University of Babylon



The chest film of elderly persons:

1-Thorax changes in shape and the AP diameter increases.

2-A kyphosis develops so that the chin overlies lung apex.

3-Frequently only AP film in the sitting position can be obtained usually with limited degree of inspiration so that lung bases are poorly visualized.

4-Bone demineralization increases, with vertebral compression and rib fractures are common.

5-Costal cartilage and vascular calcifications are common.

6-Major blood vessels become unfolded.

Pulmonary collapse:

Means partial or complete loss of volume of a lung.

Direct radiological signs of collapse:

1-displacement of interlobar fissures (most reliable sign).

2-loss of aeration.

3-Vascular and bronchial crowding.

Indirect signs:

1-Elevation of hemidiaphragm.

2-Mediastinal displacement.

3-Hilar displacement.

4-Compensatory hyperinflation.

Hilar enlargement:

Bilateral hilar enlargement is commonly due to enlarged lymph which appears as lobulated masses (lymphoma, leukemia….), or to Vascular enlargement, the adjacent bronchi may be slightly narrowed. Unilateral enlargement is common finding and it is most commonly due to a neoplasm or vascular dilatation but is also seen with infections such as tuberculosis.

Pleural Effusion:

Less than 5 ml of fluid is normally present in the pleural space. Excess pleural fluid accumulates when inflow and outflow from the pleural space are mismatched. A number of different types of fluid may accumulate in the pleural space, the commonest being transudate(less than 3 g/dl of protein, often bilateral, the commonest cause is cardiac failure, others: hypoproteinemia, constrictive pericarditis….), exudate (more than 3g/dl, the commonest causes are bacterial pneumonia, pulmonary T.B., CA of lung….), blood and chyle. Occasionally effusions are highly specific, not falling into any of the above categories and containing, for example, bile, cerebrospinal fluid or iatrogenic fluids. A small amount of free fluid may be undetectable on an erect PA chest radiograph as it tends initially to collect under the lower lobes. Such small subpulmonic effusions can be demonstrated by ultrasound or CT. An alternative technique, the lateral decubitus chest radiograph, has largely been replaced by these newer modalities .As the amount of effusion increases, the posterior and then the lateral costophrenic angles become blunted, by which time a 100-200 ml effusion is present. Following this the classical signs develop. Homogeneous opacification of the lower chest with obliteration of the costophrenic angle and the hemidiaphragm. The upper margin of the opacity is concave to the lung and is higher laterally than medially. Above and medial to the meniscus there is a hazy increase in opacity owing to the presence of fluid behind and in front of the lungs. Massive effusions cause dense opacification of the hemithorax with contralateral mediastinal shift. Large effusions sometimes cause diaphragmatic inversion, particularly on the left where the diaphragm lacks the support of the liver.

Pneumothorax:

Air in the pleural space is a pneumothorax. When air and liquid are present the nomenclature depends on their relative volumes and the type of liquid. Small amounts of liquid are disregarded and the condition is still called a pneumothorax; otherwise the prefix hydro-, haemo-, pyo-, or chylo- is added, depending on the nature of the liquid. Spontaneous pneumothorax is the commonest cause(occurs in young men), other causes: chronic bronchitis and emphysema in older patients, rupture of subpleural T.B. focus or subpleural tension cysts in Ca bronchus, trauma….

Radiologically: those are seen on erect radiographs in which the pleural air rises to the lung apex. Under these conditions the visceral pleural line at the apex becomes separated from the chest wall by a transradiant zone devoid of vessels.

Open pneumothorax: if air can move freely in and out of pleural cavity during respiration.

Closed pneumothorax: if no movement of air occurs during respiration.

Tension Pneumothorax: This life-threatening complication is present when intrapleural pressure becomes positive relative to atmospheric pressure for a significant part of the respiratory cycle. Tension has an adverse effect on gas exchange and cardiovascular performance, causing a rapid deterioration in the patient's clinical condition. The diagnosis is usually made clinically and treatment instituted without a radiograph. Should a chest radiograph be taken, it will show contralateral mediastinal shift and ipsilateral diaphragm depression. Mild degrees of contralateral mediastinal shift are not unusual with a nontension pneumothorax because of the negative pressure in the normal pleural space. Moderate or gross mediastinal shift (mainly during inspiration noticed at fluoroscopy) should be taken as indicating tension, particularly if the ipsilateral hemidiaphragm is depressed. This latter sign is the more reliable and almost invariably present with significant tension. This is particularly true of the ventilated patient in whom mediastinal shift may be absent.

