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InterstIal lung dIseases
Dr. Shrikant Nagare
Introduction
• Interstitial lung diseases (ILD’s)represent a
large number of conditions that involve the
parenchyma of lun...
• There are numerous interstitial lung diseases,
but in clinical practice only about ten diseases
account for approximatel...
Sarcoidosis
• Sarcoidosis is a systemic disorder of unknown origin.
It is characterized by non-caseating granulomas in mul...
Sarcoidosis
Sarcoidosis
• Stages:
Chest films in sarcoidosis have been classified into
four stages:
I. Bilateral hilar lymphadenopathy...
• Patient with stage I disease.
There is hilar and paratracheal adenopathy and no sign of
pulmonary involvement.
HRCT findings in Sarcoidosis.
• Common findings:
– Small nodules in a perilymphatic distribution (i.e. along
subpleural su...
Sarcoidosis: typical presentation with nodules along the bronchovascular
bundle and the fissures
Notice the partially calc...
A detailed view with the
typical HRCT-presentation
with nodules along
bronchovascular bundle (red
arrow) and fissures (yel...
Another typical presentation of sarcoidosis with mediastinal lymphadenopathy
and small nodules in a perilymphatic distribu...
Fibrosis in Sarcoidosis
• Progressive fibrosis in sarcoidosis may lead to
peribronchovascular (perihilar) conglomerate mas...
Sarcoidosis with conglomerate masses of fibrous tissue
A typical chest film of long standing
sarcoidosis (stage IV) with fibrosis in the
upper zones and volume loss of the upper...
Alveolar Sarcoidosis
In this case the appearance resembles a
ground glass attenuation, but with a close look
you may appre...
• A case of fibrosing sarcoidosis, showing fibrosis, traction
bronchiectases and crowding of the involved bronchi,
predomi...
Differential diagnosis of Sarcoidosis
• Lymphadenopathy:
– Primary TB: asymmetrical adenopathy
– Histoplasmosis
– Lymphoma...
Silicosis / Coal worker
pneumoconiosis
• Silicosis and Coal worker pneumoconiosis (CWP) are
pathologically distinct entiti...
HRCT findings in Silicosis/CWP
• Small well-defined nodules of 2 to 5mm in diameter in both
lungs.
• Upper lobe predominan...
A case of silicosis showing nodules of varying sizes with a
random and subpleural distribution. One nodule contains
calcif...
Differential diagnosis of Silicosis /
Pneumoconiosis
• Sarcoidosis : can be difficult to distinguish (look for
distributio...
Lymphangitic Carcinomatosis
• Lymphangitic Carcinomatosis results from
hematogenous spread to the lung, with subsequent
in...
HRCT findings in Lymphangitic
Carcinomatosis
• Interlobular septal thickening, thickening of fissures
and thickening of th...
A patient with Lymphangitic Carcinomatosis.
Notice the focal distribution.
This finding is helpful in distinguishing Lymph...
Differential diagnosis of Lymphangitic
Carcinomatosis
Diseases showing septal thickening:
• Cardiogenic pulmonary edema:
b...
Cardiogenic pulmonary edema
• Patients with pulmonary edema are not
imaged with HRCT as their diagnosis is usually
based o...
HRCT findings in cardiogenic
pulmonary edema
• Bilateral septal thickening and ground-glass
opacity.
• Perihilar and gravi...
Cardiogenic pulmonary edema
• Typical features of cardiogenic
pulmonary edema
There is smooth septal
thickening and some g...
Differential diagnosis of cardiogenic
pulmonary edema.
• Lymphangitic carcinomatosis
• Interstitial pneumonia (viral, myco...
Hypersensitivity Pneumonitis
• Hypersensitivity pneumonitis (HP) is also known as
extrinsic allergic alveolitis (EAA).
HP ...
Subacute hypersensitivity
pneumonitis
• The key findings in the subacute hypersensitivity
pneumonitis are:
• ill-defined c...
Subacute hypersensitivity pneumonitis with ill-defined
centrilobular nodules
Case with subacute hypersensitivity pneumonit...
Subacute hypersensitivity pneumonitis
There is subtle opacity in the centre of the secondary lobules (arrows) with
sparing...
Subacute hypersensitivity pneumonitis
with mosaic pattern
Some secondary lobules demonstrate ground-glass opacity due to l...
