Chest X-ray in Lung Consolidation

Consolidation:

Functionally the pulmonary airways can be divided into two groups. The proximal airways function purely as a conducting network: the airways distal to the terminal bronchioles are also conducting structures, but more importantly, are the site of gaseous exchange. These terminal airways are termed acini, an acinus comprising respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli arising from a terminal bronchiole. Consolidation implies replacement of air in one or more acini by fluid or solid material, but does not imply a particular pathology or aetiology. The smallest unit of consolidated lung is a single acinus, which casts a shadow approximately 7 mm in diameter. Communications between the terminal airways allow fluid to spread between adjacent acini, so that larger confluent areas of consolidation are generally visible and are frequently not confined to a single segment.

The commonest cause of consolidation is acute inflammatory exudate associated with pneumonia. Other causes include cardiogenic pulmonary edema, non-cardiogenic pulmonary edema, haemorrhage and aspiration. Neoplasms such as alveolar cell carcinoma and lymphoma can produce consolidation and alveolar proteinosis is a rare cause. In an individual patient, consolidation may be due to more than one basic aetiology. For example, a patient with major head trauma may be particularly susceptible to infection, aspiration and non-cardiogenic pulmonary edema.

When consolidation is associated with a patent conducting airway, an air bronchogram is often visible. This sign is produced by the radiographic contrast between the column of air in the airway and the surrounding opaque acini. If consolidation is secondary to bronchial obstruction, however, the air in the conducting airway is resorbed and replaced by fluid, and the affected area is of uniform density.

The volume of purely consolidated lung is similar to that of the normal lung since air is replaced by fluid or solid. However, collapse and consolidation are often associated with one another. When consolidation is due to fluid, its distribution is influenced by gravity, so that in acute pneumonitis, consolidation is often denser and more clearly demarcated inferiorly by a pleural surface, and is less dense and more indistinct superiorly.

Lobar consolidation:
Consolidation of a complete lobe produces a homogenous opacity possibly containing an air bronchogram, delineated by the chest wall, mediastinum or diaphragm and the appropriate interlobar fissure or fissures. Parts of the diaphragm and mediastinum adjacent to the non-aerated lung are obscured.

Right upper lobe consolidation:
This is confined by the horizontal fissure inferiorly and the upper half of the oblique fissure posteriorly and may obscure the right upper mediastinum.

Right middle lobe consolidation:
This is limited by the horizontal fissure above and the lower half of the oblique fissure posterioly, and may obscure the right heart border.

Lower lobe consolidation:
This is limited by the oblique fissure anteriorly and may obscure the diaphragm.

Left upper lobe and lingula consolidation:
These are limited by the oblique fissure posteriorly. Lingula consolidation may obscure the left heart border, and consolidation of the upper lobe may obscure the aortic knuckle.

Chest X-ray in Lung Collapse

Collapse:

Partial or complete loss of volume of a lung is referred to as collapse or atelectasis. This contrasts with consolidation in which a diminished volume of air in the lung is associated with normal lung volume.

Mechanisms of collapse:

1. Relaxation or passive collapse:

This is the mechanism whereby the lung tends to retract toward its hilum when air or increased fluid collects in the pleural space.

2. Cicatrisation collapse:

Normal lung expansion depends upon a balance between outward forces in the chest wall and opposite elastic forces in the lung. When the lung is abnormal stiff, this balance is disturbed, lung compliance is decreased and the volume of the affected lung is reduced. This occurs with pulmonary fibrosis.

3. Adhesive collapse:

The surface tension of the alveoli is decreased by surfactant. If this mechanism is disturbed as in the respiratory distress syndrome, collapse of alveoli occurs, although the central airways remain patent.

4. Resorption collapse:

In acute bronchial obstruction, the gases in the alveoli are steadily taken up by the blood in the pulmonary capillaries and are not replenished, causing alveolar collapse. The degree of collapse may be modified by collateral air drift if the obstruction is distal to the main bronchus, and also by infection and accumulation of secretions. If the obstruction becomes chronic, subsequent resorption of intra-alveolar secretions, and exudate may result in complete collapse. This is the ususal mechanism of collapse seen in carcinoma of the bronchus.

Radiological signs of collapse:

The radiographic appearance in pulmonary collapse depends upon the mechanism of collapse, the degree of collapse, the presence or absence of consolidation, and the pre-existing state of the pleura. Signs of collapse may be considered as direct or indirect. Indirect signs are the results of compensatory changes which occur in response to the volume loss.

Direct signs of  collapse:

1. Displacement of interlobar fissures:

This is the most reliable sign and the degree of displacement will depend on the extent of the collapse.

