
This must be a mediastinal mass.
Since there is a silhouette-sign with the right heart border - which is located
anteriorly - we can deduce that the mass must be located within the anterior
mediastinum.

The lesion on the left was a pancoast tumor.

The lesion on the right was a thymoma, located within the anterior
mediastinum.

Localize within the mediastinum

The mediastinum can be divided into anterior, middle and posterior
compartments.
It is important to remember that there is no tissue plane separating these
compartments.

On the lateral radiograph the anterior and middle compartments can be

separated by drawing an imaginary line anterior to the trachea and
posteriorly to the inferior vena cava.
The middle and posterior compartments can be separated by an imaginary
line passing 1 cm posteriorly to the anterior border of the vertebral bodies.
This division allows us to make a more narrow differential diagnosis.

In many hospitals a CT will be made to further analyze and characterize

anterior and middle mediastinal masses.
An MRI is usually made to analyze masses located in the posterior
compartment because the majority of these masses turn out to be
neurogenic in nature.
An additional CT can be performed, when bone needs to be assessed.

Anterior Mediastinum
The anterior mediastinum contains the following structures: thymus, lymph
nodes, ascending aorta, pulmonary artery, phrenic nerves and thyroid.

The most common lesions that you will see in the anterior mediastinum will
either be of thymic or lymph node origin.
Even the germ cell tumors arise from the pluripotent cells of the thymus.
Before you want to biopsy an anterior mediastinal mass, do not forget thta
some of these lesions can be vascular in origin.

The four T's make up the mnemonic for anterior mediastinal masses::

1. Thymus
2. Teratoma (germ cell)
3. Thyroid
 4. Terrible Lymphoma

On conventional radiographs look for the signs listed in the table on the left.

The finding of an obliterated retrosternal clear space is not so helpfull

anymore, since nowadays many patients are obese.
In these patients the retrosternal space can be filled with fat.

Obliterated retrosternal clear space

Describe the images on the left.
Then continue.

On the PA film there is a lobulated widening of the superior mediastinum.

On the lateral chest film the retrosternal clear space is obliterated.

This happened to be a patient with lymphoma.

On the left FDG-PET images of the same patient.

There are multiple lymphatic masses in the anterior, middle and even
posterior mediastinum, spreading to the neck.

Hilum Overlay Sign

When there is a mediastinal mass and you still can see the hilar vessels
through this mass, then you know the mass does not arise from the hilum.
This is known as the hilum overlay sign.
Because of the geometry of the mediastinum most of these masses will be
located in the anterior mediastinum.

Describe the images on the left.

Then continue.

Hilum Overlay Sign: hilar vessels are seen through a mediastinal On the chest film there is a mass that has obtuse angles with the
mass mediastinum, so it is a mediastinal mass.
The hilar vessels are seen through this mass, so it does not arise from the
hilum and probably will arise from the anterior mediastinum.
The anterior location was confirmed on a CT.
Most commonly this will be a mass of thymic or lymphatic origin.
This proved to be a lymphoma in a HIV-positive patient.
Cystic masses
The anterior mediastinum is an important location for cystic masses.
Masses can be entirely cystic (thymic cysts) or have solid components
(lymphoma or cystic thymoma).
Some masses are cystic with enhancing septations - in these cases you
should think of a germ cell tumor.
Describe the image on the left.
Then continue.

The CT shows an anterior mediastinal mass with water density attenuation.

This is typical for a thymic cyst.

Describe the image on the left.

Then continue.

The CT shows a mass located in the anterior mediastinum.

The mass is cystic but has solid enhancing septa.
This finding is very specific for a germ cell tumor.

Now many think that germ cell tumors contain fat and if a lesion does not
contain fat, it cannot be a germ cell tumor.
You have to remember, that only about 60 % of germ cell tumors contain
fat, so you must realize that the absence of fat does not exclude a germ cell
tumor from the differential diagnosis.
The more solid components a germ cell tumor has, the more likely the tumor
is to be malignant.
Describe the image on the left.
Then continue.

The CT shows a mass located in the anterior mediastinum.

The mass is cystic but has solid enhancing components, so we are worried
about lymphoma, germ cell tumor and cystic thymoma.
This proved to be a cystic thymoma.

Middle Mediastinum
The middle mediastinum contains the following structures: lymph nodes,
trachea, esophagus, azygos vein, vena cavae, posterior heart and the aortic
arch.

The majority of middle mediastinal masses will consist of foregut duplication

cysts (eg oesophageal duplication or bronchogenic cysts) or
lymphadenopathy.
Aortic arch anomalies can also present as middle mediastinal masses.

Fluid containing lesions are usually duplication cysts or necrotic lymph nodes.
A pancreatic fluid collection due to pancreatitis may also present as a
mediastinal mass.
A fibrovascular esophageal polyp is a mesenchymal lesion which almost
always contains fat.
Vascular lesions are arch anomalies, azygos continuation due to interrupted
inferior vena cava or hyperenhancing lymph nodes.
On conventional radiographs look for the signs listed in the table on the left.

Displaced azygoesophageal recess wiil be seen on the right.

On the left you may have a pseudoparavertebral line.
This is a new interface that looks like a paravertebral line.
Describe the image on the left.
Then continue.

On the AP chest radiograph of this patient there is widening of the

azygoesophageal recess on the right.
There is an apparent widening of the paravertebral line on the left.
On the lateral film the mass is anterior to the spine and therefore is located in
the middle mediastinal.

On the CT the azygoesophageal recess is displaced to the right due to

oesophageal varices (blue arrow) and there is also a new interface on the
left.
This is a patient with cirrhosis of the liver and varices as a result of portal
hypertension.

On the left a patient with a small cell lung carcinoma.

Describe the images on the left.
Then continue.

On the PA film there is a lobulated paratracheal stripe on the right.

On the lateral radiograph there is a density overlying the ascending aorta and
filling the retrosternal space.
These findings indicate a mass in the anterior aswell as in the middle
mediastinum.

The CT confirms the presence oof lymphomas in both the anterior and the
middle mediastinum.
 On the left two different patients.
One of these patients has pulmonary hypertension and the other has
sarcoidosis.
Describe the images on the left.
Then continue.

On the right image there is a lobulated mass surrounding the right bronchus
creating a 'doughnut' with the bronchus as the hole in the doughnut.
On the left image there is only density in the area from 9 o'clock to 3 o'clock
and not in the 3 - 9 o'clock area.
So the patient on the left has pulmonary hypertension with moderately
enlarged vessels while the patient on the right has sarcoidosis with
widespread lymphadenopathy.

When there is a density in the 3 - 9 o'clock area, there should always be

concern about mediastinal masses.

Posterior Mediastinum
The posterior mediastinum contains the following structures: sympathetic
ganglia, nerve roots, lymph nodes, parasympathetic chain, thoracic duct,
descending thoracic aorta, small vessels and the vertebrae.

Most masses in the posterior mediastinum are neurogenic in nature.

These can arise from the sympathetic ganglia (eg neuroblastoma) or from
the nerve roots (eg schwannoma or neurofibroma).
Don't forget lymphadenopathy, the vertebrae and the descending thoracic
aorta as potential causes for posterior mediastinal masses.
Cystic lesions will be either neuroenteric cysts, schwannomas or
meningoceles.
Fat containing lesions will be extramedullary hematopoiesis.
When the anemia is resolved the extramedullary marrow will stop producing
blood and become fatty.

On conventional radiographs look for:

 Cervicothoracic Sign
 Widening of the paravertebral stripes
Cervicothoracic sign
The anterior mediastinum stops at the level of the superior clavicle.
Therefore, when a mass extends above the superior clavicle, it is located
either in the neck or in the posterior mediastinum.
When lung tissue comes between the mass and the neck, the mass is
probably in the posterior mediastinum.
This is known as the Cervicothoracic Sign.

If we study the image on the frontal view on the left, we see a mass
extending above the level of the clavicle and there is lung tissue in front of it,
so this must be a mass in the posterior mediastinum.
 On the left the MR of the same patient.
It turned out to be a schwannoma.

On the left images of a patient, who has a disease, that is the most
commonly missed diagnosis in the emergency department resulting in the
number one cause of law suits.
Study the images and then continue.

Notice the widening of the paravertebral stripes on both the left and the right
on the PA radiograph.
On the lateral radiograph there is a severely narrowed disc space.

The diagnosis is discitis.

On MR you will notice the edema of the soft tissues and the high signal
intensity of the disc.

More than one compartment

Since there are no tissue planes separating the mediastinal compartments,
there are lesions that do not respect our approach to the mediastinum.
These lesions tend to occupy more than one compartment and include:
mediastinitis, hematomas, vascular entities, bronchogenic cancer,
metastases and lymphangiomas (fluid containing).

Characterize
Once you have localized a mediastinal mass, next try to charcterize it by
assessing whether it has any of the following characteristics:

 Does the mass contain fluid?

 Does it contain fat?/li>
 Does it enhance following the administration of intravenous contrast?
 Fluid containing masses
This is a list of mediastinal msses that may contain fluid:

 Thymic Cyst
 Thymoma
 Teratoma
 Pericardial Cyst
 Foregut Duplication
 Meningocoele
 Neuroenteric Cyst
 Cystic Lymphadenopathy
 Lymphangioma

If a mass contains fluid it could be a teratoma (on the left) or a thymic cyst
(on the right).
Note that this teratoma does not contain fat.
Teratomas are the most common benign germ cell tumors.
The most common malignant germ cell tumor is the seminoma.
Describe the image on the left.
Then continue.

There is are multiple masses in both the anterior and middle mediastinum.
The attenuation values are of water density.
These findings favor the diagnosis of cystic lymphadenopathy in a patient
with metastatic disease.

Describe the image on the left.

Then continue.

There is a cystic lesion in the middle mediastinum.

There is a fluid fluid level with milk of calcium.
Foregut duplication cysts occasionally contain milk of calcium like in this
example of an esophageal duplication cyst.
 Fat containing masses
The differential diagnosis of fat containing mediastinal masses is:

 Thymolipoma
 Teratoma (Germ cell tumors)
 Esophageal lipoma
 Fat deposition
 Lipoma
 Lipoblastoma
 Liposarcoma
 Extramedullary hematopoiesis

On the left we see an fat-containing anterior mediastinal mass.

This is the typical finding of a fat-containing teratoma.
Describe the image on the left.
Then continue.

The axial CT and sagittal MR demonstrate a lipomatous lesion within the

lumen of the esophagus.
This is typical for a esophageal lipoma and its fibrovascular stalk.

