Chest ImagingTuberculosis
disease that has existed for thousands of years and is still responsible for a large number of deaths throughout the world. As with other diseases which have diminished in incidence, tuberculosis requires at least a passing thought if the diagnosis is to be made. In hospitals that deal with immigrant, poor, indigent, inner city populations or
AIDS patients tuberculosis should be high on the differential list of acute and chronic lung disease. Pathologically, tuberculosis begins when
Mycobacterium tuberculosis bacilli are carried via aerosolized droplet nuclei into the alveoli. An exudative response occurs within the air spaces. The bacteria are phagocytized but not killed by polymorphonuclear leukocytes and macrophages and continue to multiply intracellularly. During the 2 - 6 weeks following infection, organisms proliferate, spread to
lymph nodes and then systemically. This process is usually checked by the development of antibodies and in most cases the
pulmonary lesion disappears. In a smaller percentage of patients the
lesion resolves into a
nodule which is often visible radiographically. The
radiographic changes of
pulmonary tuberculosis are generally considered in two forms: primary or postprimary.
Primary tuberculosis
should be suspected whenever children (and now increasingly adults) present with appropriate clinical findings and a chest film demonstrating homogeneous air-space consolidation (Fig.1) and ipsilateral hilar lymphadenopathy. The parenchymal process is indistinguishable from other typical bacterial pneumonias. Failure to resolve on antibiotics may be a clue to its tuberculous nature. Cavitation is unlikely in primary tuberculosis but is occasionally seen. Following therapy the consolidation clears completely in the majority of cases. In approximately one third of patients a residual nodule or Ghon lesion persists. Calcification in this region may be seen several months after the original pneumonia. Enlargement of lymph nodes occurs frequently with primary tuberculosis. Lymphadenopathy may cause compression of adjacent bronchi and atelectasis. Calcified hilar or mediastinal nodes and a peripheral Ghon lesion constitute a Ranke complex. Lymph node enlargement may occur in the absence of a radiographically visible parenchymal opacification. Pleural effusion may also be seen as the sole manifestation of primary tuberculosis. Calcification of pleura in a dense plaque-like fashion may occur as with other chronic pleural diseases.
Postprimary tuberculosis
The chest radiograph findings of postprimary tuberculosis are varied. The most common radiographic abnormality is a heterogeneous air space consolidation involving the apical and posterior segments of the upper lobes and superior segment of the lower lobes. The pattern may be unilateral or bilateral and is characterized initially by its scattered distribution, somewhat nodular shape and indistinct margination (Fig.2). With time, better defined reticulonodular opacities and associated volume loss are noted. Scattered calcifications may be seen months or years later in areas of prior parenchymal consolidation. Lymph node enlargement is not part of the appearance of reactivation tuberculosis. Cavitation occurs uni- or bilaterally with some frequency during the course of postprimary tuberculosis. The size of the cavities ranges from a few mm to several cm. The inner wall of tuberculous cavities is usually smooth but wall thickness and clarity of definition of the outer wall are commonly functions of the degree of surrounding parenchymal involvement. The activity of tuberculous disease cannot and should not be implied from the findings on chest film. A "scarred" appearance in the upper lobe does not necessarily mean inactivity, nor is the presence of an "exudative" pattern or cavity always followed by positive smear or culture for M. tuberculosis. It cannot be emphasized enough that chest films of patients suspected of having tuberculosis should be reported as "activity indeterminate", not old tuberculosis. With cavitation a large amount of caseous material and acid-fast bacilli can be introduced into the conducting airways. This endobronchial spread usually results in a fairly extensive alveolar consolidation.
Miliary tuberculosis represents the haematogenous dissemination of disease throughout the body. This event occurs in primary and postprimary forms of tuberculosis. The radiograph reveals diffuse 1–2 mm in diameter nodules. In the early stage numerous individual nodules may be difficult to distinguish, and instead a fine, hazy opacification is noted, causing loss of definition of the pulmonary vessels. With appropriate therapy the nodules will resolve in a few weeks although occasionally this takes several months. Calcification of tuberculous miliary deposits is rare. A site of reactivation tuberculosis in the upper lobes may or may not be seen.
Tuberculomas may appear as solitary pulmonary nodules. Bronchiectasis, a very common complication of tuberculosis in the pre-antibiotic era, may be seen in late stages. Pleural thickening may or may not be present but has been noted commonly in the apical regions when upper lobe bronchiectasis is advanced. Uncommon radiological manifestations include mass densities simulating neoplasm, and chronic interstitial lung disease. Some published series indicate that lung carcinoma occurs with increasing frequency in patients with tuberculosis. Whether this is a cause and effect relationship (metaplasia of epithelial scar tissue to neoplasm) or merely coincidental is undetermined.
Tuberculosis in AIDS
has an overall incidence reported with varied frequency depending on the population studied. In some US cities the rate of coexisting tuberculosis and HIV infection ranges from 23 to 31%. In one study 73% of tuberculosis patients in Zambia were HIV positive. Conversely HIV positive individuals are at greater risk of developing tuberculosis. Both reactivation of latent tuberculosis and new infection occur. Clinically patients present with more typical complaints of weight loss, fever and cough when they get the disease early in their HIV infection. With more advanced immunosuppression unusual and extrapulmonary disseminated disease may be observed. The radiographic appearance of tuberculosis also depends upon the stage of HIV infection. Early in the course of disease, tuberculosis appears in a typical fashion, that is, patients with primary tuberculosis have homogeneous lobar consolidation with adenopathy and patients with postprimary tuberculosis present with poorly marginated heterogeneous nodular opacities and occasional cavitation in the superior segments of the lower lobes and apical and posterior segments of the upper lobes. Later in HIV infection diffuse and somewhat coarse heterogeneous reticular opacities are observed with or without the presence of hilar or mediastinal lymphadenopathy (Fig.3). While tuberculosis may result in cavitation, this is uncommon late in the course of HIV infection. Pleural effusion is seen with varying incidence (9 22%).
Antituberculosis therapy should result in chest film improvement that parallels the clinical response of the patient. The radiographic abnormalities begin to resolve within weeks. Worsening of a chest film while a patient is receiving appropriate medication should prompt investigation for an alternate infection or raise the suspicion of multiple-drug-resistant tuberculosis.
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