2. Loss of aeration:

Increased density of a collapsed area of lung may not become apparent until collapse is almost complete. However, if the collapsed lung is adjacent to the mediastinum or diaphragm, obscuration of the adjacent structures may indicate loss of aeration.

3. Vascular and bronchial signs:

If a lobe is partially collapsed, crowding of its vessels may be visible, if an air bronchogram is visible, the bronchi may be crowded.

Indirect signs of collapse:

1. Elevation of the hemidiaphragm:

This sign may be seen in lower lobe collapse, but is rare in collapse of the other lobes.

2. Mediastinal displacement:

In upper lobe collapse, the trachea is often displaced toward the affected side, and in lower lobe collapse, the heart may be displaced.

3. Hilar displacement:

The hilum may be elevated in upper lobe collapse and depressed in lower lobe collapse.

4. Compensatory hyperinflation:

The normal part of the lung may become hyperinflated, and it may appear hypertransradiant with its vessels more widely spaced than in the corresponding area of the contralateral lung. If there is considerable collapse of a lung, compensatory hyperinflation of the contralateral lung may occur, with herniation across the midline.

Patterns of collapse:

An air bronchogram is almost never seen in resorption collapse, but is usual in passive and adhesive collapse, and may be seen in cicatrisation collapse if fibrosis is particularly dense. Pre-existing lung disease such as fibrosis and pleural adhesions may alter the expected displacement of anatomic landmarks in lung collapse. There also tends to be a reciprocal relationship between the compensatory signs, e.g. in lower lobe collapse, if diaphramatic elevation is marked, hilar depression will be diminished.

Complete collapse of a lung:

Complete collapse of a lung in the absence of pneumothorax or large pleural effusion or extensive consolidation, causes opacification of the hemithorax, displacement of the mediastinum to the affected side and elevation of the diaphragm. compensatory hyperinflation of the contralateral lung occurs, often with herniation across the midline. Herniation most often occurs in the retrosternal space, anterior to the ascending aorta, but may occur posterior to the heart or under the aortic arch.

Lobar collapse:

a. Right upper lobe collapse:

The normal horizontal fissure is usually at the level of the right fourth rib anteriorly. As the right upper lobe collapses, the horizontal fissure pivots about the hilum, its lateral end moving upward and medially toward the superior mediastinum, and its anterior end moving upward toward the apex. The upper half of the oblique fissure moves anteriorly. The two fissures become concave superiorly. In severe collapse, the lobe may be flattened against the superior mediastinum, and may obscure the upper pole of the hilum. The hilum is elevated, and its lower pole may be prominent. Deviation of the trachea to the right is usual, and compensatory hyperinflation of the right middle and lower lobes may be apparent.

b. Right middle lobe collapse:

In right middle lobe collapse, the horizontal fissure and lower half of the oblique fissure move toward one another. This can best be seen in the lateral projection. The horizontal fissure tends to be more mobile, and therefore usually shows greater displacement. Signs of right middle lobe collapse are often subtle on the frontal projection since the horizontal fissure may not be visible, and increased opacity does not become apparent until collapse is almost complete. However, obscuration of the right heart border is often present, and may be the only clue in this projection. The lordotic AP projection brings the displaced fissure into the line of the X-ray beam, and may elegantly demonstrate right middle lobe collapse. Since the volume of this lobe is relatively small, indirect signs of volume loss are rarely present.

c. Lower lobe collapse:

The normal oblique fissures extend from the level of the fourth thoracic vertebra posteriorly to the diaphragm close to the sternum anteriorly. The position of these fissures on the lateral projection is the best index of lower lobe volumes. When a lower lobe collapses, its oblique fissure moves posteriorly but maintains its normal slope. In addition to posterior movement, the collapsing lower lobe causes medial displacement of the oblique fissure, which may then become visible in places on the frontal projection.

d. Right lower lobe collapse:

This causes depression and medial rotation of the hilum, elevation of the right hemidiaphragm and hyperinflation of the right upper lobe. A completely collapsed lower lobe may be so small that it flattens and merges with the mediastinum, producing a thin, wedge-shaped shadow. On the left, this shadow may be obscured by the heart and a penetrated view with a grid may be required for its visualization.

e. Lingula collpase:

The lingula is often involved in collapse of the left upper lobe, but it may collapse individually, when the radiological features are similar to right middle lobe collapse. However, the absence of a horizontal fissure on the left makes anterior displacement of the lower half of the oblique fissure and increased opacity anterior to it important signs. On the frontal projection the left heart border becomes obscured.

f. Left upper lobe collapse:

The pattern of upper lobe collapse is different in the two lungs. Left upper lobe collapse is apparent on the lateral  projection as anterior displacement of the entire oblique fissure, which becomes oriented almost parallel to the anterior chest wall. With increasing collapse the upper lobe retracts posteriorly and loses contact with the anterior chest wall. The space between the collapsed lobe and the sternum becomes occupied by either hyperinflated left lower lobe or herniated right upper lobe. With complete collapse, the left upper lobe may lose contact with the chest wall and diaphragm and retract medially against the mediastinum. On a lateral film, therefore, left upper lobe collapse appears as an elongated opacity extending front the apex and reaching, or almost reaching, the diaphragm: it is anterior to the hilum and is bounded by displaced oblique fissure posteriorly, and by hyperinflated lower lobe anteriorly.

