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RADIOLOGIC MANIFESTATIONS OF PULMONARY

H. Page McAdams, MD, Jeremy Erasmus, MD, and James A. Winter, MD

Among the difficulties inherent in a radio-logic discussion of tuberculosis (TB) are the many excellent prior reviews of the subject .2,

12, 14, 25, 53, 60, 95 There is also the question of organization. Does one approach the subject from a purely pattern oriented approach? Or should it be addressed from a pathophysiologic perspective, attempting to differentiate primary from postprimary disease? We have chosen the latter approach because it stresses the fundamental importance of pathology in understanding the various radiologic mani-festations of TB.

There are, however, certain weaknesses in this approach. The overlap in the radiologic manifestations of primary and postprimary disease often makes it difficult to confidently differentiate between the two. Moreover, as far as the patient is concerned, correct classification is often a moot point. Far more important is correct, timely diagnosis and therapeutic intervention. Also, certain radiologic findings that are seen in either type, such as cavitation or miliary disease, are of greater clinical significance than the type of disease itself.

For the purpose of this discussion, we adopt the pathophysiologic approach and we stress, where appropriate, differentiating features between primary and postprimary disease. Radiologic findings that are seen in ei

ther form (e.g., miliary disease) are discussed in the setting in which they most commonly occur.

PRIMARY TB

Pathogenesis and Pathologic Features

Mycobacterium tuberculosis is a strictly aero-bic, acid fast, gram-positive rod whose viru-lence is related to its ability to survive and reproduce within the cytoplasm of macro-phages.", 62 Humans are the most common natural reservoir and spread is by person to person transmission." The pathogenesis and pathologic manifestations of clinical TB are the result of both a cellular immune response and the development of delayed hypersensi-tivity to M. tuberculosis antigens." 3' Although humoral antibodies are produced, they do not seem to be important in the host response."

Primary TB occurs in patients not pre-viously exposed to M. tuberculosis. Exposure results in clinical infection in 5% to 15% of cases.", 19,25 Infection begins with inhalation and intraalveolar deposition of small (2-5 pg) droplets containing one to three bacilli."- 64

These droplets most commonly deposit in the middle and lower lobes3' where the bacilli

From the Departments of Radiology (HPM, JE) and Pathology (JAW), Duke University Medical Center, Durham, North Carolina

RADIOLOGIC CLINICS OF NORTH AMERICA

VOLUME 33 • NUMBER 4 • JULY 1995 655

2 McADAMS et al

attract a nonspecific, loosely organized infil-trate of lymphocytes, alveolar macrophages, and neutrophils (the primary focus)." 25 The bacilli are ingested by "nonactivated" macro-phages, proliferate within their cytoplasm, and ultimately cause cell lysis."- Zs This pro-cess may result in extensive alveolar consoli-dation or tuberculous pneumonia .64

Until the cellular immune response devel-ops, infection can progress locally and spread beyond the primary focus.31, 64 Lymphatic dissemination can result in more extensive disease in the hilar and mediastinal lymph nodes than at the primary focus.64 Low grade, usually subclinical, hematogenous spread is also common. 2-1 Although any organ can be secondarily infected, certain sites such as the subapical regions of the lung, renal cortex, brain, meninges, and epiphyseal bone marrow are preferentially involved .31, 62, 64, 83

In the first few weeks after infection, T cells sensitized to M. tuberculosis antigens accumulate and produce cytokines, which activate macrophages for effective mycobacterial killing. 17, 17,19 Clonal expansion of this sensitive T-cell population also occurs. The result is the development of both cell mediated immunity (activated macrophages) and tissue hypersensitivity (expansion of the sensitive T-cell population) to M. tuberculosis.8 This is clinically manifested as a delayed cutaneous reaction to the intradermal injection of purified protein derivative (PPD) .17

Effective cellular immunity and tissue hy-persensitivity usually develops 2 to 6 weeks after infection .62 Subsequent pathologic manifestations reflect the balance between bacillary proliferation and destruction within activated macrophages (antigen load) and the strength of the hypersensitivity response.19 In hosts with a normal response and low antigen load, the initial infiltrate organizes into wel l-defined tubercles by fusion of activated mac-rophages into epithelioid and multinucleate giant cells. 19,3' Tubercle encapsulation occurs by peripheral fibroblast proliferation and collagen deposition. 14 Such proliferative (productive) foci develop at both the primary and secondary sites19 (Fig. 1). Higher antigen burdens or less effective macrophage function result in more loosely organized areas of consolidation and caseous necrosis (exudative lesions) .19, 64 Granulomatous nodal inflammation and enlargement can result in either extrinsic bronchial compression or endobronchial inflammation and ulceration .25 This can lead to atelectasis of the affected pulmonary

segment or lobe. Rupture of caseous nodes into the airways or blood stream can cause massive endobronchial or hematogenous dis-semination 64 (Fig. 2).