Chronic hypersensitivity pneumonitis
The key findings in chronic hypersensitivity
pneumonitis are:
• Mosaic pattern with a...
Chronic hypersensitivity pneumonitis:
Nonspecific chest film, typical HRCT-findings.
The HRCT shows a mosaic pattern.
Addi...
Differential diagnosis of
Hypersensitivity Pneumonitis
• Subacute stage:
– RB-ILD: seen in smokers, upper lobe predilectio...
UIP with honeycombing (left) and chronic HP (right)
Tuberculosis
• Primary TB: Initial infection with consolidation, adenopathy and
pleural effusion.
• Secondary TB : Post-pr...
HRCT findings in TB
• Primary TB:
– Consolidation anywhere, lymphadenopathy and pleural
effusion. Usually regresses to cal...
TB: cavitating lesion and
endobronchial spread
There is a cavitating lesion and typical tree-in-bud appearance. The
blue a...
Miliary TB
• This represents a haematogenous
dissemination of infection and may occur in
association with either primary o...
Miliary TB
Uniform small nodules with a random distribution
Endobronchial spread of TB
• This can occur with primary or postprimary infection.
• In most subjects, the primary infecti...
Endobronchial spread of TB with tree-
in-bud
Differential diagnosis of TB
• Primary TB: Acute bacterial pneumonia
• Secondary TB: Sarcoidosis, Silicosis, Pneumoconiosi...
LEFT: miliary TB
RIGHT: metastases
Chronic eosinophilic pneumonia
• Chronic eosinophilic pneumonia is an idiopathic condition
characterized by filling of the...
HRCT/CT findings in Chronic
eosinophilic pneumonia
• Contrast enhanced CT in a patient with chronic
eosinophilic pneumonia...
Differential diagnosis of Chronic
eosinophilic pneumonia
• Organizing pneumonia (COP)
• Löffler syndrome (eosinophilia and...
Chronic eosinophilic pneumonia (left)
versus Organizing pneumonia (right)
The images show the similarities between chronic...
Pneumocystis carinii pneumonia
• Pneumocystis carinii pneumonia (PCP) or
pneumocystis jiroveci as it is currently named, i...
HRCT findings in PCP
• Perihilar or diffuse ground-glass opacification.
• Sometimes thickened septal lines in association ...
Immunocompromised patient with
PCP
The CT findings are diffuse ground-glass opacification.
The findings are not specific f...
ARDS
• Acute respiratory distress syndrome (ARDS) is a sudden, life-threatening
lung failure requiring mechanical ventilat...
Extra-pulmonary ARDS
• A patient who was involved in a traffic accident and within hours
developed ARDS.
The dominant patt...
Pulmonary ARDS
• Patient who developed ARDS as a result of pneumonia (i.e. pulmonary
ARDS).
Note the patchy distribution o...
Idiopathic interstitial pneumonias
• The idiopathic interstitial pneumonias (IIPs) comprise a
heterogeneous group of disor...
Usual Interstitial Pneumonitis (UIP)
• UIP is a histological diagnosis.
UIP has distinctive HRCT findings and is usually s...
UIP due to IPF
• The findings on the chest film comprise volume loss and fibrotic changes in the basal
lung area.
The radi...
HRCT findings in UIP
• Honeycombing consisting of multilayered thick-walled
cysts.
• Architectural distortion with tractio...
Nonspecific interstitial pneumonia
(NSIP)
• NSIP representing cases of idiopathic interstitial pneumonia
that cannot be cl...
• This patient had a rash and muscle
weakness.
• The predominant finding is ground
glass opacity (GGO).
There is very subt...
COP / BOOP
• Cryptogenic organizing pneumonia (COP) used to be described as
bronchiolitis obliterans with organizing pneum...
HRCT findings in OP
• Bilateral peripheral consolidations, sharply
demarcated.
• Consolidations may be migratory.
• Lesion...
A patient with the typical bilateral peripheral consolidations of OP.
After exclusion of other diseases such as lymphoma, ...
• A patient with rheumatoid arthritis and bilateral
peripheral consolidations as a result of organizing
pneumonia.
Patient...
Differential diagnosis of Organizing
Pneumonia
• Chronic eosinophilic pneumonia
• Bronchoalveolar cell carcinoma
• Aspirat...
Chronic eosinophilic pneumonia (left)
versus Organizing pneumonia (right)
The images show the similarities between chronic...