Enhancing masses
The differential diagnosis of enhancing mediastinal masses is:

 Hyperenhancing lymph nodes

 Thyroid tissue
 Paragangliomas
 Hemangiomas
 Vascular Etiologies

On the left multiple enhancing lesions.

This is typical for hyperenhancing lymph nodes.

Enhancing lymphomas can be seen in:

 Melanoma
Multiple enhancing lesions in multiple compartments
 Renal cell carcinoma
 Thyroid carcinoma
 Castlemann's disease (as in this case)
 Describe the image.
Then continue.

First notice the large thymus in this young child.

There is also an enhancing mass in the posterior mediastinum extending into
the vertebral canal.
This is typical for a hemangioma.

Enhancing posterior mediastinal mass in a child.

Describe the image.
Then continue.

Somewhat irregular enhancing mass in the anterior mediastinum.

This proved to be a thyroid mass.

Non-Small Cell Lungcancer : staging

IJsbrand Zijlstra, Otto van Delden, Cornelia Schaefer-Prokop and Robin Smithuis
Department of Radiology of the Academical Medical Centre, Amsterdam and the Rijnland Hospital, Leiderdorp, the Netherlands
 TNM-classification
 T-Staging back to overview print
 T1 - tumor Publicationdate 20-8-
 T2 - tumor : 2007
Lungcancer is the leading cause of cancer-related mortality in bo
 T3 - tumor
men and women.
 T4 - tumor
Lungcancer is classified into two categories, small cell lung cance
 Pancoast tumor
(SCLC) and non-small cell lung cancer (NSCLC).
 N - Staging SCLC usually has metastasized by the time of presentation.
 Regional Lymph Node Classification System It is therefore not curable and will not be discussed in this review
 N1 - Nodes NSCLC is a group of primary lung neoplasms with the same
 N2 - Nodes staging system and therapy and it can be cured with resection if
 N3 - Nodes is in an early stage.
 CT vs PET-CT in N-staging .
 M-Staging Therefore the most important question in a patient with NSCLC
 PET-CT whether the tumor is resectable.
 In this review we will discuss:
 TNM-classification of NSCLC.
 T-staging with CT.
 N- and M-staging with CT and PET-CT.

TNM-classification
NSCLC includes adenocarcinoma (35-40%), squamous cell
carcinoma (25-30%) and large cell carcinoma (10-15%).
NSCLC is staged according to the TNM-staging system.

TNM subsets are grouped into certain stages, because these

patients share similar prognostic and therapeutic options.
For instance all stage IIIA patients have a 5 year-survival of
10%.

In the table on the left resectable stages are indicated in

Stages of bronchial carcinoma adapted from Mountain 1998.
green and unresectable stages are indicated in red.
Stages in green are surgical candidates. In red are uresectable.
Stage IIIA is possibly resectable, usually after combined-
modality therapy consisting of platinum-based chemotherapy
and radiation.
Stage IIIB, i.e. any patient who has T4 or N3 disease is
virtually unresectable, but in some countries there are
subgroups of patients that will get a resection.
Evidently all patients with distant metastases (stage IV) are
inoperable.
The goal of imaging is to decide whether the tumor is
resectable and whether it should be a lobectomy or a
pneumonectomy.

On the left a patient with a tumor near the fissure.

On coronal reconstructions it was demonstrated that there
was no transfissural growth.
Lobectomy therefore is a possibilty.

LEFT: Axial image of tumor near fissure.

RIGHT: Coronal reconstruction showing no transfissural growth.
Lobectomy is not possible if there is:

 Tranfissural growth.
 Pulmonary vascular invasion.
 Invasion of main bronchus.
 Involvement of upper and lower lobe bronchi.

Thin collimation and MPR are necessary in order to clearly

demonstrate the relation of a tumor with the fissure.

On the left a case with transfissural growth on both coronal

Coronal and sagital reconstruction showing transfissural growth. and sagittal reconstructions.
Lobectomy is not possible.

T-Staging
 In the Table on the left an overview of T-staging.

T-staging is best done with CT to determine the local extent

and to look for satellite nodules.
There are advantages if CT precedes bronchoscopy and the
information from CT is used by the bronchoscopist.
CT however has important limitations in overall staging.
Preoperative predictions with CT differ from operative staging
in 45% of cases.
Patients are being both over- and understaged.
CT staging remains unsatisfactory for detecting hilar (N1)
and mediastinal (N2 and N3) lymph node metastases, and
for chest wall involvement (T3) or mediastinal invasion (T4),
in which sensitivity and specificity can be less than 65%.

MR is more useful than CT in the following cases:

 mediastinal ingrowth
 pancoast tumor
 vertebral ingrowth

PET has a limited role in T-staging because of its lack of

resolution.
PET however is of great value in N- and M-staging.
T1 - tumor
 Diameter of 3 cm or smaller and surrounded by lung or visce
pleura or
 endobronchial tumor distal to the lobar bronchus

On the left a typical T1 tumor.

T1 tumor
T2 - tumor
 Greater than 3 cm
 Invasion of the visceral pleura
 Atelectasis or obstructive pneumopathy involving less than th
whole lung
 Tumor involving the main bronchus 2 cm or more distal to th
carina.

On the left a typical T2 tumor with obstructive infiltrate of the

left lower lobe.
The tumor is located in the main bronchus, but the distance
is more than 2 cm from the carina.
T2 tumor
 T3 - tumor
 Tumor with atelectasis or obstructive pneumonitis of the enti
lung
 Tumor in the main bronchus within 2 cm of the carina but no
invading it
 Tumor of any size with invasion of non-vital structures such a
the chest wall, mediastinal pleura, diaphragm, pericardium.

Chest pain usually indicates chest wall invasion (i.e.T3).

A Pancoast tumor is a tumor that involves the superior sulcus
and the chest wall is almost always involved in these patients
T3 tumor with invasion of the chest wall. (i.e. T3).
Local chest wall invasion can be treated with en-bloc
resection.

On the left a typical T3 tumor.

T4 - tumor
 Invasion of vital mediastinal structures ((heart, trachea,
esophagus, great vessels).
 Invasion of vertebral body
 Malignant pleural or pericardial effusion (cytologically proven)
 Satellite tumor within the same lung as the primary tumor
(biopsy proven).

On the left an endobronchial tumor of the left main bronchus

within 2 cm of the carina.
This means that it is at least a T3 tumor.
There is also invasion of the mediastinum (blue arrow) and
invasion of the pulmonary artery (small yellow arrow),
indicating that this is a T4-tumor.
T4 tumor. Coronal reconstruction at the level of the carina.
In many cases T4-tumors do not pose a diagnostic dilemma.
On the left we see a large mass that invades the
mediastinum.
There is complete obliteration of the superior vena cava with
collaterals in the para-aortic and paraspinal regions.
The aortic arch is partially surrounded by tumor.

T4 tumor with invasion of the mediastinum

 T4 - tumor (2)
On the left another straight forward case.
The tumor invades the mediastinum and surrounds and
narrows the right pulmonary artery.

T4 tumor constricting the right pulmonary artery (blue arrow)

T4 - tumor (3)- mediastinal invasion
In many cases it is not certain whether there is mediastinal
invasion.
These are patients with a mass that is not clearly invading
the mediastinum but that do not have an intervening fat-
plane (Figure).

In the case on the left there is an intimate relationship of the

tumor with the right brachiocephalic vein.
This should be dagnosed as 'indeterminate mediastinal
invasion'.
This patient should be given the benefit of the doubt and get
an operation, since that is the only chance for definitive cure.
At surgery the tumor fell away from the mediastinum and
Tumor with possible invasion of the mediastinum was subsequently succesfully resected.
On the left an odd case, that was recently published in the
NEJM, to illustrate the difficulty of determining mediastinal
invasion (11).

A CT showed a mass in the right upper lobe, closely

associated with the paratracheal soft tissues, indicating
possible mediastinal invasion.
A needle biopsy of the mass resulted in a pneumothorax.
Repeat CT imaging with the patient in a right decubitus
position revealed that the mass had moved with the lung and
had separated completely from the trachea and
'Staging' pneumothorax (Courtesy Robert C. Hoch, M.D. Minnesota mediastinum.
Lung Center (11) Evidently this is not a T4-tumor, but a T2-tumor.
The patient underwent resection of the right upper lobe.
 T4 - tumor (4)- Satellite nodules
In patients with NSCLC the presence of satellite metastatic
nodules may be considered a contraindication to surgical
treatment.
However the use of multidetector CT has led to the detection
of a considerable number of indeterminate satellite lesions.
Obtaining a differential diagnosis of these lesions is extremely
important in defining the therapeutic strategy (12).

CT demonstrates satellite nodule in ipsilateral lobe (arrow) next to In many institutions T4-tumors due to satellite metastatic
tumor in lower lobe. PET demonstrates FDG-uptake only in large nodules in the ipsilateral lung will be resected, since these
tumor. patients have a slightly better prognosis than other T4-
patients and have a chance of completeness of resection.

PET scan is of limited value in the detection and

differentiation of satellite nodules.
Many nodules are not detected by PET because of their small
size (figure).
On the left a patient with a lungcancer in the left upper lobe.
In the right upper lobe a second nodule is seen.
Both lesions show FDG-uptake.

A malignant node in another lobe can either be a metastasis

or a synchronous primary tumor.
In this case, if it is a metastasis, this means stage IV disease,
which is not resectable, because it is not in the ipsilateral
lung.
If it is a synchronous primary tumor, it is possibly resectable.
CT and PET demonstrate second nodule in right upper lobe in a
patient with lungcancer in left upper lobe.
T4 - tumor (5)- pleural effusion
Malignant pleural effusion has a poor prognosis.
These patients usually die within 3 months.
In patients with malignant pleural effusion aspiration will yield
a false negative results in about a third of the cases.
If the cytology is negative, you can either do another
thoracocenthesis or do a VATS-procedure (video assisted
thoracoscopy) and obtain pleural biopsies.
T4 - tumor (6) - resectability
There is some controversy concerning the resectability of
certain T4-tumors.
As mentioned above in some institutions T4-tumors due to
ipsilateral satellite nodules will be resected.
In some institutions even limited invasion of the vertebral
body or the heart is no contraindication for surgery.

On the left a T4 tumor with invason of the left atrium.

The invasion is usually through the pulmonary veins.