Pneumomediastinum:

Air may enter the mediastinum from a perforation of the pharynx, oesophagus or major airways. In many instances, however, a pneumomediastinum is the result of an air leak from a tear in a small intrapulmonary airway, the air dissecting through the lung via the hilum into the mediastinum. Asthma is the commonest precipitating cause. In other cases the leak is probably related to abrupt changes in intrathoracic pressure such as those associated with vomiting. Occasionally, air tracks into the mediastinum from retroperitoneal air collections.

On imaging examinations: the condition is recognized as streaky translucencies within the mediastinum that are usually most obvious adjacent to the left heart border, aortic knuckle, main pulmonary artery and adjacent left hilum .The air dissects through the perivascular areolar tissues and may track up into the neck, supraclavicular areas and axillae as well as down into the retroperitoneum.

Pneumonia:

Pneumonia is infective consolidation of the lung, and radiology plays a key role in its diagnosis and management.

LobarPneumonia:Streptococcus pneumonia is the classical cause, it begins as localized infection of terminal airspaces and then spreads to adjacent lung via terminal airways and pores of Kohn forming uniform (sometimes non-uniform) consolidation of all or part of lobe. it is limited by fissures, the affected lobe retain its normal volume, and it is often shows airbronchogram.Karely-B-line may appear in the affected area. On the other hand, the consolidation in a bronchopneumonia is usually multifocal and centred on airways affected by a bronch(iol)itis. The process is initially patchy and distributed in a way that reflects the course of the airways, i.e. it is segmental. Inflammatory involvement of the airways commonly leads to obstruction and atelectasis and occasionally to pneumatocele formation. Thus, radiologically a bronchopneumonia is characterized by a non homogeneous (patchy), segmental consolidation which only later, with confluence, becomes uniform. An air bronchogram is usually absent and volume loss is common. The commonest cause is Staphylococcus aureus.

Pulmonary T.B.:

Primary Tuberculosis: This develops about 1–2 months after exposure and is usually occult. Simply there is an area of peripheral consolidation (Ghon' focus), and spread from this along draing lymphatics may lead to enlargement of regional lymph nodes, this combination called primary complex.

Radiological Findings:

1. Inactive: Should the primary focus arrest early with minor scarring, the chest radiograph will appear normal but the Mantoux status will be positive. If significant scarring results it will be visible as well-defined, rounded or irregular (linear) opacities, and should caseous necrosis have occurred, calcification may be present. Parenchymal calcification consists of one or more homogeneous nodules, usually less than 5 mm in diameter, which may occur anywhere. Nodal calcification is typically inhomogeneous and irregular.

2. Consolidation: Consolidation tends to be more common on the right, may occur in any zone (but most commonly in subpleural site in well ventilated lower lobes), and has no specific features. When it is indolent or combined with nodal enlargement, however, tuberculosis should be considered as a strong possibility. Consolidation is usually homogeneous and may be relatively well defined. The size of the involved area can range from 10 mm or less to an entire lobe. Multifocal involvement is unusual and cavitation rare, the occurrence of the latter suggesting progressive primary disease.

3. Lymphadenopathy: Lymphadenopathy is the most common manifestation and it occurs with or without radiological consolidation. In the former case, the nodes involved are those draining the consolidated area, and the consolidation is sometimes sufficiently extensive to obscure the adenopathy. With apparently isolated nodal enlargement, the patterns commonly seen are unilateral hilar, unilateral hilar plus right paratracheal, or isolated right paratracheal adenopathy. Bilateral hilar involvement is also described, and when present it is almost always asymmetrical. Nodal pressure and erosion affecting adjacent structures may cause the following complications:

a. Airways: Narrowing of major airways may lead to obstructive over-inflation or segmental/lobar collapse; the collapse is commonly right-sided. A segmental consolidation can follow bronchial perforation and distal aspiration of infective caseous material.

B.Blood vessels: Haematogenous dissemination from nodes can lead to miliary tuberculosis or to an isolated lesion such as a soft tissue abscess. Metastases from nodes may lie dormant for years before becoming active and presenting particularly as bone, joint, or renal tuberculosis.

c.Pericardium: Erosion of a node into the pericardial sac can cause a pericarditis which may also be seen with miliary spread. Late constrictive pericarditis is a recognized sequel and may occur with or without pericardial calcification.

d.Pleura: Similarly, pleural erosion by a node is one of several mechanisms by which a pleural effusion forms in primary tuberculosis.

