Chest X Ray Lung Pathology
Carlos Beirise
Your lungs are part of a complex system, expanding and relaxing thousands of times each day to bring in oxygen and send out carbon dioxide. Lung disease can happen when there are problems in any part of this system.
The interstitium is the thin, delicate lining between your alveoli. Tiny blood vessels run through the interstitium and let gas transfer between the alveoli and your blood. Various lung diseases affect the interstitium:
The pleura is the thin lining that surrounds your lung and lines the inside of your chest wall. A tiny layer of fluid lets the pleura on your lung's surface slide along the chest wall with each breath. Lung diseases of the pleura include:
Your chest wall also plays an important role in breathing. Muscles connect your ribs to each other, helping your chest expand. Your diaphragm descends with each breath, also causing chest expansion. Diseases that affect your chest wall include:
Consolidation is the result of replacement of air in the alveoli by transudate, pus, blood, cells or other substances.
Pneumonia is by far the most common cause of consolidation.
The disease usually starts within the alveoli and spreads from one alveolus to another.
When it reaches a fissure the spread stops there.
Now it is obvious that some diseases can have more than one pattern.
For instance a lobar pneumonia caused by streptococcus pneumoniae may become diffuse if the patient does not respond to the treatment.
Other examples are organizing pneumonia (OP) and chronic eosinophilic pneumonia.
These diseases typically present as multifocal consolidations, but sometimes they may become diffuse.
Lobar consolidation is the result of disease that starts in the periphery and spreads from one alveolus to another through the pores of Kohn.
At the borders of the disease some alveoli will be involved, while others are not, thus creating ill-defined borders.
As the disease reaches a fissure, this will result in a sharp delineation, since consolidation will not cross a fissure.
In consolidation there should be no or only minimal volume loss, which differentiates consolidation from atelectasis.
Expansion of a consolidated lobe is not so common and is seen in Klebsiella pneumoniae and sometimes in Streptococcus pneumoniae, TB and lung cancer with obstructive pneumonia.
In the proper clinical setting this is most likely a lobar or segmental pneumonia.
However if this patient had weight loss or long standing symptoms, we would include the list of causes of chronic consolidation.
Based on the images alone, it is usually not possible to determine the cause of the consolidation.
Other things need to be considered, like acute or chronic illness, clinical data and other non-pulmonary findings.
The radiographic features of acute pulmonary thromboembolism are insensitive and nonspecific.
The most common radiographic findings in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study were atelectasis and patchy pulmonary opacity.
It is a congenital abnormality.
A nonfunctioning part of the lung lacks communication with the bronchial tree and receives arterial blood supply from the systemic circulation.
Patients present with recurrent infection when bacteria migrate through the pores of Kohn.
The increased heart size is usually what distinguishes between cardiogenic and non-cardiogenic.
Look for other signs of heart failure like redistribution of pulmonary blood flow, Kerley B-lines and pleural fluid.
However some patients, who have an acute cardiac infarction, may still have a normal heart size, while other patients who have a large heart due to a chronic heart disease, may have non-cardiac pulmonary edema due to a superimposed pulmonay infection, ARDS, near-drowning etc.
Unlike lobar pneumonia, which starts in the alveoli, bronchopneumonia starts in the airways as acute bronchitis.
It will lead to multifocal ill-defined densities.
When it progresses it can produce diffuse consolidation.
The disease does not cross the fissures, but usually starts in multiple segments.
The CT-image is not very helpful in the differentiation.
There are hypodense areas, which could be masses.
On the other hand this also could be areas of consolidation with hypodense areas due to necrosis.
Batwing
A bilateral perihilar distribution of consolidation is also called a Batwing distribution.
The sparing of the periphery of the lung is attributed to a better lymphatic drainage in this area.
It is most typical of pulmonary edema, both cardiogenic and non-cardiogenic.
Sometimes it is seen in pneumonias.
In some cases however the underlying pathology of multiple ill-defined densities is interstitial disease, like in the alveolar form of sarcoidosis in which the granulomas are very small and fill up the alveoli.
This patient had a several month history of chronic non-productive cough, that did not respond to antibiotics.
So we are dealing with the differential diagnosis of chronic consolidation.
The lab-findings were normal which makes bronchoalveolar carcinoma and lymphoma less likely.
There was no eosinophilia, which excludes eosinophilic pneumonia.