T4 tumor with invason of the left atrium (arrow)

 Pancoast tumor
A Pancoast tumor is a tumor of the superior pulmonary
sulcus characterized by pain due to invasion of the brachial
plexus, Horner's syndrome and destruction of bone due to
chest wall invasion.
MR is superior to CT for local staging due to its superior soft
tissue contrast.
Sagittal T1WI will best demonstrate ingrowth into thoracic
and cervical nerves.
Axial MR will best demonstrate ingrowth into mediastinum
and vertebral canal.
Pancoast tumors are staged at least as T3, because there is
almost always chest wall invasion.
When there is ingrowth into a vertebral body or vital
mediastinal structures, the tumor is staged as T4.
Nodes in pancoast tumors are treated differently than in
other tumors.
Pancoast tumor in the right upper lobe with displacement of the Ipsilateral supraclavicular nodes (N3) are potentially
superior mediastium and trachea. resectable with en bloc resection, while mediastinal nodes
(N2) are not.
In 20% of patients there will be N2 nodes, so all patients with
a pancoast tumor should undergo mediastinoscopy with
sampling of mediastinal nodes before surgery.
On the left a detail of an AP-film of the cervical spine of a
patient with pain in the neck and shoulder.
A mass is seen in the apex of the left lung.
This proved to be a Pancoast with ingrowth in the brachial
plexus.

Pancoast tumor seen on AP-film of cervical spine

On the left the chest film of the same patient.
Notice how difficult it is to depict the tumor.
We will continue with the MR-images.
 On the left sagittal T1-weighted images after the
administration of Gadolinium.
Scroll through the images by clicking on the arrows.
Notice how the tumor grows through the chest wall and
invades the structures of the neck.
Only a small part of the tumor is actually within the lung.

View more images: 1/5

Pancoast tumor. Scroll through the images by clicking on the
arrows.
Pancoast tumors are potentially resectable if only one of the
following occurs:

1. Rib destruction.
2. Limited vertebral body involvement < 50%.
3. T1 nerve involvement.

Patients are nowadays treated with a trimodality approach.

First they undergo preoperative radiotherapy and
chemotherapy (chemoradiation), followed by restaging and
finally en-bloc resection of the upper lobe and the chest wall i
there is no evidence of progressive disease.

On the left a Pancoast tumor.

The tumor abuts the root T1 (long white arrow), but the
Operable Pancoast tumor. Sagittal contrast-enhanced T1-weighted other roots of the brachial plexus are free in the interscalene
image. The tumor abuts the root T1 (long arrow), but the other triangle (green arrow).
roots of the brachial plexus are not involved. A = subclavian artery, This patient is operable.
ASM = anterior scalene muscle. (Courtesy of Wouter van Es, MD.
St. Antonius Hospital Nieuwegein, The Netherlands)
Pancoast tumors are unresectable if one of the following
occurs:

1. Brachial plexus involvement above T1 (Ingrowth of C8

higher level).
2. Elevated diaphragm (i.e. ingrowth of nerves C3-4-5).
3. Esophageal or tracheal involvement (i.e. vital mediastin
structures).
4. Vertebral body involvement > 50%.
5. N2 (mediastinal) or N3 (contralateral).
6. Distant metastases.

On the left another patient with a Pancoast tumor.

The tumor is seen as an enhancing mass and invades the
Inoperable Pancoast tumor. Sagittal contrast-enhanced T1-weighted interscalene triangle, where the roots and trunks of the
image. Invasion of brachial plexus (white arrow). Encasement of the brachial plexus are located.
subclavian artery (A). (Courtesy of Wouter van Es, MD. St. Antonius There is encasement of the subclavian artery (A).
Hospital Nieuwegein, The Netherlands)

N - Staging
Regional Lymph Node Classification System
Lymph node staging is done according to the American
Thoracic Society mapping scheme.
Read more about mediastinal lymph node staging in the
article called 'Mediastinal Lymph Node Stations'.

Superior Mediastinal Nodes

 1. Highest Mediastinal: above left brachiocephalic vein

 2. Upper Paratracheal: below 1. and above aortic arch
 3. Pre-vascular and Retrotracheal
 4. Lower Paratracheal (including Azygos Nodes): below uppe
margin of aortic arch down to level of main bronchus

Aortic Nodes

 5. Subaortic (A-P window): nodes lateral to ligamentum

arteriosum or lateral to aorta or left pulmonary artery.
 6. Para-aortic (ascending aorta or phrenic): nodes lying anter
and lateral to the ascending aorta and the aortic arch beneat
the upper margin of the aortic arch.
Adapted from the American Thoracic Society mapping scheme
Inferior Mediastinal Nodes

 7. Subcarinal
 8. Paraesophageal (below carina)
 9. Pulmonary Ligament: nodes lying within the pulmonary
ligament

Hilar, Interlobar, Lobar, Segmental and Subsegmenta

Nodes

 10-14: these are nodes that are outside of the mediastinum.

These are all N1-nodes.

N1 - Nodes
N1-nodes are ipsilateral nodes within the lung up to hilar
nodes.
N1 alters the prognosis but not the management.
A T1-tumor without positive nodes within the lung has a 5-y
survival of 61%.
The same T1-tumor with N1-nodes has a 5-y survival of
34%.

On the left a T2 tumor (> 3cm) in the right lower lobe with
ipsilateral hilar node (N1).
 N2 - Nodes
Although we all have learned, that N2-nodes are resectable,
there is only a subset of patients with N2 disease that
benefits from resection.
Those are the patients who, after a negative
mediastinoscopy, are found to have microscopic metastatic
disease at the time of thoracotomy.
Those patients have a better prognosis.
Patients however with bulky N2-nodes on CT and FDG-PET
will not undergo surgery.
They are treated with neo-adjuvant therapy followed by
definitive locoregional treatment, which may consist of either
radiotherapy or surgery.

T4N2-tumor On the left a tumor in the right upper lobe with progression
into the mediastinum (T4) with ipsilateral mediastinal N2
nodes in station 4R.
On the left a patient with a lungcancer and hilar nodes (N1),
right paratracheal (station 4R = N2) and a prevascular node
(station 3 = N2).

N3 - Nodes
N3-nodes are clearly unresectable.
These are contralateral mediastinal or contralateral hilar
nodes or any scalene or supraclavicular nodes.

On the left a central tumor in the right lung.

Lymphadenopathy all the way up to the lower paratracheal
station on the left (i.e. station 4L).
This is N3-stage due to contralateral mediastinal nodes.

N3-stage disease.
 On the left two patients with lungcancer in the right lung.
Both have contralateral nodes.
If these lymph nodes contain tumor cells, this means
inoperable stage IIIB-disease.

Two patients with N3-disease.

On the left another patient with lungcancer.
Scroll through the images and stage the tumor.

There is possible ingrowth into the mediastinum.

Notice the extensive spread into the mediastinal lymphnodes
up to the highest level.
The next step should be US-guided FNA.

View more images: 1/5

CT vs PET-CT in N-staging
Regardless of the threshold size of lymph node chosen, CT
findings in isolation can not be taken as clear evidence of
malignant nodal involvement.
20% of all nodes deemed malignant on CT criteria will be
benign.
Size alone cannot be an exclusion criterion and proof is
needed by biopsy or resection that a node is indeed
malignant.

It is now well established that PET is a much better technique

than CT in the determining the lymph node status in patients
with NSCLC.
In the Table on the left a list of studies that clearly
demonstrated the superiority of PET over CT.
False-positive mediastinal nodal scans occur in sarcoid,
tuberculosis and other infections.

In normal-sized mediastinal lymph nodes PET has a

sensitivity and specificity of 74 and 96%, respectively, for
detecting metastasis.
This means that if the PET is positive in these normal-sized
nodes, there is almost always a lymph node metastasis.
Only in 4% of cases PET is false negative.

In enlarged mediastinal lymph nodes (short axis diameter of

10 mm or more) PET has a sensitivity and specificity of 95
 and 76%, respectively.
This means that PET depicts almost all the metastases, but is
false positive due to reactive nodes in 24%.
On the left a patient who during follow up for obstructive
pulmonary disease presented with a mass in the left upper
lobe.
On the chest film enlarged nodes are seen in the AP-window
(i.e. station 5 nodes).

The next diagnostic step was a PET-CT which clearly depicted

the tumor, many positive mediastinal nodes, but also nodes
in the neck on the left side (i.e. N3-disease).
This indicates stage IIIB, non-operable.
The PET also showed activity in the right upper lung, which
can be a metastasis or a synchronous tumor.

There were no palpable nodes in the neck region, but

ultrasound depicted the nodes that were PET-positive.
Fine needle aspiration was performed and the diagnosis of
NSCLC was made (i.e. N3-disease).

Enlarged lymph node lateral to the carotid artery.

On the left a patient with a solitary pulmonary nodule.
There is FDG-uptake in the nodule, but not in the
mediastinaum or elsewhere in the body.
This is probably a T1N0M0 tumor (Stage I)

Classification of disease as stage I on the basis of a clinical

examination and negative results from CT and PET
examinations appears sufficient to exclude mediastinal
disease.
In this case there is no need for mediastinoscopy, because
the accuracy of PET-CT is as high as it is.

Classification of stage II and III diseases is more

FDG-uptake in solitary pulmonary nodule, but no evidence of nodal controversial.
disease or distant metastases. The negative predictive value of PET decreases in relation to
the size of the metastases, the presence of centrally located
primary disease or N1 nodes, and the avidity of the primary
tumor for 18F-FDG.
In addition, the presence of hypermetabolic central tumors or
hilar lymph nodes can decrease the detectability of
mediastinal lymph nodes and thus the negative predictive
value of mediastinal PET.
For stage II and III diseases, the incidence of false-negative
results is still greater with PET than with mediastinoscopy
(respectively 11.7% and 3%).
Mediastinoscopy likely will remain part of the standard
protocol for mediastinal staging for stage II and III diseases.

M-Staging
PET-CT
We will soon present an article focussed on the role of PET-
CT in the staging of lungcancer and the evaluation of solitary
pulmonary nodules.
In this review only some brief remarks are made.

Distant metastases are very common in patients with lung

cancer.
Almost every organ may be involved but the extra-thoracic
sites posing common clinical problems are brain metastases,
bone metastases, sometimes with cord compression, nodal
spread, adrenal and liver involvement.

