University of Babylon



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.

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