In most cases, bacilli in all sites are eventu-ally contained and destroyed with minimal pathologic residua .3' Healing of larger paren-chymal lesions may leave fibrous scars or persistent nodules (known as tuberculomas), both of which may calcify.25, 31, 64 In a small percentage of cases, viable intracellular bacilli persist at the secondarily infected sites .25 Later, with waning of immunity, these dormant foci may reactivate, causing postpri-mary TB .31 Tuberculomas may also harbor viable intracellular bacilli and may slowly en-large with time .25

Children younger than 1 year of age, the elderly, and patients with T-cell immunode-ficiencies may not mount an adequate im-mune response to M. tuberculosis infection.'2, 25, 31 This happens in up to 5% of all primary infections and results in progressive primary tuberculosis .62 These patients can remain PPD skin test negative even though intracellular bacterial proliferation proceeds unabated.', 19 Pathologically, early nonspecific infiltrates progress to more extensive exudative le-sions." Proteolytic enzymes released by mac-rophage lysis result in caseous necrosis .31 Cavitation and endobronchial spread may result. 19, 64 Symptomatic hematogenous dissemination (miliary TB) also can occur .62

Pleural effusion in the setting of primary TB is thought to be caused by intrapleural rupture of small peripheral tubercles and an ensuing pleural hypersensitivity response .22 The pleural fluid is typically a serous exudate with a low glucose level and a marked lymphocytosis.9, 23 The fluid contains few ba-cilli and cultures are positive in only 30% to 40% of cases .22 Pleural biopsy and culture, however, yield the diagnosis in more than two thirds of cases .1, 22, 66 Sputum cultures are usually negative unless concomitant paren-chymal disease is present.9 Primary TB effu-sions are often self-limited.9 Timely diagnosis and appropriate therapy are imperative, as up to 65% of untreated patients develop active pulmonary disease within 5 years.9, 22,60

Radiologic Features

Primary TB traditionally has been consid-ered a disease of childhood, and its radio-graphic manifestations were initially de-

RADIOLOGIC MANIFESTATIONS OF PULMONARY TUBERCULOSIS 3

A

BFigure 1. TB in a 65-year-old woman. A, Large confluent caseating tubercles (arrowheads) and a marked fibroblastic response in the surrounding lung parenchyma (hematoxylin-eosin, original magnification x 40). 8, Higher magnification of a tubercle shows amorphous central caseous necrosis (N) surrounded by epithelioid (arrowheads) and Langerhans giant cells (arrows) with surrounding fibrosis (hematoxylin-eosin, original magnification x 200).

Figure 2. Miliary TB in a 4-year-old girl. Low power photomicrograph reveals numerous small discrete caseating granulomata (arrows) due to hematogenous dissemination (hematoxylin-eosin, original magnification x 10).

4 McADAMS et

scribed in the pediatric population. It remains the most common form of the disease in infants and children, with the highest prevalence in the 0- to 5-year age group.2, 53, 95 Although it continues to be almost exclusively a pediatric affliction in many parts of the world, primary TB is increasingly an adult disease in the United States. 14, 9s With the introduction of effective public health measures and antituberculous chemotherapy, the overall incidence of TB has (until recently) steadily declined in the United States.", 95 The pop-ulation of nonexposed adults who are at risk for primary TB has concomitantly increased.14, s1 Thus, primary disease now accounts for 23% to 34% of all adult cases of tuberculosis .53

Chest radiography remains essential for the diagnosis of primary TB. Up to 65% of pediatric patients are asymptomatic at presentation, with the chest radiographic abnormality or a positive PPD skin test the only clue to the diagnosis .z Primary TB manifests radiographically in five major ways: (1) parenchymal consolidation, (2) atelectasis, (3) lymphadenopathy, (4) pleural effusion, and (5) miliary disease .6° Chest radiographs are normal, however, in up to 15% of patients who have proved primary tuberculosis .53

