Showing posts sorted by relevance for query BASICS OF HRCT INTERPRETATION-PART 2- RETICULAR PATTERN. Sort by date Show all posts
Showing posts sorted by relevance for query BASICS OF HRCT INTERPRETATION-PART 2- RETICULAR PATTERN. Sort by date Show all posts

BASICS OF HRCT INTERPRETATION-PART 2- 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.       
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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.
c carcinomatosis
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.
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 made based on clinical and radiographic findings, but sometimes 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.
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
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).


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BASICS OF HRCT PART 7 - DIFFERENTIAL DIAGNOSIS OF ILD

This is the last post in the series of basics of HRCT. links to the previous posts are given at the end of this post.

DIFFERENTIAL DIAGNOSIS OF INTERSTITIAL LUNG DISEASE
Reticular pattern 

1.     Lymphangitic carcinomatosis: irregular septal thickening, usually focal 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 of 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 glass 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 consolidation.
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 traction 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. Notice the centrilobular artery in the center.
2.     Langerhans cell histiocytosis (LCH): multiple thick walled cysts; smoking history.
3.     Honeycombing.

BASICS OF HRCT INTERPRETATION-PART 3- NODULAR PATTERN

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.
Here 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).
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.

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.

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).
Here 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).
Random distribution

HRCT of 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 extensive, it spreads along the bronchovascular bundle to the periphery of the lung and may reach 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.




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BASICS OF HRCT PART 6 - DISTRIBUTION PATTERN AND ADDITIONAL FEATURES

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 .


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