A collapsed left upper lobe does not produce a sharp outline on the frontal view. An ill-defined hazy opacity is present in the upper, mid and sometimes lower zones, the opacity being densest near the hilum. Pulmonary vessels in the hyperinflated lower lobe are usually visible through the haze. The aortic knuckle is usually obscured, unless the upper lobe has collapsed anterior to it, allowing it to be outlined by lower lobe. If the lingula is involved, the left heart border is obscured. The hilum is often elevated, and the trachea is often deviated to the left.

Rounded atelectasis:

This is an unusual form of pulmonary collapse which may be misdiagnosed as a pulmonary mass. It appears as a homogeneous mass upto 5 cm in diameter, with ill-defined edges. It is always pleural based and associated with pleural thickening. Vascular shadows may be seen to radiate from part of the opacity, resembling a comet's tail. The appearance is caused by peripheral lung tissue folding in on itself. It is often related to asbestos exposure, but may occur secondary to any exudative pleural effusion.

Cardiomegaly in Chest X-ray

Cardiomegaly:

It is a general term used to describe any condition that results in an enlarged heart.

1. Dilative
2. Hypertrophic

1. Dilative: 

The heart can become enlarged due to dilation of the myocardium. Dilated Cardiomyopathy (DCM) is the most common form of non-ischaemic cardiomyopathy. In DCM, the heart becomes weakened and enlarged and cannot pump blood efficiently. The decreased heart function can affect the lungs, liver and other systems (the most common form of non-ischaemic cardiomyopathy). Generalized enlargement of the heart is seen upon normal chest x-ray. Pleural effusion may also be noticed which is due to pulmonary venous hypertension.

2.Hypertrophic:

Just as skeletal muscle, hypertrophy grow in size in response to increase demand, cardiac muscle undergoes hypertrophy when placed under a high workload for a prolong period of time. Some cardiac hypertrophy is normal and reversible. Pathologic hypertrophy is the result of diseases that place increased demand on the heart, such as chronic hypertension, MI and valvular damage.Gross RA enlargement evidence of shift of right border very much into right hemithorax. MPA and RPA shadows prominent. Elevated left bronchial shadow and filling of appendage region of left border indicate left atrial enlargement.

 LVH is the most common type of hypertrophic heart disease. A common cause of LVH is chronic hypertension, which increase the afterload on the left ventricle. This means the left ventricle has to increase contractibility and/or preload to maintain same stroke volume. Overtime the added stress on the left ventricular myocardium results in muscle hypertrophy and remodelling of left ventricle to a less efficient shape and size. This leads to a diminishing ejecting fraction, meaning the heart must work even harder to maintain cardiac output. The larger heart also demands more blood flow and so becomes more susceptible to ischaemic injury.

Causes of Cardiomegaly:

1. Hypertension
2. Valvular heart disease
3. Ischaemic heart disease - previous MI
4. Dilated cardiomyopathy
5. Pericardial effusions e.g. malignancy
6. Right heart dilatation - PHTN
7. ASD
8. Thyroid disorders
9. Infiltrative heart disease - amyloid
10. Congestive heart disease

Extracardiac causes of cardiac enlargement:

1. Portable AP films
2. Obesity
3. Pregnancy
4. Ascites
5. Straight back syndrome
6. Pectus excavatum

 Cardiomegaly is often detected on postero-anterior projection of chest x-ray. The standard method for measuring heart size (Danzer Method) involves measuring the distance from the midline of the spine to the most lateral aspect of the cardiac apex and adding this distance to that found from the same midline to the most lateral aspect of the right atrium. This number is divided by the largest horizontal width of the chest from right to left pleural space (usually found just above the left hemidiaphragmatic surface). This value is known as cardiothoracic ratio i.e. CTR (more than 0.5 indicates cardiomegaly).
CTR = a ratio of
1. Max. horizontal cardiac diameter
2. Max. horizontal thoracic diameter (inner edge of ribs or edge of pleura)

In cardiomegaly chest x-ray, there will be markedly enlarged cardiac silhouette, double contour to the right heart border and splaying of carina. The most lateral contour is of right atrium and the most medial contour is of left atrium.