Parenchymal

Primary TB typically manifests as a unifo-cal parenchymal consolidation43.95 (Figs. 3 and 4). Multilobar consolidation is less common, seen in up to 25% of cases4', 95 (Fig. 5). The

Figure 4. Primary tuberculosis in a 3-year-old child. A, Coned-down view of a posteroanterior chest radiograph shows left lower lobe homogeneous opacity. B, Followup examination 11 months later shows a residual calcified scar or Ghon lesion (arrow).

opacity is typically homogeneous, has ill-de-fined borders, and can contain an air-bronchogram.43,1° It is often indistinguishable from typical bacterial pneumonia. Important clues to the correct diagnosis include asso-ciated lymphadenopathy, lack of systemic toxicity, and/or failure to respond to conven-tional antibacterial therapy. 'z The consolida-tion is usually sublobar and subpleural.43

Complete lobar opacification with bulging fissures can occur,47, 60 usually due to associated endobronchial obstruction .43

The most common location of the paren

Figure 3. Primary TB in a 14-year-old boy. Posteroanterior chest radiograph demonstrates right upper lobe homogeneous opacity and right hilar and right paratracheal adenopathy. These findings suggest primary TB.

Figure 5. Primary TB in a 39-year-old man. Posteroanterior chest radiograph demonstrates extensive left lung opacification without adenopathy. Adenopathy is less common in adults with primary TB.


Figure 6. Ranke complex in a 65-year-old man. Coned-down view of a posteroanterior chest radiograph shows a 1.5-cm calcified nodule in the right lower lobe (Ghon focus, arrow) and calcified hilar lymph nodes. There is a smaller calcified nodule (open arrow) in the superior segment, which may represent a Simon focus.

festation of TB 6° seen in 7%95 to 9%39 of cases. They usually are considered to be the result of healed primary disease 60 but are most often encountered in asymptomatic adults.10, 3°. 93, 95 The true frequency of these lesions is difficult to determine because up to 11% of patients with proved tuberculomas are PPD negative .82 In the general population, tuberculomas account for 14%82 to 24%$$ of resected solitary nodules.

The majority of tuberculomas are less than 3 cm in size; 8

z, $

8 although lesions up to

5.0 cm are reported 25, 6° (Figs. 7 and 8). They usually occur in the upper lobes (75%) .82 Multiple similar-sized tuberculomas are seen in 20% of cases'° and smaller "satellite" lesions are seen in up to 80%" (Fig. 8). Cavitation is reported in 10% to 50%60,77 (Fig. 7). Up to 50% will eventually calcify 12,60,77 (Fig. 8). Calcified hilar lymphadenopathy supports the diagnosis .6° Although tuberculomas can gradually enlarge with time, most remain stable in size .6o

Pulmonary cavitation and endobronchial

chymal focus is controversial. In most series, there is a right-sided predominance, both in children and adults.43, 47, 90 In some series, an upper lobe predominance is cited, especially in infants and children." A middle and lower lobe predilection, particularly in adults, is also reported .95 Still, other series report no significant lobar bias .47 For practical purposes, primary TB can cause consolidation of any lobe (Figs. 3-5).

In two thirds of cases, the parenchymal focus resolves without radiologic sequelae.25,

47, 90 Resolution is typically slow, however, requiring 6 months to 2 years for complete clearing.47 In one third, a radiographically visible scar persists.25, 90 A calcified scar, known as a Ghon focus, is seen in 15% to 17%91 (Figs. 4 and 6). Healing of the secondarily infected sites also can result in radiographically visible scars and/or calcification .25 Calcified secondary foci in the lungs are known as Simon foci83 (Fig. 6). Antituberculous chemotherapy typically speeds the resolution of radiographic findings, although paradoxic worsening in the first 3 months of therapy is not uncommon. 3, 4', 10 The American Thoracic Society recommends radiographic evaluation at 2to 3-month intervals after initiation of therapy until all parenchymal findings resolve or stabilize.''

Persistent masslike opacities, or tuberculomas, are an uncommon parenchymal mani

Figure 7. Tuberculoma in a 74-year-old woman. A, Coned-down view of a posteroanterior chest radiograph shows a 2-cm nodule in the right upper lobe (arrows). There is a central lucency but no evidence of calcification. 8, Chest CT (lung window) confirms central cavitation (arrowhead). At surgery, necrotizing granulomatous in-flammation with viable M. tuberculosis organisms was found.