PET-CT is extremely helpful in the detection of distant

metastases.
In a study of 100 patients PET was compared with
conventional imaging, which consisted of CT of chest and
upper abdomen, bone scintigraphy, brain-CT or MR (3).
PET had superior sensitivity and specificity in the lung, liver,
adrenals and bone.
Not suprisingly PET was only less sensitive in the brain due to
the high glucose uptake in the normal brain.
In this study 9% of patients had metastases demonstrated
by PET that were not found with conventional imaging,
whereas 10% of patients suspected of having metastases
because of conventional imaging findings were correctly
shown with PET not to have metastases.

Because of the high negative predictive value, PET scanning

should be performed in all patients with no evidence of
metastatic disease on CT who are considered candidates for
surgery.
On the left a CT- and corresponding PET image of a tumor in
the right lung.
Continue with the PET-overview.
 PET-image demonstrates FDG-uptake in mediastinal nodes,
but also in the liver (yellow arrows) and the spine (red arrow)
indicating distant metastases.

References
1. STATE OF THE ART - Lung Cancer - Where Are We Today? - Current Advances in Staging and Nonsurgical
Treatment
by Stephen G. Spiro and Joanna C. Porter.
American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 1166-1196, (2002)
2. Effectiveness of positron emission tomography in the preoperative assessment of patients with suspected non-
small-cell lung cancer: the PLUS multicentre randomised trial.
H. van Tinteren et al.
The Lancet, Volume 359, Issue 9315, Pages 1388-1392
3. Staging Non-Small Cell Lung Cancer with Whole-Body PET
Edith M. Marom et al
Radiology. 1999;212:803-809
4. Staging of Non Small-Cell Lung Cancer with Integrated Positron-Emission Tomography and Computed
Tomography
Didier Lardinois et al.
NEJM, Volume 348:2500-2507, June 19, 2003, Number 25
5. Non Small Cell Lung Cancer: Prospective Comparison of Integrated FDG PET/CT and CT Alone for Preoperative
Staging
Sung Shine Shim et al.
Radiology 2005;236:1011-1019.
 6. Integrated PET-CT for the Characterization of Adrenal Gland Lesions in Cancer Patients: Diagnostic Efficacy and
Interpretation Pitfalls
Semin Chong et al
RadioGraphics 2006;26:1811-1824
7. State of the Art: Integrated PET/CT: Current Applications and Future Directions
Gustav K. von Schulthess et al
Radiology 2006;238:405-422
8. The Role of PET Scan in Diagnosis, Staging, and Management of Non-Small Cell Lung Cancer
Liesbet Schrevens, Natalie Lorent, Christophe Dooms, Johan Vansteenkiste
The Oncologist, Vol. 9, No. 6, 633-643, November 2004
9. Clinical Applications of PET in Oncology
Eric M. Rohren, MD, PhD, Timothy G. Turkington, PhD and R. Edward Coleman, MD
Radiology 2004;231:305-332
10. PET Evaluation of Lung Cancer
by Tira Bunyaviroch, MD and R. Edward Coleman, MD
Journal of Nuclear Medicine Vol. 47 No. 3 451-469, 2006
11. 'Staging' Pneumothorax.
Images in Clinical Medicine by Robert C. Hoch, M.D., Minnesota Lung Center.
NEJM Volume 356:2312 May 31, 2007 Number 22
12. Positron Emission Tomography to Evaluate Lung Lesions

Solitary pulmonary nodule: benign versus malignant

Differentiation with CT and PET-CT
Ann Leung and Robin Smithuis
Department of Radiology, Stanford University Medical Center, Stanford, California and the Department of Radiology, Rijnland Hospital, Leiderdorp, the
Netherlands
 CT: benign versus malignant
 Calcification back to overview print
 Size Publicationdate 20-5-
 Growth : 2007
The differential diagnosis of a solitary pulmonary nodule is broad and
 Shape
management depends on whether the lesion is benign or malignant.
 Margin
In this overview we will discuss some of the new features that can help to
 Air Bronchogram sign
differentiate between benign and malignant nodules based upon CT and PET
 Solid and Ground-glass components CT findings.
 Contrast enhancement
 PET-CT: benign versus malignant
 Conclusion

CT: benign versus malignant

Calcification
Diffuse, central, laminated or popcorn calcifications are benign patterns of
calcification.
These types of calcification are seen in granulomatous disease and
hamartomas.
All other patterns of calcification should not be regarded as a sign of
benignity.
Benign pattern of calcification
The exception to the rule above is when patients are known to have a
primary tumor.
For instance the diffuse calcification pattern can be seen in patients with
osteosarcoma or chondrosarcoma.
Similarly the central and popcorn pattern can be seen in patients with GI-
 tumors and patients who previously had chemotherapy.
Size
A solitary pulmonary nodule (SPN) is defined as a single intraparenchyma
lesion less than 3 cm in size and not associated with atelectasis or
lymphadenopathy.
A lesion greater than 3 cm in diameter is called a mass.
This distinction is made, because lesions greater than 3 cm are usually
malignant, while smaller lesions can be either benign or malignant.

Swensen et al studied the relationship between the size of a SPN and the
chance of malignancy in a cohort at high risk for lung cancer (1).
Their findings are listed in the table on the left.
Relationship between SPN-size and chance of malignancy in patients They concluded that benign nodule detection rate is high, especially if
with high risk for lung cancer lesions are small.
Of the over 2000 nodules that were less than 4 mm in size, none was
malignant.
Growth
Comparison with prior imaging studies is often the most useful procedure
to determine the importance of the finding of a SPN, since stability over 2
years is highly associated with benignity.
Shape
Japanese screening studies showed that a polygonal shape and a three-
dimensional ratio > 1.78 was a sign of benignity (2,3).
A polygonal shape means that the lesion has multiple facets (multi-sided).
A peripheral subpleural location was also a sign of benignity in this study.

The three-dimensional ratio is measured by obtaining the maximal

transverse dimension and dividing it by the maximal vertical dimension.
A large three-dimensional ratio indicates that the lesion is relatively flat,
which is a benign sign.
Transverse image (left) and coronal reconstruction (right)
Three-dimensional ratio = transverse dimension : vertical dimension
Margin
 Corona radiata sign - highly associated with malignancy (figure)
 Lobulated or scalloped margins - intermediate probability
 Smooth margins - more likely benign unless metastatic in origin

Corona radiata sign in a malignant lesion with spiculation at the

margin.
 Air Bronchogram sign
Recent studies have showed that an air bronchogram is more commonly
seen in malignant pulmonary nodules.
It is most commonly seen in BAC (bronchoalveolar cell carcinoma) and
adenocarcinoma.

The case on the left shows an airbronchogram seen as a linear lucency

(broad arrow) and as a more cystic lucency (small arrow) due to the fact
that the bronchus is seen en face.

Air bronchogram sign seen in

On the left two solitary pulmonary nodules.
Based upon the morphology, which lesion has the most malignant
features?

The lesion on the far left has a spicuated margin and has lucencies within
it.
The lesion next to it is lobulated in contour and has some spicules
radiating to the pleura.
It is however homogeneous in attenuation.
Based on these findings we should be most concerned that the lesion on
the far left is malignant.
It proved to be an adenocarninoma, while the other one was a fungal
infection.
The lucencies and frank air bronchograms should not mislead you in
thinking that it probably is infection.
Solid and Ground-glass components
Another result from screening studies is that nodules containing a ground-
glass component are more likely to be malignant (5).

 Partly solid lesions with ground-glass components had a malignancy rate

63%.
 Nonsolid - only ground-glass lesions had a malignancy rate of 18%.
 Only solid lesions had a malignancy rate of only 7%.

Partly solid nodule containing ground-glass component most likely to

be malignant
 On the far left a lesion that only has a ground-glass appearance and next
to it a lesion that has both ground-glass and solid components.
The likelihood of malignancy is 1:5 for the lesion on the far left and 2:3 for
the lesion with both ground-glass and solid components.

LEFT: 1 in 5 malignant
RIGHT: 2 in 3 malignant
Contrast enhancement
Contrast enhancement less than 15 HU has a very high predictive value
for benignity (99%).
After a baseline scan, 4 consecutive scans at 1 minute interval are
performed.

This applies only for nodules with the following selection criteria:

Baseline scan and scans after contrast enhancement. Benign lesion 1. Nodule > 5mm
with < 15 HU enhancement. 2. Relatively spherical
3. Homogeneous, no necrosis, fat or calcification
4. No motion or beam hardening artifacts

PET-CT: benign versus malignant

PET-CT plays an increasingly important role in the evaluation of solitary
nodules.

When you perform PET-CT, you have to realize the following:

1. PET has a very high sensitivity 95%, but a lesser specificity of only
81%
2. PET is false positive in granulomatous disease
3. PET is usually false negative in size < 10 mm and low-grade
malignancy including bronchoalveolar carcinoma and carcinoid
False negative PET in a patient with adenocarcinoma.
Activity is not sufficient for the diagnosis malignancy. With these specificity numbers, there will be false positives in about 20%,
depending on the background prevalence of granulomatous disease.
On the left a patient with an adenocarcinoma, that was not
hypermetabolic on the PET, so it is a false negative PET.

Conclusion
In the differentiation of benign versus malignant solitary pulmonary
nodules nowadays new imaging features have to be added.
We especially have to look for the presence of areas of ground-glass
opacity, air bronchograms or cavities and the three-dimensional ratios of
a lesion.
 With the increasingly important role of PET-CT, we have to be aware of
the accuracy of PET-CT and we should have an idea about the prevalence
of infectious and non-infectious granulomatous disease in the area that
we practice.
References
1. CT Screening for Lung Cancer: Five-year Prospective Experience
Stephen J. Swensen et al
Radiology 2005;235:259-265.
2. Indeterminate Solitary Pulmonary Nodules Revealed at Population-Based CT Screening of the Lung: Using First
Follow-Up Diagnostic CT to Differentiate Benign and Malignant Lesions
Shodayu Takashima et al.
AJR 2003; 180:1255-1263
3. Small Solitary Pulmonary Nodules (1 cm) Detected at Population-Based CT Screening for Lung Cancer: Reliable
High-Resolution CT Features of Benign Lesions
Shodayu Takashima et al.
AJR 2003; 180:955-964
4. CT Screening for Lung Cancer Frequency and Significance of Part-Solid and Nonsolid Nodules
Claudia I. Henschke et al
AJR 2002; 178:1053-1057

Lung cancer - New TNM

IJsbrand Zijlstra, Otto van Delden, Cornelia Schaefer-Prokop and Robin Smithuis
Department of Radiology of the Academical Medical Centre, Amsterdam and the Rijnland Hospital, Leiderdorp, the Netherlands
 TNM-overview
 What is new in 7th edition of TNM back to overview print
 T-Staging Publicationdate 2-7-
 T1 - tumor : 2010
This is an updated version of the 2005 article 'Lung cancer -
 T2 - tumor
staging'.
 T3 - tumor
It is adapted to the new guidelines in the 7th Edition of TNM in
 T4 - tumor
Lung Cancer of the International Association for the Study of Lu
 Pancoast tumor Cancer (IASLC) Staging Committee in 2009.
 N - Staging
 Regional Lymph Node Classification System Lungcancer is classified into two categories: small cell lung cance
 N1 - Nodes (SCLC) and non-small cell lung cancer (NSCLC).
 N2 - Nodes NSCLC is a group of primary lung neoplasms with the same
 N3 - Nodes staging system and therapy and can be cured with resection if it
 CT vs PET-CT in N-staging in an early stage.
 M-Staging
 PET-CT In this review we will discuss:
 TNM-classification.
 T-staging with CT.
 N- and M-staging with CT and PET-CT.