E.Other manifestations: Other complications are occasionally seen, including oesophageal involvement, nerve paresis (phrenic and recurrent laryngeal), superior vena caval obstruction and fistula formation.

4. Pleural Effusion: Pleural effusion as a manifestation of primary tuberculosis occurs either in children, who usually show radiological evidence of parenchymal or nodal disease or in teenagers and young adults, when it is frequently isolated. In this latter form, accumulation is slow and painless, so that at presentation the effusions are often large. Effusions are unilateral except in a situation in which they complicate miliary spread.

5. Miliary Tuberculosis: Although classically a manifestation of primary disease, miliary tuberculosis is now more commonly seen as a post-primary process in older patients. Early on, the chest radiograph may be normal before the development of multiple small (1–2 mm) discrete nodules scattered evenly throughout both lungs. These are of soft tissue density and are characteristically very well defined. Other features of primary tuberculosis may or may not be present, but nodal enlargement, for example, is not uncommon.

6. Tuberculoma.

Post-primary T.B.: this follows the primary infection after a latent period, and it is now generally accepted that almost all post-primary T.B. is due to reinfection.

Major Radiological Findings: while glandular involvement is the hallmark of primary tuberculosis, post-primary disease is characterized by a strong site preference, chronicity, cavity formation, and fibrosis. It should be noted that although glandular involvement is not a feature of post-primary disease, the sequelae of adenopathy are very similar to those of endobronchial tuberculosis, which does occur with postprimary disease. In 95% of patients the initial lesion arises in the apicoposterior segment of an upper lobe or the apical segment of a lower lobe. The lesion consists of a peripheral consolidation, often patchy and multifocal with nodular elements (acinar nodules) interspersed with linear opacities which may extend along the bronchovascular bundles towards the hilum. Changes may be unilateral or bilateral. With progression the consolidation may become confluent and early volume loss appears.

Cavitation is common and seen in 40–80% of cases. It arises in areas showing the changes described above and has the same distribution. Cavities have no diagnostic features and may be single or multiple, large or small. The thickness of the wall varies from a hairline to a few millimetres. It is usually smooth. Air–fluid levels are unusual. A Rasmussen aneurysm is a rare life-threatening complication of cavitary tuberculosis caused by granulomatous weakening of a pulmonary arterial wall.

Healing results in scar formation. Cavities are usually obliterated by this scarring process, but occasionally healed cavities remain as such or as thin-walled ring shadows. The fibrosis results in well-defined, upper zone nodular and linear opacities, often with evidence of marked volume loss and pleural thickening. Some of the opacities calcify, though this occurs less commonly than in primary tuberculosis. With gross scarring, bronchiectasis and the formation of cysts and bullae are common. Bronchiectasis, because of its site, drains well and is usually asymptomatic, apart from sometimes causing haemoptysis.

Radiology of Other Features and Complications:

These include various entities, many of which are shared by the primary disease:

1. Bronchogenic spread. This can occur with or without cavitary disease and spread may be ipsi- or contralateral often in a segmental distribution. The bronchopneumonic consolidation that follows tends to be rather nodular, with acinar lesions that may later become confluent. The combination of localized consolidation and/or cavitation with remote segmental nodular consolidation is very suggestive of tuberculosis.

2. Endobronchial infection. Although this is not related, as in primary tuberculosis, to lymphadenopathy but rather to tuberculous bronchitis, it has essentially the same sequelae.

3. Pleural effusion. Effusion accompanying post-primary tuberculosis is usually an empyema and it carries a worse prognosis than does effusion in primary tuberculosis, often leading to pleural thickening and calcification and very occasionally directly involving the chest wall. Should a bronchopleural fistula form, a hydropneumothorax will result.

4. Miliary tuberculosis. This now occurs more commonly as a manifestation of postprimary than of primary disease. The chest radiograph may initially be clear but sooner or later the characteristic miliary nodulation described above appears.

5. Tuberculoma. A tuberculoma may occur in the setting of primary or postprimary tuberculosis. This produces a nodule 10–15 mm in diameter that may be situated in any zone but most commonly the right upper. These nodules are commonly single but may be multiple, and in this case may all be confined to a single segment. The margins of the nodule are usually fairly well defined and there may be satellite lesions nearby, though this is not a specific finding. Calcification is not uncommon and cavitation has been described, though it is unusual.