Right cardiomediastinal contour: (from superior to inferior)

1. Right paratracheal stripe seen in 2/3rd of normal films, made up of right brachiocephalic vein and SVC
2. Arch of azygous vein
3. Ascending aorta in older patients often projects to the right of SVC
4. Superior venacava
5. Right Atrium
6. Inferior venacava

Left cardiomediastinal contour: (from superior to inferior)

1. Left paratracheal stripe made up of LCCA, LSA, LJV
2. Aortic arch +/- aortic nipple
3. Pulmonary artery
4. Auricle of left atrium
5. Left ventricle

Chest X-ray findings in Inactive Tuberculosis

1. Discrete fibrotic scar or linear opacity
2. Discrete nodule(s) without calcification
3. Discrete fibrotic scar with volume loss or retraction
4. Other- any other findings prior TB- such as upper lobe bronchiectasis

1. Discrete fibrotic scar or linear opacity: the edges of these densities should be distinct and there should be no suggestion of airspace opacification or haziness between or surrounding these densities. Calcification can be present within the lesion and the lesion is called as "fibrocalcific" scar.

2. Discrete nodules without calcification: one or more nodular densities with distinct borders and without any surrounding airspace opacification. Nodules are generally round or have rounded edges. These features allow them to distinguish from infiltrates or airspace opacities. To be included here, these nodules must be non-calcified. No follow up needed for calcified nodules.

3. Discrete fibrotic scar with volume loss or retraction: discrete linear densities with reduction in the space occupied by the upper lobe. Associated signs include upward deviation of the fissure or hilum on the corresponding side with asymmetry of the volume of two thoracic cavities.

4. Discrete nodule(s) with volume loss or retraction: one or more nodular densities with distinct borders and no surrounding airspace opacification with reduction in the space occupied by the upper lobe. Nodules are generally round or have rounded edges.

5. Other - prior TB i.e. upper lobe bronchiectasis (bronchial dilatation with bronchial wall thickening).

Follow up:

• Musculoskeletal abnormalities
• Cardiac abnormalities
• Pulmonary abnormalities

No follow up:

• Pleural thickening: irregularity or abnormal prominence of the pleural margin including apical capping (thickening of the pleura in apical region); may be calcified.
• Diaphragmatic tenting: localized accentuation of the normal convexity of the hemidiaphragm as if pulled upwards by a string.
• Blunting of costophrenic angle: loss of sharpness of both costophrenic angles or one. Blunting can be related to a small amount of fluid in pleural space or to pleural thickening. Large pleural effusion is a sign of actve TB at any age.
• Minor musculoskeletal abnormalities
• Minor cardiac abnormalities
• Solitary calcified nodules or granuloma: discrete calcified nodules or granuloma or calcified lymph node. The calcified nodule can be within the lung, hila or mediastinum.

Chest X-ray findings in Active Pulmonary Tuberculosis

1. Infiltrate or consolidation
2. Any cavitary lesion
3. Nodule with poorly defined margin
4. Pleural effusion
5. Hilar or mediastinal lymphadenopathy
6. Linear, interstitial disease (in children only)
7. Other - any other findings of active TB, such as miliary TB.

In active PTB, infiltrates or consolidations and/or cavities are often seen in the upper lungs with or without mediastinal or hilar lymphadenopathy. Old healed TB usually presents as pulmonary nodules in the hilar area or upper lobes, with or without fibrotic scars and volume loss. Bronchiectasis and pleural thickening may be present.

1. Infiltrate or consolidation: opacification of airspaces within the lung parenchyma; may be dense or patchy and might have irregular, ill-defined or hazy borders.

2. Any cavitary lesion: lucency (darkened area) within the lung, with or without irregular margins that might be surrounded by an area of air space consolidation or infiltrates or by nodular or fibrotic (reticular) densities or both. The walls surrounding the lucent area can be thick or thin. Calcification can exist around the cavity.

3. Nodule with poorly defined margins: Round density within the lung parenchyma also called as tuberculoma; tree in bud sign. The surrounding haziness can be either subtle or readily apparent and suggests co-existing airspace consolidation.

4. Pleural effusion: presence of significant amount of fluid within the pleural space; blunting of costophrenic angle, which may or may not represent a small amount of fluid within the pleural space.

5. Hilar or mediastinal lymphadenopathy: enlargement of lymph nodes in one or both hila or within the mediastinum with or without associated atelectasis or consolidation.

6. Linear, interstitial disease:(in children only) prominence of linear, interstitial or septal markings.

7.Other: miliary TB: nodules of millet size (1-2mm) distributed throughout the parenchyma.