TNM-overview
 T1
Tumor < 3 cm diameter, surrounded by lung or visceral
pleura, without invasion more proximal than lobar bronchus.

T2
Tumor > 3 cm but < 7 cm, or tumor with any of the
following features:

 Involves main bronchus > 2 cm distal to carina

 Invades visceral pleura
 Associated with atelectasis or obstructive pneumonitis that
extends to the hilar region but does not involve the entire lun

New T-staging according to the 7th edition of the TNM-staging of T3

lungcancer Tumor > 7 cm or any of the following:
Click on image to enlarge
 Directly invades any of the following: chest wall, diaphragm,
phrenic nerve, mediastinal pleura, parietal pericardium, main
bronchus < 2 cm from carina without involvement of the
carina.
 Atelectasis or obstructive pneumonitis of the entire lung
 Separate tumor nodules in the same lobe

T4
Tumor of any size that invades the mediastinum, heart,
great vessels, trachea, recurrent laryngeal nerve, esophagus,
vertebral body, carina, or with separate tumor nodules in a
different ipsilateral lobe.
In 2009 a new Lung cancer lymph node map was proposed
by the International Association for the Study of Lung Cancer
(IASLC) in order to reconcile the differences between the
Naruke and the MD-ATS maps and refine the definitions of
the anatomic boundaries of each of the lymph node stations.

 go to the IASLC lymph node map 2009

Stages
NSCLC includes adenocarcinoma, squamous cell carcinoma
and large cell carcinoma and is staged according to the TNM-
staging system.
TNM subsets are grouped into certain stages, because these
patients share similar prognostic and therapeutic options.
For instance all stage IIIA patients have a 5 year-survival of
10%.

In the table on the left resectable stages are indicated in

Stages of lung cancer adapted from the 7th Edition of TNM in Lung green and unresectable stages are indicated in red.
Cancer Stage IIIA is possibly resectable, usually after combined-
modality therapy consisting of platinum-based chemotherapy
and radiation.
Stage IIIB, i.e. any patient who has T4 or N3 disease is
virtually unresectable, but in some countries there are
subgroups of patients that will get a resection.
Evidently all patients with distant metastases (stage IV) are
inoperable.
What is new in 7th edition of TNM

1. T1 tumors
o T1 is subclassified in T1a: 2 cm or less and T1b: > 2
cm but 3 cm or less, since they have a different
prognosis.
2. T2 tumors
o Small T2 tumors (> 3 cm but < 5 cm) become T2a
and T2a N1 M0 cases are downstaged from stage II
to IIA.
o Large T2 tumors > 5 cm but < 7 cm become T2b.
o Large T2 > 7 cm is reclassified as T3.
T2b N0 M0 cases change from stage IB to IIA.
3. T3 tumors
o T3 N0 M0 is reclassified from IB to IIB
o T3 N1 M0 from IIB to IIIA.
4. T4 tumors
o T4 by additional tumor nodules in the lobe of the
primary is now downstaged to T3.
These tumors will be down-staged from stage IIIB t
IIIA (if N1 or N2) or to stage IIB (if N0).
o Those cases with additional tumor nodules in other
ipsilateral lobes are downstaged to T4 and not M1.
They will be down-staged from stage IV to IIIB (if N
or N3) and to stage IIIA (if N0 or N1).
Tumors that are T4 due to other features will be dow
staged if N0 or N1 from stage IIIB to stage IIIA.
5. M tumors
o Tumors associated with pleural or pericardial nodule
or effusions become M1a instead of T4 and are
consequently up-staged from IIIB to stage IV.
o M tumors are subclassified into M1a (contralateral lu
nodules and pleural dissemination) and M1b (distan
metastasis).
In the table on the left the changes for the new stage
grouping in the revised TNM staging system .
 The goal of imaging is to decide whether the tumor is
resectable and whether it should be a lobectomy or a
pneumonectomy.

On the left a patient with a tumor near the fissure.

On coronal reconstructions it was demonstrated that there
was no transfissural growth.
Lobectomy therefore is a possibilty.

LEFT: Axial image of tumor near fissure.

RIGHT: Coronal reconstruction showing no transfissural growth.
Lobectomy is not possible if there is:

 Transfissural growth.
 Pulmonary vascular invasion.
 Invasion of main bronchus.
 Involvement of upper and lower lobe bronchi.

Thin collimation and MPR are necessary in order to clearly

demonstrate the relation of a tumor with the fissure.

On the left a case with transfissural growth on both coronal

Coronal and sagital reconstruction showing transfissural growth. and sagittal reconstructions.
Lobectomy is not possible.

T-Staging
In the Table on the left the new T-staging according to the
7th edition of the TNM-staging of lungcancer.

T-staging is best done with CT to determine the local extent

and to look for satellite nodules.
There are advantages if CT precedes bronchoscopy and the
information from CT is used by the bronchoscopist.
CT however has important limitations in overall staging.
Preoperative predictions with CT differ from operative staging
in 45% of cases.
Patients are being both over- and understaged.
CT staging remains unsatisfactory for detecting hilar (N1)
and mediastinal (N2 and N3) lymph node metastases, and
for chest wall involvement (T3) or mediastinal invasion (T4),
in which sensitivity and specificity can be less than 65%.

MR is more useful than CT in the following cases:

 mediastinal ingrowth
 pancoast tumor
 vertebral ingrowth

PET has a limited role in T-staging because of its lack of

resolution.
PET however is of great value in N- and M-staging.
 T1 - tumor
 Diameter of 3 cm or smaller and surrounded by lung or visce
pleura or
 endobronchial tumor distal to the lobar bronchus
 T1A= < 2 cm
 T1B= 2 cm - 3 cm

On the left a typical T1 tumor.

T1 tumor
T2 - tumor
 Greater than 3 and smaller than 7 cm
 T2a= 3 cm - 5 cm
 T2b= 5 cm - 7 cm
 Invasion of the visceral pleura
 Atelectasis or obstructive pneumopathy involving less than th
whole lung
 Tumor involving the main bronchus 2 cm or more distal to th
carina.

On the left a typical T2 tumor with obstructive infiltrate of the

left lower lobe.
T2 tumor The tumor is located in the main bronchus, but the distance
is more than 2 cm from the carina.
T3 - tumor
 Tumor with atelectasis or obstructive pneumonitis of the enti
lung
 Tumor in the main bronchus within 2 cm of the carina but no
invading it
 Tumor of any size with invasion of non-vital structures such a
the chest wall, mediastinal pleura, diaphragm, pericardium.
 Separate tumour nodules in the same lobe as the primary
tumor.

Chest pain usually indicates chest wall invasion (i.e.T3).

T3 tumor with invasion of the chest wall. A Pancoast tumor is a tumor that involves the superior sulcus
and the chest wall is almost always involved in these patients
(i.e. T3).
Local chest wall invasion can be treated with en-bloc
resection.

On the left a typical T3 tumor.

 T4 - tumor
 Invasion of vital mediastinal structures: fat, heart, trachea,
esophagus, great vessels, recurrent laryngeal nerve, carina.
 Invasion of vertebral body.
 Malignant pleural or pericardial effusion (cytologically proven)
 Separate tumour nodule(s) in a different ipsilateral lobe to th
of the primary tumor.

On the left an endobronchial tumor of the left main bronchus

within 2 cm of the carina.
This means that it is at least a T3 tumor.
There is also invasion of the mediastinum (blue arrow) and
invasion of the pulmonary artery (small yellow arrow),
indicating that this is a T4-tumor.
T4 tumor. Coronal reconstruction at the level of the carina.
In many cases T4-tumors do not pose a diagnostic dilemma.
On the left we see a large mass that invades the
mediastinum.
There is complete obliteration of the superior vena cava with
collaterals in the para-aortic and paraspinal regions.
The aortic arch is partially surrounded by tumor.

T4 tumor with invasion of the mediastinum

T4 - tumor (2)
On the left another straight forward case.
The tumor invades the mediastinum and surrounds and
narrows the right pulmonary artery.

T4 tumor constricting the right pulmonary artery (blue arrow)

 T4 - tumor (3)- mediastinal invasion
In many cases it is not certain whether there is mediastinal
invasion.
These are patients with a mass that is not clearly invading
the mediastinum but that do not have an intervening fat-
plane (Figure).

In the case on the left there is an intimate relationship of the

tumor with the right brachiocephalic vein.
This should be dagnosed as 'indeterminate mediastinal
invasion'.
This patient should be given the benefit of the doubt and get
an operation, since that is the only chance for definitive cure.
At surgery the tumor fell away from the mediastinum and
Tumor with possible invasion of the mediastinum was subsequently succesfully resected.
On the left an odd case, that was recently published in the
NEJM, to illustrate the difficulty of determining mediastinal
invasion (11).

A CT showed a mass in the right upper lobe, closely

associated with the paratracheal soft tissues, indicating
possible mediastinal invasion.
A needle biopsy of the mass resulted in a pneumothorax.
Repeat CT imaging with the patient in a right decubitus
position revealed that the mass had moved with the lung and
had separated completely from the trachea and
'Staging' pneumothorax (Courtesy Robert C. Hoch, M.D. Minnesota mediastinum.
Lung Center (11) Evidently this is not a T4-tumor, but a T2-tumor.
The patient underwent resection of the right upper lobe.
T3/T4 - tumor (4)- Satellite nodules
In patients with NSCLC the presence of satellite metastatic
nodules may be considered a contraindication to surgical
treatment.
However the use of multidetector CT has led to the detection
of a considerable number of indeterminate satellite lesions.
Obtaining a differential diagnosis of these lesions is extremely
important in defining the therapeutic strategy (12).