6. Mycetoma formation. Chronic tuberculous cavities of more than 25 mm in diameter may become saprophytically colonized by a fungus, usually Aspergillus fumigatus. CT is more sensitive than the chest radiograph in demonstrating mycetoma formation.

7. Chest wall involvement. Chest wall involvement may be due to haematogenous seeding or direct spread from the lung and may affect soft tissue, rib, or costal cartilage.

Bronchiectasis:

Bronchiectasis is the irreversible dilatation of a bronchus, and it is usually the results of severe, recurrent or chronic infections. Bronchiectasis may be localized, multifocal, or generalized depending on its aetiology. It is commonly basal or basally predominant but in some conditions it may be confined to the upper zones (e.g. tuberculosis) or be predominantly in the upper zones (e.g. cystic fibrosis).It may be cylindrical(tubular), varicoid(the walls are irregular) or saccular(or cystic).

The chest radiograph is usually abnormal in moderate or severe bronchiectasis, but is commonly normal in mild disease. Airway walls become visible because they are thickened. Side-on they produce single thin lines or parallel-line opacities that are more widely separated than would be expected with normal diameter airways. End-on dilated airways produce ring and curvilinear opacities with relatively thin walls that may contain air-fluid levels. When filled with secretions airways parallel to the film generate simple or branched band opacities (5–10 mm diameter) that point towards the hilum and may have expanded distal ends. Seen end-on, such dilated fluid filled airways produce rounded or oval nodular opacities. In generalized forms of bronchiectasis lung volume is often increased but with focal disease there is commonly volume loss.

Emphysema:

Defined in morphological terms as an increase beyond normal of airspaces distal to the terminal bronchiole, due either to dilatation or destruction of their walls.

Radiologically: The diaphragm is usually at the level of the 6th or 7th anterior rib at the end of a deep inspiration. Normal individuals may contract their diaphragm below this level and a low position alone is not therefore sufficient evidence for over-inflation, the most reliable sign for which is associated flattening of the diaphragmatic dome. Films exposed at the end of inspiration and expiration respectively will reveal limited diaphragmatic excursion (well under the normal lower limit of 3 cm). The low, flat diaphragm results in an apparently small heart and a decreased cardiothoracic ratio. Enlargement of the retrosternal translucent zone on the lateral radiograph (measured from the back of the sternum to the anterior aspect of the lower ascending aorta) provides additional evidence of over-inflation, but should be 4 cm or greater to be considered abnormal.

In emphysema, in addition to overinflation of the lungs, the pulmonary vessels are abnormal. In widespread generalized emphysema, the midfield and peripheral vessels are attenuated in both size and number. The normal smooth gradation in size of vessels from the hilum outwards is lost, with the hilar vessels being larger than normal and tapering abruptly. With the development of cor pulmonale, or left heart failure, the radiographic appearances will alter and may become less obviously abnormal. The heart may then appear to be normal in size, or sometimes enlarged, the diaphragm becomes less flat and the pulmonary vessels less attenuated.

Bullae: These are recognized by their transradiancy, their hairline walls and a distortion of adjacent pulmonary vessels. Bullae vary greatly in size and are occasionally large enough to occupy the whole hemithorax. They can be identified in about one-third of patients with other radiographic evidence of emphysema and they are sometimes seen independently of emphysema.

Bronchial carcinoma:

Types:

1-Squamous cell carcinoma (central, cavitates more often than other types).

2-Adenocarcinoma (peripheral).

3-small cell carcinoma (central and often associated with extensive hilar and mediastinal lymphadenopathy).

4-large cell tumors (undifferentiated type).

Radiological features: There are no radiological features that can reliably differentiate between a benign and malignant pulmonary nodule or mass. However, malignant tumors are usually larger than benign lesions at the time of presentation. Peripheral lung cancers tend to have poorly defined, lobulated or umbilicated margins, or may appear speculated. Satellite opacities around the main lesion are more frequently seen with benign masses, but may be associated with carcinoms.Diffuse or central calcification in the peripheral pulmonary mass is very suggestive of benign lesion, but occasionally calcified granuloma will have been engulfed by malignant tumors. Doubling time of Ca bronchus between (1-18) months. Any mass or nodule that has not changed in appearance over 2 year is almost certainly benign.Cavitation is seen in about (10-15) % of peripheral lung cancers on plain CXR (thick walled with an irregular, nodular inner margins, but some may appear as thin walled cavities).

