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).


See my  article on HRCT




 



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 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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BASICS OF HRCT INTERPRETATION

In this article a practical approach is given for the interpretation of HRCT examinations

We will discuss the following subjects:
  • Anatomy of the secondary lobule
  • Basic HRCT patterns
  • Distribution of abnormalities
  • 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.
  • There are two lymphatic systems: a central network, that runs along the bronchovascular bundle towards the centre of the lobule and a peripheral network, that is located within the interlobular septa and along the pleural linings.


Centrilobular area is the central part of the secondary lobule.
It is usually the site of diseases, that enter the lung through the airways ( i.e. hypersensitivity pneumonitis, respiratory bronchiolitis, centrilobular emphysema ).
Perilymphatic area is the peripheral part of the secondary 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.


Basic Interpretation
A structured approach to interpretation of HRCT involves the following questions:
  • What is the dominant HR-pattern:
    • reticular
    • nodular
    • high attenuation (ground-glass, consolidation)
    • low attenuation (emphysema, cystic)
  • Where is it located within the secondary lobule (centrilobular, perilymphatic 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 lung carcinoma 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.
Read my next article in the series