CT demonstrates satellite nodule in ipsilateral lobe (arrow) next to In many institutions T3/T4-tumors due to satellite metastatic
tumor in lower lobe. PET demonstrates FDG-uptake only in large nodules in the ipsilateral lung will be resected, since these
tumor. patients have a slightly better prognosis than other T4-
patients and have a chance of completeness of resection.

PET scan is of limited value in the detection and

differentiation of satellite nodules.
Many nodules are not detected by PET because of their small
size (figure).
 On the left a patient with a lungcancer in the left upper lobe.
In the right upper lobe a second nodule is seen.
Both lesions show FDG-uptake.

A malignant node in another lobe can either be a metastasis

or a synchronous primary tumor.
In this case, if it is a metastasis, this means stage IV disease,
which is not resectable, because it is not in the ipsilateral
lung.
If it is a synchronous primary tumor, it is possibly resectable.
CT and PET demonstrate second nodule in right upper lobe in a
patient with lungcancer in left upper lobe.
T4 - tumor (6) - resectability
There is some controversy concerning the resectability of
certain T4-tumors.
As mentioned above in some institutions T4-tumors due to
ipsilateral satellite nodules will be resected.
In some institutions even limited invasion of the vertebral
body or the heart is no contraindication for surgery.

On the left a T4 tumor with invason of the left atrium.

The invasion is usually through the pulmonary veins.

T4 tumor with invason of the left atrium (arrow)

Pancoast tumor
A Pancoast tumor is a tumor of the superior pulmonary
sulcus characterized by pain due to invasion of the brachial
plexus, Horner's syndrome and destruction of bone due to
chest wall invasion.
MR is superior to CT for local staging due to its superior soft
tissue contrast.
Sagittal T1WI will best demonstrate ingrowth into thoracic
and cervical nerves.
Axial MR will best demonstrate ingrowth into mediastinum
and vertebral canal.
Pancoast tumors are staged at least as T3, because there is
almost always chest wall invasion.
When there is ingrowth into a vertebral body or vital
mediastinal structures, the tumor is staged as T4.
Nodes in pancoast tumors are treated differently than in
other tumors.
Pancoast tumor in the right upper lobe with displacement of the Ipsilateral supraclavicular nodes (N3) are potentially
superior mediastium and trachea. resectable with en bloc resection, while mediastinal nodes
(N2) are not.
In 20% of patients there will be N2 nodes, so all patients with
a pancoast tumor should undergo mediastinoscopy with
sampling of mediastinal nodes before surgery.
 On the left a detail of an AP-film of the cervical spine of a
patient with pain in the neck and shoulder.
A mass is seen in the apex of the left lung.
This proved to be a Pancoast with ingrowth in the brachial
plexus.

Pancoast tumor seen on AP-film of cervical spine

On the left the chest film of the same patient.
Notice how difficult it is to depict the tumor.
We will continue with the MR-images.

On the left sagittal T1-weighted images after the

administration of Gadolinium.
Scroll through the images by clicking on the arrows.
Notice how the tumor grows through the chest wall and
invades the structures of the neck.
Only a small part of the tumor is actually within the lung.

View more images: 1/5

Pancoast tumor. Scroll through the images by clicking on the
arrows.
 Pancoast tumors are potentially resectable if only one of the
following occurs:

1. Rib destruction.
2. Limited vertebral body involvement < 50%.
3. T1 nerve involvement.

Patients are nowadays treated with a trimodality approach.

First they undergo preoperative radiotherapy and
chemotherapy (chemoradiation), followed by restaging and
finally en-bloc resection of the upper lobe and the chest wall i
there is no evidence of progressive disease.

On the left a Pancoast tumor.

The tumor abuts the root T1 (long white arrow), but the
Operable Pancoast tumor. Sagittal contrast-enhanced T1-weighted other roots of the brachial plexus are free in the interscalene
image. The tumor abuts the root T1 (long arrow), but the other triangle (green arrow).
roots of the brachial plexus are not involved. A = subclavian artery, This patient is operable.
ASM = anterior scalene muscle. (Courtesy of Wouter van Es, MD.
St. Antonius Hospital Nieuwegein, The Netherlands)
Pancoast tumors are unresectable if one of the following
occurs:

1. Brachial plexus involvement above T1 (Ingrowth of C8

higher level).
2. Elevated diaphragm (i.e. ingrowth of nerves C3-4-5).
3. Esophageal or tracheal involvement (i.e. vital mediastin
structures).
4. Vertebral body involvement > 50%.
5. N2 (mediastinal) or N3 (contralateral).
6. Distant metastases.

On the left another patient with a Pancoast tumor.

The tumor is seen as an enhancing mass and invades the
Inoperable Pancoast tumor. Sagittal contrast-enhanced T1-weighted interscalene triangle, where the roots and trunks of the
image. Invasion of brachial plexus (white arrow). Encasement of the brachial plexus are located.
subclavian artery (A). (Courtesy of Wouter van Es, MD. St. Antonius There is encasement of the subclavian artery (A).
Hospital Nieuwegein, The Netherlands)

N - Staging
 Regional Lymph Node Classification System
Lymph node staging is done according to the American
Thoracic Society mapping scheme.

Supraclavicular zone (1)

 1. Low cervical, supraclavicular and sternal notch nodes

Superior Mediastinal Nodes (2-4)

 2. Upper Paratracheal: above the aortic arch, but below the

clavicles.
 3A. Pre-vascular: these nodes are not adjacent to the trache
like the nodes in station 2, but they are either anterior to the
vessels.
 3P. Pre-vertebral: these nodes are not adjacent to the trache
like the nodes in station 2, but they are behind the esophagu
which is prevertebral (3P).
 4. Lower Paratracheal (including Azygos Nodes): below uppe
margin of aortic arch down to level of main bronchus.

Aortic Nodes (5-6)

 5. Subaortic (A-P window): nodes lateral to ligamentum

arteriosum. These nodes are not located between the aorta a
the pulmonary trunk, but lateral to these vessels.
Adapted from the American Thoracic Society mapping scheme
 6. Para-aortic (ascending aorta or phrenic): nodes lying ante
and lateral to the ascending aorta and the aortic arch.

Inferior Mediastinal Nodes (7-9)

 7. Subcarinal.
 8. Paraesophageal (below carina).
 9. Pulmonary Ligament: nodes lying within the pulmonary
ligaments.

Hilar, Interlobar, Lobar, Segmental and Subsegmenta

Nodes (10-14)

 10-14. N1-nodes: these are located outside of the

mediastinum.
They are all N1-nodes.
 go to the IASLC lymph node map 2009
 N1 - Nodes
N1-nodes are ipsilateral nodes within the lung up to hilar
nodes.
N1 alters the prognosis but not the management.
A T1-tumor without positive nodes within the lung has a 5-y
survival of 61%.
The same T1-tumor with N1-nodes has a 5-y survival of only
34%.

On the left a T2 tumor (> 3cm) in the right lower lobe with
ipsilateral hilar node (N1).

N2 - Nodes
Although we all have learned, that N2-nodes are resectable,
there is only a subset of patients with N2 disease that
benefits from resection.
Those are the patients who, after a negative
mediastinoscopy, are found to have microscopic metastatic
disease at the time of thoracotomy.
Those patients have a better prognosis.
Patients however with bulky N2-nodes on CT and FDG-PET
will not undergo surgery.
They are treated with neo-adjuvant therapy followed by
definitive locoregional treatment, which may consist of either
radiotherapy or surgery.

T4N2-tumor On the left a tumor in the right upper lobe with progression
into the mediastinum (T4) with ipsilateral mediastinal N2
nodes in station 4R.
On the left a patient with a lungcancer and hilar nodes (N1),
right paratracheal (station 4R = N2) and a prevascular node
(station 3A = N2).
 N3 - Nodes
N3-nodes are clearly unresectable.
These are contralateral mediastinal or contralateral hilar
nodes or any scalene or supraclavicular nodes.

On the left a central tumor in the right lung.

Lymphadenopathy all the way up to the lower paratracheal
station on the left (i.e. station 4L).
This is N3-stage due to contralateral mediastinal nodes.

N3-stage disease.
On the left two patients with lungcancer in the right lung.
Both have contralateral nodes.
If these lymph nodes contain tumor cells, this means
inoperable stage IIIB-disease.

Two patients with N3-disease.

On the left another patient with lungcancer.
Scroll through the images.

There is possible ingrowth into the mediastinum.

Notice the extensive spread into the mediastinal lymph
nodes up to the station 1 level, i.e. N3.
The next step should be US-guided FNA.

View more images: 1/5

CT vs PET-CT in N-staging
Regardless of the threshold size of lymph node chosen, CT
findings in isolation can not be taken as clear evidence of
malignant nodal involvement.
20% of all nodes deemed malignant on CT criteria will be
benign.
Size alone cannot be an exclusion criterion and proof is
needed by biopsy or resection that a node is indeed
malignant.

It is now well established that PET is a much better technique

than CT in the determining the lymph node status in patients
with NSCLC.
 In the Table on the left a list of studies that clearly
demonstrated the superiority of PET over CT.
False-positive mediastinal nodal scans occur in sarcoid,
tuberculosis and other infections.

In normal-sized mediastinal lymph nodes PET has a

sensitivity and specificity of 74 and 96%, respectively, for
detecting metastasis.
This means that if the PET is positive in these normal-sized
nodes, there is almost always a lymph node metastasis.
Only in 4% of cases PET is false negative.

In enlarged mediastinal lymph nodes (short axis diameter of

10 mm or more) PET has a sensitivity and specificity of 95
and 76%, respectively.
This means that PET depicts almost all the metastases, but is
false positive due to reactive nodes in 24%.
On the left a patient who during follow up for obstructive
pulmonary disease presented with a mass in the left upper
lobe.
On the chest film enlarged nodes are seen in the AP-window
(i.e. station 5 nodes).

The next diagnostic step was a PET-CT which clearly depicted

the tumor, many positive mediastinal nodes, but also nodes
in the neck on the left side (i.e. N3-disease).
This indicates stage IIIB, non-operable.
The PET also showed activity in the right upper lung, which
can be a metastasis or a synchronous tumor.

There were no palpable nodes in the neck region, but

ultrasound depicted the nodes that were PET-positive.
Fine needle aspiration was performed and the diagnosis of
NSCLC was made (i.e. N3-disease).

Enlarged lymph node lateral to the carotid artery.