Biopsy revealed the diagnosis of organizing pneumonia (OP) also known as BOOP.
Wegener's is a collagen vascular disease with vasculitis involving the lung, kidney and sinuses.
In the lung the vasculitis causes infarcts which first present as ill-defined areas of consolidation.
In a later stage these infarcts become more circumscribed and can be seen as multiple nodules or masses, sometimes with cavitation.
On a CXR the most common pattern is reticular.
The ground-glass pattern is frequently not detected on a chest x-ray.
The cystic pattern is also difficult to appreciate on a cest x-ray.
When the cysts have thick walls like in Langerhans cell histiocytosis or honeycombing, it frequently presents as a reticular pattern on a CXR.
The CXR is of a patient with Langerhans cell histiocytosis (LCH).
LCH is called a cystic disease.
On the CXR it is difficult to see if this is a cystic or a reticular pattern.
In many of such cases a HRCT will give you more information.
This problem is also seen in patients with UIP.
One of the prominent findings in UIP is honeycombing.
This creates a reticular pattern on the chest x-ray, because the cysts in honeycombing have thick walls.
We will show a case in a moment.
The is volume loss in the upper lobes as a result of fibrosis.
The image on the left also shows densities in the lung.
On a HRCT fine nodules were seen.
A follow-up CXR shows resorption of most of the lung abnormalities.
The fibrosis persists.
On a chest X-ray UIP manifests as a reticular pattern particularly at the lung bases.
In many cases you can suspect UIP on the CXR.
A HRCT is needed to confirm the diagnosis by demonstrating honeycombing.
Here a CXR with a reticular pattern at the lung bases.
This pattern was first attributed to chronic congestive heart failure, but persisted on follow-up CXR's despite therapy.
HRCT demonstrated honeycombing.
Atelectasis or lung-collapse is the result of loss of air in a lung or part of the lung with subsequent volume loss due to airway obstruction or compression of the lung by pleural fluid or a pneumothorax.
In many cases atelectasis is the first sign of a lung cancer.
Evidently it is very important to recognize the various presentations of atelectasis, since some of them can be easily misinterpretated.
Notice the abnormal right border of the heart.
The right interlobar artery is not visible, because it is not surrounded by aerated lung but by the collapsed lower lobe, which is adjacent to the right atrium.
There is an atelectasis of the left upper lobe.
You would not expect the apical region to be this dark, but in fact this is caused by overinflation of the lower lobe, which causes the superior segment to creep all the way up to the apical region.
These findings indicate a total atelectasis of the left upper lobe and possibly also partial atelectasis on the right.
Since the silhouette of the right heart border is still visible, there is probably partial atelectasis of the lower lobe and not of the middle lobe.
There is a total collaps of the left upper lobe.
Notice the high position of the left hilum.
There is only a subtle band of density projecting behind the sternum.
This is the collapsed upper lobe.
There is a triangular density seen through the cardiac shadow.
This must be an abnormality located posterior to the heart.
This is confirmed on the lateral view.
The contour of the left diaphragm is lost when you go from anterior to posterior.
As the title suggests this is lower lobe atelectasis.
The chest x-ray shows a nearly total opacification of the left hemithorax.
This patient was known to have pleuritic carcinomatosis.
The left lung is almost completely compressed by the pleural fluid.
Unlike most of the above cases, which were caused by obstruction, in this case the atelectasis is a result of compression.
The theory is that a local pleuritis causes the pleura to thicken and contract.
The underlying lung shrinks and atelectasis develops in a round configuration.
The distorted vessels appear to be pulled into the mass and resemble a comet tail (4).
However there is also some pleural thickening (red arrow) and vessels seem to swirl around the mass (blue arrows).
This is also described as the comet tail sign (4).
Whenever you see a pleural-based lesion that looks like a lungcancer, also consider the possibility of rounded atelectasis.
Rounded atelectasis is a benign lesion and when the findings are convincing, then biopsy is not needed.
During follow up these lesions usually do not change in configuration.
Rounded atelectasis is frequently seen in patients with a history of asbest exposure.
The images show a density posteriorly in the left lower lobe.
On the PA-film this looks like a mass or possibly a consolidation.
On the lateral film however the boundaries seem to be sharp, which is in favor of a mass.
Also notice that the pleura is thickened (red arrow).