Secondary signs of malignancy: hilar and mediastinal LAP, atelectasis, obstructive pneumonia, pleural effusion, interstial patterns (lymphatic tumor spread) and metastasis (ipsi-, contralateral lungs…..).

Cardiac imaging

Selective Left Atrial Enlargement:

1. Frontal View (Posteroanterior):

a. The enlarging left atrium may elevate the left main bronchus and if gross may lead to splaying of the carina.

b. As the enlarging left atrium bulges to the right, from the mediastinum out into the right lung, it produces a double shadow seen through the right side of the heart, until it eventually forms the right heart border. On the right side the borders of right and left atria may be distinguished because the left atrial border passes medially towards the spine before fading, whereas the right atrial border is limited below by the entry of the inferior vena cava.

c. Particularly in rheumatic mitral valve disease, there may be left atrial enlargement with specific enlargement of the left atrial appendage, first seen as a straightening of the left heart border, then as a discrete bulge on the left, immediately below the pulmonary bay and left main bronchus.

d. The enlarged left atrium may displace the descending aorta to the left. It may also displace the oesophagus to the side of the spine, usually to the right.

e. When the grossly enlarged left atrium bulges to the left and right of the cardiac silhouette and approaches to within an inch of the chest wall the term 'aneurysmal enlargement' is used.

2. Lateral View:

The enlarging left atrium may displace the left main bronchus, its direct posterior relation, backwards, a specific feature of selective enlargement. If the oesophagus is opacified with barium a localized posterior displacement at the level of the upper posterior heart border may be seen, stopping at the level of the mitral valve if overall cardiac enlargement is not gross.

Selective Left Ventricular Enlargement:

The following are the plain film radiographic signs of left ventricular enlargement:

1. Rounding of the apex of the heart. This may be the only sign and may be seen before overall cardiac enlargement has occurred. It appears as a characteristic rounding of the apex of the heart as seen in the frontal view.

2. Elongation of the long axis of the left ventricle. The earliest sign of LV cavity dilatation is an elongation of the axis of the left ventricle, which occurs mainly to the left and in a downward direction. On the plain radiograph, it is usual to see cardiac enlargement which has occurred mainly in a leftward direction so that the axis of the heart shadow extends to the left and downwards to a variable degree.

3. In the lateral view, the dilatation of the body of the left ventricular cavity may be recognized when the soft tissue shadow of the heart muscle bulges behind the barium-filled oesophagus (normally left ventricle on lateral CXR forms the posterior aspect of the heart below the level of the atrioventricular ring).

Selective Right Ventricular Enlargement:

The right ventricle is a flattened, triangular-shaped structure occupying the front of the heart. It forms the front surface of the heart in the lateral projection but contributes no part of the normal cardiac outline in the frontal projection. The normal heart shadow is in contact with the sternum (in the normally shaped chest) only in the lower half of its extent, in the lateral view. With progressive enlargement of the right ventricle the area of contact between the front surface of the heart and the sternum increases until eventually the whole heart lies in contact with the sternum. This is the earliest and most sensitive radiological sign of right ventricular enlargement.

Dilatation of the right ventricle frequently becomes so gross that the left border of the right ventricle may move so far to the left that it makes up the left heart border, and thus in the frontal view, the cardiac outline takes the triangular shape of the right ventricle.

Dilatation of the right ventricle usually involves the whole of the chamber, this dilatation results in a tilting-up and a posterior displacement of the left ventricle if this is normal in size. Thus in the frontal view, right ventricular enlargement results in an overall increase in the cardiac shadow, which adopts a triangular configuration whose long axis is elongated in a downward direction, and there may be elevation of the apex of the heart which is usually formed by the left ventricle.

Other radiographic evidence pointing to selective right ventricular enlargement may frequently be obtained by studying the main pulmonary artery, which is usually enlarged, and the peripheral pulmonary vessels, which may be increased, pruned or decreased, and thus point to the presence or cause of some right ventricular abnormalities.

Selective Right Atrial Enlargement:

Plain radiographic signs of right atrial enlargement:

1. Increase in size of the right atrium displaces the right heart border to the right.

2. Selective right atrial enlargement may either increase the radius of the curvature of the right heart border, or increase the convex curvature of the right heart border. Thus the right heart border may be 'flatter' or more curved than usual.

3. A step-like angle between the right atrium and the superior vena cava may be seen. It is less obvious in acquired disease leading to right atrial enlargement, as the superior vena cava is itself often dilated as well, and these smoothes out the step.

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