 On the left a patient with a solitary pulmonary nodule.
There is FDG-uptake in the nodule, but not in the
mediastinaum or elsewhere in the body.
This is probably a T1N0M0 tumor (Stage I)

Classification of disease as stage I on the basis of a clinical

examination and negative results from CT and PET
examinations appears sufficient to exclude mediastinal
disease.
In this case there is no need for mediastinoscopy, because
the accuracy of PET-CT is as high as it is.

Classification of stage II and III diseases is more

FDG-uptake in solitary pulmonary nodule, but no evidence of nodal controversial.
disease or distant metastases. The negative predictive value of PET decreases in relation to
the size of the metastases, the presence of centrally located
primary disease or N1 nodes, and the avidity of the primary
tumor for 18F-FDG.
In addition, the presence of hypermetabolic central tumors or
hilar lymph nodes can decrease the detectability of
mediastinal lymph nodes and thus the negative predictive
value of mediastinal PET.
For stage II and III diseases, the incidence of false-negative
results is still greater with PET than with mediastinoscopy
(respectively 11.7% and 3%).
Mediastinoscopy likely will remain part of the standard
protocol for mediastinal staging for stage II and III diseases.

M-Staging
 M0: No distant metastasis
 M1: Distant metastasis
o M1a: Separate tumour nodule(s) in a contralateral lobe o
tumour with pleural nodules or malignant pleural or
pericardial effusion.
o M1b Distant metastasis

PET-CT
Distant metastases are very common in patients with lung
cancer.
Almost every organ may be involved but the extra-thoracic
sites posing common clinical problems are brain metastases,
bone metastases, sometimes with cord compression, nodal
spread, adrenal and liver involvement.

On the left a CT- and corresponding PET image of a tumor in

the right lung.
PET-CT is extremely helpful in the detection of distant
metastases.
In a study of 100 patients PET was compared with
conventional imaging, which consisted of CT of chest and
upper abdomen, bone scintigraphy, brain-CT or MR (3).
PET had superior sensitivity and specificity in the lung, liver,
adrenals and bone.
Not suprisingly PET was only less sensitive in the brain due to
the high glucose uptake in the normal brain.
In this study 9% of patients had metastases demonstrated
by PET that were not found with conventional imaging,
whereas 10% of patients suspected of having metastases
because of conventional imaging findings were correctly
shown with PET not to have metastases.

Because of the high negative predictive value, PET scanning

should be performed in all patients with no evidence of
metastatic disease on CT who are considered candidates for
surgery.
PET-image demonstrates FDG-uptake in mediastinal nodes,
but also in the liver (yellow arrows) and the spine (red arrow)
indicating distant metastases.

M1a-tumor and pleural effusion

 Malignant pleural effusion has a poor prognosis.
These patients usually die within 3 months.
In patients with malignant pleural effusion aspiration will yield
a false negative results in about a third of the cases.
If the cytology is negative, you can either do another
thoracocenthesis or do a VATS-procedure (video assisted
thoracoscopy) and obtain pleural biopsies.
References
1. The 7th Edition of TNM in Lung Cancer: What Now?
By Peter Goldstraw
Journal of Thoracic Oncology: June 2009 - Volume 4 - Issue 6 - pp 671-673
2. STATE OF THE ART - Lung Cancer - Where Are We Today? - Current Advances in Staging and Nonsurgical
Treatment
by Stephen G. Spiro and Joanna C. Porter.
American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 1166-1196, (2002)
3. Effectiveness of positron emission tomography in the preoperative assessment of patients with suspected non-
small-cell lung cancer: the PLUS multicentre randomised trial.
H. van Tinteren et al.
The Lancet, Volume 359, Issue 9315, Pages 1388-1392
4. Staging Non-Small Cell Lung Cancer with Whole-Body PET
Edith M. Marom et al
Radiology. 1999;212:803-809
5. Staging of Non Small-Cell Lung Cancer with Integrated Positron-Emission Tomography and Computed
Tomography
Didier Lardinois et al.
NEJM, Volume 348:2500-2507, June 19, 2003, Number 25
6. Non Small Cell Lung Cancer: Prospective Comparison of Integrated FDG PET/CT and CT Alone for Preoperative
Staging
Sung Shine Shim et al.
Radiology 2005;236:1011-1019.
7. Integrated PET-CT for the Characterization of Adrenal Gland Lesions in Cancer Patients: Diagnostic Efficacy and
Interpretation Pitfalls
Semin Chong et al
RadioGraphics 2006;26:1811-1824
8. State of the Art: Integrated PET/CT: Current Applications and Future Directions
Gustav K. von Schulthess et al
Radiology 2006;238:405-422
9. The Role of PET Scan in Diagnosis, Staging, and Management of Non-Small Cell Lung Cancer
Liesbet Schrevens, Natalie Lorent, Christophe Dooms, Johan Vansteenkiste
The Oncologist, Vol. 9, No. 6, 633-643, November 2004
10. Clinical Applications of PET in Oncology
Eric M. Rohren, MD, PhD, Timothy G. Turkington, PhD and R. Edward Coleman, MD
Radiology 2004;231:305-332
11. PET Evaluation of Lung Cancer
by Tira Bunyaviroch, MD and R. Edward Coleman, MD
Journal of Nuclear Medicine Vol. 47 No. 3 451-469, 2006
12. 'Staging' Pneumothorax.
Images in Clinical Medicine by Robert C. Hoch, M.D., Minnesota Lung Center.
NEJM Volume 356:2312 May 31, 2007 Number 22
13. Positron Emission Tomography to Evaluate Lung Lesions
Smith-Bindman et al.
JAMA.2001; 285: 2711-2712.
14. The Revised TNM Staging System for Lung Cancer
by Ramon Rami-Porta et al
Ann Thorac Cardiovasc Surg 2009; 15: 4 - 9
 Chest X-Ray - Heart Failure
by Simone Cremers, Jennifer Bradshaw and Freek Herfkens
Radiology department of the Albert Schweitzer Hospital in Dordrecht and the Medical Centre Alkmaar, the Netherlands, the Netherlands
 Introduction
 Congestive Heart Failure back to overview print
 Stage I - Redistribution Publicationdate 1-9-
 Stage II - Interstitial edema : 2010
In this article we will discuss the radiographic signs of congestive heart failure o
 Stage III - Alveolar edema
the chest X-ray.
 Cardiothoracic ratio
 Pleural effusion
 Vascular pedicle
 Dilatation of azygos vein
 Right ventricular failure

Introduction
Congestive heart failure (CHF) is the result of insufficient output because of
cardiac failure, high resistance in the circulation or fluid overload.
Left ventricle (LV) failure is the most common and results in decreased
cardiac output and increased pulmonary venous pressure.
In the lungs LV failure will lead to dilatation of pulmonary vessels, leakage of
fluid into the interstitium and the pleural space and finally into the alveoli
resulting in pulmonary edema.

Right ventricle (RV) failure is usually the result of long standing LV failure or
pulmonary disease and causes increased systemic venous pressure
resulting in edema in dependent tissues and abdominal viscera.

In the illustration on the left some of the features, that can be seen on a
chest-film in a patient with CHF.

Increased pulmonary venous pressure is related to the pulmonary capillary

wedge pressure (PCWP) and can be graded into stages, each with its own
radiographic features on the chest film (Table).
This grading system provides a logical sequence of signs in congestive heart
failure.
In daily clinical practice however some of these features are not seen in this
sequence and sometimes may not be present at all.
This can be seen in patients with chronic heart failure, mitral valve disease
and in chronic obstructive lung disease.

Congestive Heart Failure

 Stage I - Redistribution
In a normal chest film with the patient standing erect, the pulmonary
vessels supplying the upper lung fields are smaller and fewer in number
than those supplying the lung bases.
The pulmonary vascular bed has a significant reserve capacity and
recruitment may open previously non-perfused vessels and causes
distension of already perfused vessels.
This results in redistribution of pulmonary blood flow.
First there is equalisation of blood flow and subsequently redistribution of
flow from the lower to the upper lobes.

The term redistribution applies to chest x-rays taken in full inspiration in the
erect position.
In daily clinical practice many chest films are taken in a supine or semi-erect
Views of the upper lobe vessels of a patient in good condition (left) position and the gravitational difference between the apex and the lung
and during a period of CHF (right). Notice also the increased width of bases will be less.
the vascular pedicle (red arrows). In the supine position, there will be equalisation of blood flow, which may
give the false impression of redistribution.
In these cases comparison with old fims can be helpful.
Artery-to-bronchus ratio
Normally the vessels in the upper lobes are smaller than the accompanying
bronchus with a ratio of 0.85 (3).
At the level of the hilum they are equal and in the lower lobes the arteries
are larger with a ratio of 1.35.
When there is redistribution of pulmonary blood flow there will be an
increased artery-to-bronchus ratio in the upper and middle lobes.
This is best visible in the perihilar region.

On the left a patient with cardiomegaly and redistribution.

The upper lobe vessels have a diameter > 3 mm (normal 1-2 mm).
Notice the increased artery-to-bronchus ratio at hilar level (arrows).

Increased artery-to-bronchus ratio in CHF

Stage II - Interstitial edema
Stage II of CHF is characterized by fluid leakage into the interlobular and
peribronchial interstitium as a result of the increased pressure in the
capillaries.
When fluid leaks into the peripheral interlobular septa it is seen as Kerley B
or septal lines.
Kerley-B lines are seen as peripheral short 1-2 cm horizontal lines near the
costophrenic angles.
These lines run perpendicular to the pleura.

LEFT: normal. RIGHT: CHF stage II with Kerley B-lines due to

interstitial edema
 When fluid leaks into the peribronchovascular interstitium it is seen as
thickening of the bronchial walls (peribronchial cuffing) and as loss of
definition of these vessels (perihilar haze).

On the left a patient with congestive heart failure.

There is an increase in the caliber of the pulmonary vessels and they have
lost their definition because they are surrounded by edema.

Click to enlarge.

Perihilar haze in interstitial stage of CHF

On the left another patient with congestive heart failure.
The lateral view nicely demonstrates the increased diameter of the
pulmonary vessels and the hazy contours.
Notice also the septal lines and the accentuated interstitium.
Furthermore the fissura major is markedly thickened.

Previous normal chest x-ray (left) and CHF stage II with perihilar
haze (right)
CT will also demonstrate signs of congestive heart failure.