RB-ILD and DIP
• Respiratory bronchiolitis (RB), respiratory
bronchiolitis-associated interstitial lung
disease (RB-ILD), ...
• All smokers have various degrees of respiratory bronchiolitis,
but it is usually asymptomatic.
• The term RB-ILD was pro...
HRCT findings in RB-ILD
• Centrilobular nodules of ground glass opacity
with upper lobe predominance
• Bronchial wall thic...
RB-ILD
The dominant feature is ground glass opacification and there are some thickened
interlobular septa (arrow).
Usually...
RIGHT: Hypersensitivity pneumonitis in non-
smoker
Note the difference in severity of ground glass opacities and the well ...
Acute interstitial pneumonia AIP
• AIP, earlier named Hamman Rich Pneumonitis
is a rare idiopathic lung disease characteri...
HRCT characteristics of AIP
• Diffuse or patchy consolidation, often with a
crazy paving.
AIP
There are areas of consolidation and extensive areas of ground-glass density
with a crazy-paving appearance.
These abn...
Lymphocytic interstitial pneumonitis
LIP
• LIP is uncommon, being seen mainly in
patients with autoimmune disease,
particu...
HRCT findings are usually nonspecific.
A patient with Sjogren's syndrome with LIP.
Uncommon interstitial lung
diseases
Lymphangiomyomatosis
• Rare disease, that occurs only in premenopausal
women
• Characterized by progressive proliferation ...
Key findings in
Lymphangiomyomatosis
• Numerous thin-walled cysts, surrounded by normal
parenchyma.
• Cysts range from 2mm...
Lymphangiomyomatosis
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 sh...
Langerhans cell histiocytosis
• Langerhans cell histiocytosis is also known as
pulmonary histiocytosis X or eosinophilic g...
HRCT findings in Langerhans cell
histiocytosis
• Early stage:
– Small irregular or stellate nodules in centrilobular
locat...
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 coa...
Late stage Langerhans' cell histiocytosis. Cysts
progress to typical bizarre shaped cysts.
Radiological pathological correlation of
Langerhans cell histiocytosis in respectively
nodular stage and early and late cy...
Differential diagnosis of Langerhans
cell histiocytosis
• Nodular LCH:
– Sarcoidosis: perilymphatic distribution.
– Metast...
Alveolar proteinosis
• Alveolar proteinosis is a rare disease characterized by filling of
the alveolar spaces with PAS pos...
Key findings in alveolar proteinosis
• Crazy paving pattern: reticular pattern
superimposed on ground glass opacification....
A typical case of alveolar proteinosis with extensive
thickening of interlobular and intra-lobular septa.
This is caused b...
Differential diagnosis of alveolar
proteinosis
• The crazy paving pattern is a rather non-specific finding.
Many other dis...
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Interstitial lung diseases radiology
Interstitial lung diseases radiology
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Interstitial lung diseases radiology

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Interstitial lung diseases radiology

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Interstitial lung diseases radiology

  1. 1. InterstIal lung dIseases Dr. Shrikant Nagare
  2. 2. Introduction • Interstitial lung diseases (ILD’s)represent a large number of conditions that involve the parenchyma of lung- the alveoli, the alveolar epithelium, the capillary endothelium, and the spaces between these structures, as well as perivascular and lymphatic tissues.
  3. 3. • There are numerous interstitial lung diseases, but in clinical practice only about ten diseases account for approximately 90% of cases. • Knowledge of both, the radiological and clinical appearance of these more common interstitial lung diseases, is therefore important for recognizing them in the daily practice and including them in the differential diagnosis.
  4. 4. 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. • Less than 5% of patients die from sarcoidosis usually as a result of pulmonary fibrosis.
  5. 5. Sarcoidosis
  6. 6. Sarcoidosis • Stages: Chest films in sarcoidosis have been classified into four stages: I. Bilateral hilar lymphadenopathy II. Bilateral hilar lymphadenopathy + pulmonary disease III. Only pulmonary disease IV. Irreversible fibrosis These stages do not indicate disease chronicity or correlate with changes in pulmonary function.
  7. 7. • Patient with stage I disease. There is hilar and paratracheal adenopathy and no sign of pulmonary involvement.