On the image on the left notice the following:

 Thickened septal lines due to interstitial edema

 Subtle ground glass opacity in the dependent part of the lungs (HU differenc
of 100-150 between the dependent and non-dependent part of the lung).
 Bilateral pleural fluid.

In a patient with a known malignancy lymphangitic carcinomatosis would be

high in the differential diagnostic list.
Ground glass opacity is the first presentation of alveolar edema and a
precursor of consolidation.

Thickened septal lines due to interstitial edema in CHF

 Stage III - Alveolar edema
This stage is characterized by continued fluid leakage into the interstitium,
which cannot be compensated by lymphatic drainage.
This eventually leads to fluid leakage in the alveoli (alveolar edema) and to
leakage into the pleural space (pleural effusion).

The distribution of the alveolar edema can be influenced by:

 Gravity: supine or erect position and right or left decubitus position

 Obstructive lung disease, i.e. fluid leakage into the less severe diseased area
of the lung

On the left a patient who was admitted with severe dyspnoe due to acute
heart failure.
The following signs indicate heart failure: alveolar edema with perihilar
consolidations and air bronchograms (yellow arrows); pleural fluid (blue
arrow); prominent azygos vein and increased width of the vascular pedicle
(red arrow) and an enlarged cardiac silhouette (arrow heads).
View more images: 1/3 After treatment we can still see an enlarged cardiac silhouette, pleural fluid
and redistribution of the pulmonary blood flow, but the edema has resolved.
On the left another patient with alveolar edema at admission, which
resolved after treatment.
When you scroll through the images and go back and forth, you will notice
the difference in vascular pedicle width and distribution of pulmonary flow.

View more images: 1/2

Both on the chest x-ray and on the CT the edema is gravity dependent and
differences in density can be measured.

Notice that even within each lobe there is a gravity dependent difference in
density.
This is only seen when the consolidations are the result of transudate like in
CHF.
This is not seen when the consolidations are the result of exsudate due to
infection, blood due to hemorrhage or when there is a capillary leak like in
ARDS.

On the left a patient who first had a chest film in a supine position.
Notice the pulmonary edema, which is almost exclusively seen in the right
lung.
A possible explanation for this phenomenon could be, that the patient had
been lying on his right side for a while before the x-ray was taken.
 Cardiothoracic ratio
The cardiothoracic ratio (CTR) is the ratio of the transverse diameter of the
heart to the internal diameter of the chest at its widest point just above the
dome of the diaphragm as measured on a PA chest film.
An increased cardiac silhouette is almost always the result of cardiomegaly,
but occasionally it is due to pericardial effusion or even fat deposition.
The heart size is considered too large when the CTR is > 50% on a PA chest
x-ray.
A CTR of > 50% has a sensitivity of 50% for CHF and a specificity of 75-
80%.
An increase in left ventricular volume of at least 66% is necessary before it
is noticeable on a chest x-ray.
Old film for comparison (left)
CHF with redistribution, interstitial edema and some pleural fluid
On the left a patient with CHF.
There is an increase in heart size compared to the old film.
Other signs of CHF are visible, such as redistribution of pulmonary flow,
interstitial edema and some pleural fluid.

On a supine film the cardiac silhouette will be larger due to magnification

and high position of the hemidiafragms.
Exact measurements are not that helpful, but comparison to old supine
films can be of value.
On the left a patient, who recently underwent a valve replacement.
There is a large cardiac silhouette, which could be the result of
cardiomegaly.
Because of the recent cardiac surgery, the possibility of pericardial effusion
was taken into account, which is nicely demonstrated on the CT-image.

Increased CTR due to pericardial effusion

On the left another patient with a large cardiac silhouette on the chest x-ray
due to pericardial effusion.
Pericardial effusion is demonstrated on the coronal CT-reconstruction.
 Pleural effusion
Pleural effusion is bilateral in 70% of cases of CHF.
When unilateral, it is slightly more often on the right side than on the left
side.
There has to be at least 175 ml of pleural fluid, before it will be visible on a
PA image as a meniscus in the costophrenic angle.
On a lateral image effusion of > 75 ml can be visible.
If pleural effusion is seen on a supine chest film, it means that there is at
least 500 ml present.

On the left images of a patient who has bilateral pleural effusions.

Notice that it is more evident on the lateral view.

Pleural effusion more evident on lateral view

Pleural effusion is not always visible as a meniscus in the costophrenic angle

A subpulmonic effusion may follow the contour of the diaphragm making it

tricky to discern.
In these cases, the only way to detect pleural effusion, is when you notice
that there is an increased distance between the stomach bubble and the
lung.
The stomach is normally located directly under the diaphragm, so, on an
erect PA radiograph, the stomach bubble should always appear in close
proximity to the diaphragm and the lung.

On the left images of a patient with signs of CHF.

At first glance you might get the impression that there is a high position of
the diaphragm.
Subpulmonic pleural effusion with increased distance of the stomach However when you notice the increased distance of the stomach air bubble
air bubble to the lung base (arrow) to the lung base, you realize that there is a large amount of pleural fluid on
both sides (arrow).

Vascular pedicle
The vascular pedicle is bordered on the right by the superior vena cava and
on the left by the left subclavian artery origin (6).
The vascular pedicle is an indicator of the intravascular volume.
A vascular pedicle width less than 60 mm on a PA chest radiograph is seen
in 90% of normal chest x-rays.
A vascular pedicle width of more than 85 mm is pathologic in 80% of cases.
5 mm increase in diameter corresponds to 1 liter increase of intravascular
fluid.
An increase in width of the vascular pedicle is accompanied by an increased
width of the azygos vein.
 There are three principal varieties of pulmonary edema: cardiac,
overhydration and increased capillary permeability (ARDS).

The vascular pedicle width (VPW) can help in differentiating these different
forms of pulmonary edema (6):

 Normal VPW: most common in capillary permeability or acute cardiac failure

 Widened VPW: most common in overhydration/renal failure and chronic
cardiac failure.
 Narrowed VPW: most common in capillary permeability.

Subtle increased width of vascular pedicle (left) and normalisation

(right)
On the left a patient with ARDS.
There is alveolar edema in both lungs.
Notice that the VPW is normal.
The vessels in the upper lobes are not dilated and the cardiac silhouette is
not enlarged.

Normal VPW in a patient with ARDS

 The VPW is best used as a measure to compare serial chest x-rays of the
same patient, as there is a wide range of values for the VPW.
The VPW may increase due to rotation to the right.
On an AP-view the VPW will increase 20% compared to a PA-view.

On the left a patient with subtle signs of congestive heart failure on the initia
chest x-ray (image 1/2).
There is a slightly enlarged vascular pedicle, which becomes more obvious
when you compare to the chest film after diuretic therapy (image 2/2).

View more images: 1/2

Dilatation of azygos vein

Dilation of the azygos vein is a sign of increased right atrial pressure and is
usually seen when there is also an increase in the width of the vascular
pedicle.
The diameter of the azygos vein varies according to the positioning.
In the standing position a diameter > 7 mm is most likely abnormal and a
diameter > 10 mm is definitely abnormal.
In a supine patient > 15 mm is abnormal.
An increase of 3 mm in comparison to previous films is suggestive of fluid
overload.
The difference of the azygos diameter on an inspiration film compared to an
expiration film is only 1mm.
This means that the diameter of the azygos is a valuable tool whether or not
there is good inspiration.

Right ventricular failure

RV failure is most commonly caused by longstanding LV failure, which
increases the pulmonary venous pressure and leads to pulmonary arterial
hypertension, thus overloading the RV.

Other less common causes of RV failure are:

 Severe lung disorder (cor pulmonale)

 Multiple pulmonary emboli
 RV infarction
 Primary pulmonary hypertension
 Tricuspid regurgitation or stenosis, mitral stenosis and pulmonary valve
Dilatation of IVC and hepatic veins on US images in a patient with RV stenosis.
failure
 Radiographic signs of RV failure:

 Increased VPW due to dilatation of the superior vena cava

 Dilatation of azygos vein
 Dilatation of the right atrium
 In many cases there will be both signs of RV and LV failure

Sonographic signs of RV failure:

 Dilatation of the inferior vena cava (IVC) and hepatic veins

 Hepatomegaly
 Ascites

The indication for ultrasound examination in many of these patients is

abnormal liver function tests.
It is therefore important to consider the possibility of RV failure when a
patient presents with liver enzyme abnormalities.
Under normal conditions dynamic ultrasound will demonstrate changes in
caliber of the IVC.
These changes in caliber can be attributed to variations in blood flow in the
IVC in accordance with the respiratory and cardiac cycles.

References
1. Heart Failure (HF) (Congestive Heart Failure)
in Merck manual
2. Radiographic analysis of vascular distribution: a review (PDF)
by Carle Ravin
Presented as part of a Conference on Chest Radiology 1982
3. Pulmonary artery-bronchus ratios in patients with normal lungs, pulmonary vascular plethora, and congestive
heart failure.
by J H Woodring
April 1991 Radiology, 179, 115-122.
4. American College of Radiology ACR Appropriateness Criteria: Congestive Heart Failure
5. The Radiologic Distinction of Cardiogenic and Noncardiogenic Edema (PDF)
by Eric Milne et al
American Journal of Roentgenology, Vol 144, Issue 5, 879-894
6. The vascular pedicle of the heart and the vena azygos. Part II: Acquired heart disease.
by M Pistolesi, E N Milne, M Miniati and C Giuntini
July 1984 Radiology, 152, 9-17.
7. Pulmonary hypertension secondary to left-sided heart disease: a cause for ventilation-perfusion mismatch
mimicking pulmonary embolism.
by Au VW, Jones DN, Slavotinek JP.
British Journal of Radiology. 2001 Jan; 74(877) 86-88.
8. The pulmonary vessels in incipient left ventricular decompensation
by M. Simon
Circulation 1961; 24:185-190
9. Pulmonary vascular congestion in acute myocardial infarction: Hemodynamic and radiologic correlation
by McHugh, T. J., Forrester, J. S., Adler, L., et al.
Ann. Intern. Med., 1972; 76:29-33
10. Radiological detection of clinically occult cardiac failure following myocardial infarction
Harrison M.O., Conte P.J., Heitzman E.R.
Br J Radiol. 1971; 44:265-272
11. Absolute lungdensity in experimental canine pulmonary edema
by Gamsu G,Kaufman K ,Swann S ,Brito A.
Invest Radiol 1979 ; 14: 261-269
12. Aging and the respiratory system
Bonomo L., et al.
Radiologic Clinics of North America, vol. 46, nr 4, July 2008: 685-702