  8. 8. HRCT findings in Sarcoidosis. • Common findings: – Small nodules in a perilymphatic distribution (i.e. along subpleural surface and fissures, along interlobular septa and the peribronchovascular bundle). – Upper and middle zone predominance. – Lymphadenopathy in left hilus, right hilus and paratracheal (1-2- 3 sign). Often with calcifications. • Uncommon findings: – Conglomerate masses in a perihilar location. – Larger nodules (> 1cm in diameter, in < 20%) – Grouped nodules or coalescent nodules surrounded by multiple satellite nodules (Galaxi sign) – Nodules so small and dense that they appear as ground glass or even as consolidations (alveolar sarcoidosis)
  9. 9. Sarcoidosis: typical presentation with nodules along the bronchovascular bundle and the fissures Notice the partially calcified node in the left hilum.
  10. 10. 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.
  11. 11. 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.
  12. 12. 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: • Silicosis • Tuberculosis • Talcosis
  13. 13. Sarcoidosis with conglomerate masses of fibrous tissue
  14. 14. 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.
  15. 15. Alveolar Sarcoidosis 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
  16. 16. • 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.
  17. 17. Differential diagnosis of Sarcoidosis • Lymphadenopathy: – Primary TB: asymmetrical adenopathy – Histoplasmosis – Lymphoma – Small cell lung cancer with nodal metastases • Nodular pattern: – Silicosis / Pneumoconiosis: predominantly centrilobular and subpleural nodules. – Miliary TB: random nodules. • Fibrotic pattern: – Usual Interstitial Pneumonia (UIP): basal and peripheral fibrosis, honeycombing. – Chronic Hypersensitivity Pneumonitis: mid zone fibrosis with mosaic pattern. – Tuberculosis (more unilateral).
  18. 18. 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. • Silicosis and CWP occur in a specific patient group (construction workers, mining workers, workers exposed to sandblasting, glass blowing and pottery).
  19. 19. 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.
  20. 20. 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.
  21. 21. Differential diagnosis of Silicosis / Pneumoconiosis • Sarcoidosis : can be difficult to distinguish (look for distribution of nodules). • Infection: miliary TB, fungus. • Hematogenous metastases: silicotic nodules in subpleural and peribronchiolar location up to the level of the secondary pulmonary lobule, may have a seemingly random distribution and simulate metastases and miliary infections. • Langerhans cell histiocytosis: can be difficult to distinguish from silicosis in the early stage, when LCH is solely characterized by the presence of small nodules. Look for nodules with cavitation.
  22. 22. Lymphangitic Carcinomatosis • Lymphangitic Carcinomatosis results from hematogenous spread to the lung, with subsequent invasion of interstitium and lymphatics. • Lymphangitic Carcinomatosis is seen in carcinoma of the lung, breast, stomach, pancreas, prostate, cervix, thyroid and metastatic adenocarcinoma from an unknown primary.
  23. 23. 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 irregular 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).
  24. 24. 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.
  25. 25. Differential diagnosis of Lymphangitic Carcinomatosis Diseases showing septal thickening: • Cardiogenic pulmonary edema: bilateral abnormalities, filling of alveoli, enlarged heart, rapid response to diuretics, ground-glass opacity due to filling of alveoli with fluid, gravitational distribution of the alveolar fluid. • Alveolar proteinosis: sharply demarcated secondary lobules with ground glass attenuation as opposed to secondary lobules with normal aeration, superimposed inter and intralobular septal thickening (crazy paving).
  26. 26. 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.
  27. 27. 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.
  28. 28. Cardiogenic pulmonary edema • 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.
  29. 29. Differential diagnosis of cardiogenic pulmonary edema. • Lymphangitic carcinomatosis • Interstitial pneumonia (viral, mycoplasma) • ARDS • Pulmonary hemorrhage
  30. 30. 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.
  31. 31. 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
  32. 32. Subacute hypersensitivity pneumonitis with ill-defined centrilobular nodules Case with subacute hypersensitivity pneumonitis with a typical mosaic pattern and without any signs of septal thickening or distortion of the airways.
  33. 33. Subacute hypersensitivity pneumonitis There is subtle opacity in the centre of the secondary lobules (arrows) with sparing of the subpleural region.
  34. 34. Subacute hypersensitivity pneumonitis with mosaic pattern Some secondary lobules demonstrate ground-glass opacity due to lung infiltration, while others are more lucent due to bronchiolitis with air trapping.
  35. 35. Chronic hypersensitivity pneumonitis The key findings in chronic hypersensitivity pneumonitis are: • Mosaic pattern with areas of ground-glass attenuation and areas of low attenuation. • Fibrosis and parenchymal distortion in a mid zone distribution.
  36. 36. Chronic hypersensitivity pneumonitis: Nonspecific chest film, typical HRCT-findings. The HRCT shows a mosaic pattern. Additionally there is septal and intralobular reticular thickening, indicating already existing irreversible fibrosis.
  37. 37. Differential diagnosis of Hypersensitivity Pneumonitis • Subacute stage: – RB-ILD: seen in smokers, upper lobe predilection, usually associated with centrilobular emphysema. – Alveolar proteinosis. • Chronic stage: – UIP: may show very similar HRCT findings. UIP has a strong lower zone distribution. In chronic HP fibrotic changes are typically seen throughout the whole lung parenchyma from the periphery towards the centre.
  38. 38. UIP with honeycombing (left) and chronic HP (right)
  39. 39. 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.
  40. 40. HRCT findings in TB • Primary TB: – Consolidation anywhere, lymphadenopathy and pleural effusion. Usually regresses to calcified lung nodule and calcified ipsilateral lymph node. • Secondary TB: – Consolidation in apical segments of upper lobes or superior segments of lower lobes. – Cavitation • Endobronchial spread: – Tree in bud appearance • Miliary TB: – 2-3 mm nodules with random distribution.
  41. 41. TB: cavitating lesion and endobronchial spread There is a cavitating lesion and typical tree-in-bud appearance. The blue arrow indicates the biopsy needle.
  42. 42. Miliary TB • This represents a haematogenous dissemination of infection and may occur in association with either primary or post primary disease. • It is characterized by uniform small nodules with a random distribution.
  43. 43. Miliary TB Uniform small nodules with a random distribution
  44. 44. 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.
  45. 45. Endobronchial spread of TB with tree- in-bud
  46. 46. Differential diagnosis of TB • Primary TB: Acute bacterial pneumonia • Secondary TB: Sarcoidosis, Silicosis, Pneumoconiosis • Endobronchial spread of TB: Bronchopneumonia, Hypersensitivity pneumonitis • Miliary TB: metastases of medullary thyroid ca, chorion ca and melanoma. In both miliary TB and metastases the nodules have a random distribution. In miliary TB the nodules are more uniform in size.
  47. 47. LEFT: miliary TB RIGHT: metastases
  48. 48. 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.
  49. 49. HRCT/CT findings in Chronic eosinophilic pneumonia • Contrast enhanced CT in a patient with chronic eosinophilic pneumonia. Notice peripheral distribution of the consolidations.
  50. 50. Differential diagnosis of Chronic eosinophilic pneumonia • Organizing pneumonia (COP) • Löffler syndrome (eosinophilia and vanishing peripheral consolidations) • Churg-Strauss syndrome (also serum eosinophilia, asthma, systemic vasculitis affecting multiple organs: renal insufficiency, arthralgia and myocarditis and pericarditis) • Pulmonary infarcts
  51. 51. Chronic eosinophilic pneumonia (left) versus Organizing pneumonia (right) The images show the similarities between chronic eosinophilic pneumonia and organizing pneumonia. Differentiation has to be made on the basis of clinical and laboratory findings.
  52. 52. 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.
  53. 53. 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 complete disappearance, or residual nodules or scars • Pneumothorax in 35% of patients with cysts
  54. 54. 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.
  55. 55. 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 irreversible fibrosis. Why some people develop ARDS and others do not is unknown.
  56. 56. Extra-pulmonary ARDS • 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.
  57. 57. Pulmonary ARDS • Patient who developed ARDS as a result of pneumonia (i.e. pulmonary ARDS). Note the patchy distribution of lung disease and the almost complete distortion 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.
  58. 58. Idiopathic interstitial pneumonias • The idiopathic interstitial pneumonias (IIPs) comprise a heterogeneous 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 in order of relative frequency. • These diseases have specific patterns of morphologic findings on HRCT and histology.
  59. 59. Usual Interstitial Pneumonitis (UIP) • UIP is a histological diagnosis. UIP has distinctive HRCT findings and is usually shown at lung biopsy, 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 (asbestos), and collagen vascular diseases like RA, SLE, polyarteritis nodosa and scleroderma. • 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).
  60. 60. 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.
  61. 61. 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
  62. 62. Nonspecific interstitial pneumonia (NSIP) • NSIP 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 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.
  63. 63. • This patient had a rash and muscle weakness. • 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. 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. NSIP
  64. 64. COP / BOOP • 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 exudates 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.
  65. 65. 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 volume 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.
  66. 66. 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.
  67. 67. • 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.
  68. 68. Differential diagnosis of Organizing Pneumonia • Chronic eosinophilic pneumonia • Bronchoalveolar cell carcinoma • Aspiration pneumonia • Pulmonary infarction • Lymphoma
  69. 69. Chronic eosinophilic pneumonia (left) versus Organizing pneumonia (right) The images show the similarities between chronic eosinophilic pneumonia and organizing pneumonia. Differentiation has to be made on the basis of clinical and laboratory findings.
  70. 70. 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.
  71. 71. • All smokers have various degrees of respiratory bronchiolitis, but it is usually asymptomatic. • 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.
  72. 72. 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)
  73. 73. 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.
  74. 74. RIGHT: Hypersensitivity pneumonitis in non- smoker Note the difference in severity of ground glass opacities and the well defined areas of air trapping 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. Somehow smoking seems to protect against HP. This is not a 100% specific criterion but is quite helpful for differential diagnosis. LEFT: RB-ILD in smoker.
  75. 75. Acute interstitial pneumonia AIP • 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 as well as the HRCT findings in AIP are indistinguishable from acute respiratory distress syndrome (ARDS).
  76. 76. HRCT characteristics of AIP • Diffuse or patchy consolidation, often with a crazy paving.
  77. 77. AIP There are areas of consolidation and extensive areas of ground-glass 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.
  78. 78. Lymphocytic interstitial pneumonitis LIP • 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
  79. 79. HRCT findings are usually nonspecific. A patient with Sjogren's syndrome with LIP.
  80. 80. Uncommon interstitial lung diseases
  81. 81. 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).
  82. 82. 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 or less uniform. • Cysts are distributed diffusely throughout the lungs and upper and lower lobes 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%).
  83. 83. Lymphangiomyomatosis A typical case of LAM with multiple evenly spread thin walled cysts complicated by a pneumothorax.
  84. 84. Differential diagnosis of Lymphangiomyomatosis • Langerhans cell histiocytosis: > 90% are smokers, cysts have irregular shapes and the basal costophrenic angles are spared. • Centrilobular emphysema: characterized by airspaces that have no perceptible wall, centrilobular artery seen as dot in the centre. • Lymphoid interstitial pneumonitis: seen in patients with HIV and Sjögren syndrome.
  85. 85. 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.
  86. 86. HRCT findings in Langerhans cell histiocytosis • Early stage: – Small irregular or stellate nodules in centrilobular location. • Late stage (more commonly seen) – Cystic airspaces < 10 mm in diameter with walls that range from barely perceptible to several millimetres thick. – Cysts have bizarre shapes, they may coalesce and than become larger. – Upper and mid lobe predominance. – Recurrent pneumothorax.
  87. 87. Early stage Langerhans cell histiocytosis with small nodules There are no cysts visible.
  88. 88. • 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.
  89. 89. Late stage Langerhans' cell histiocytosis. Cysts progress to typical bizarre shaped cysts.
  90. 90. Radiological pathological correlation of Langerhans cell histiocytosis in respectively nodular stage and early and late cystic stage.
  91. 91. Differential diagnosis of Langerhans cell histiocytosis • Nodular LCH: – Sarcoidosis: perilymphatic distribution. – Metastases: random distribution. • Cystic LCH: – LAM: round cysts, evenly distribution in women in the child-bearing age – Cystic bronchiectasis: 'signet ring sign'. – Centrilobular emphysema: no walls, central dot. – LIP
  92. 92. 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 bronchoalveolar lavage.
  93. 93. Key findings in alveolar proteinosis • Crazy paving pattern: reticular pattern superimposed on ground glass opacification. • Opacifications range from ground glass to consolidation.
  94. 94. 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.
  95. 95. Differential diagnosis of alveolar proteinosis • 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. • Non cardiogenic edema, ARDS, Acute Interstitial Pneumonia. • Pneumonia: – Infection (PCP and CMV). – OP (organizing pneumonia). – Chronic eosinophilic pneumonia. • Haemorrhage. • Bronchoalveolar ca.
  96. 96. thank You

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