6 McADAMS et al

Figure 8. Tuberculoma in a 70-year-old man. A, Chest CT (lung window), coned down to the right lung, shows a 1.5cm nodule with spiculated margins and eccentric calcification (arrow). 8, A smaller, also calcified, "satellite lesion" (arrow) is seen elsewhere in the right lower lobe.

uncomplicated primary TB.47, 78, 80, 90

Although cavitation is reported in 7% to 29% of adults with primary disease,",'-' it is more likely a manifestation of progressive primary TB (see below). Pneumatocoeles are also an uncommon finding in children 8' but are reported in up to 12% of adults with primary TB.95

Atelectasis

Lobar or segmental atelectasis is a frequent radiologic manifestation of primary TB in children younger than 2 years of age.', 26, 90 It is less commonly observed in older children (9%)4' and adults (18%).25, 95 Collapse is caused either by endobronchial disease or extrinsic bronchial compression by enlarged hilar lymph nodes.26, 110 The bronchi of young children are particularly susceptible to extrin-sic compression 2, 26 (Fig. 9). Atelectasis most often involves the anterior segment of an upper lobe or the medial segment of the middle lobe .26 It typically persists until lymph node enlargement regresses .2. 25 Residual distortion or displacement of the involved bronchi may result.2, 25 Rarely, lobar hyperinflation secondary to a check-valve mechanism results from bronchial disease. 2,

80, 90

Lymphadenopathy

Radiographic evidence of hilar and/or me-diastinal lymphadenopathy is seen in 10% to 43% of adults", 14, 81, 95 and in up to 96% of children", 60, 91 with primary tuberculosis (Figs. 3, 9, 10, and 11). It is the radiologic hallmark of the disease in children" and is

more common in nonwhite patients in the United States.38, 49 The enlarged lymph nodes are typically in the hila, the right paratracheal, and less commonly, the subcarinal and the aortopulmonary window regions .25, 90 Although typically unilateral and rightsided 31, 90 (Figs. 3 and 10), bilateral adenopathy occurs in up to 31% of cases", 4' (Fig. 11). Adenopathy usually is seen in association with parenchymal consolidation or atelectasis2, 58, 80 (Figs. 3 and 9); however, it can be the sole radiographic manifestation of disease (Figs. 10 and 11). Adenopathy alone is a finding that decreases in frequency with age ,43 being encountered in up to 49% of children age 0 to 3 years," in 9% of children age 4 to 15 years," and only rarely in adults .4, 30, 39, 49, 52, 56

The radiographic detection of adenopathy requires high quality, high kilovoltage radiographs .2, 43 In children, adenopathy can manifest as ill-defined hilar prominence rather than distinct nodal enlargement. This is often best detected on the lateral chest radiograph i2, 80 CT is more sensitive than chest radiography for detecting intrathoracic tuberculous adenopathy.s8 Tuberculous nodes greater than 2 cm in diameter are typically of low attenuation on CT because of central caseous necrosis36, 63 (Fig. 12). Peripheral rimlike enhancement after the administration of intravenous contrast material also is seen .36, 63 Smaller nodal masses may show little or no contrast enhancement.36, 63 Tuberculous adenopathy can be gallium-67-avid.19

Tuberculous lymphadenopathy typically resolves at a slower rate than the associated parenchymal disease and it usually resolves


Figure 9. Primary TB in a 4-month-old boy. A, Coronal chest MR image (TR = 805,TE = 15,1.5 T) reveals marked right paratracheal, right hilar, and subcarinal adenopathy, which compresses the right and left upper lobe bronchi and the bronchus intermedius. 8, Axial chest MR image (TR = 805,TE = 15,1.5 T) further demonstrates the extent of adenopathy as well as the primary parenchymal focus in the right lower lobe (arrow). (Case courtesy of George Bisset, MD.)

without significant radiographic sequelae, al-though nodal calcification may result." Nodal calcification usually develops 6 months or more after the initial infection and is more common than parenchymal calcification .80, 90

Nodal calcification is also more common in adults than in children .80 The finding of calcified hilar nodes and a calcified parenchymal lesion (Ghon focus) is known as a Ranke complex25 (see Fig. 6). This finding, although suggestive of primary TB, also can result from histoplasmosis.25 The American Thoracic Society recommends yearly radiographic evalua

tion until tuberculous adenopathy either re-solves or stabilizes.'

In some cases, tuberculous adenitis evolves into tuberculous mediastinitis.93 This can lead to tracheal compression 6 the superior vena cava syndrome 6, 11 esophageal compression and fistula formation '21, 92 and tuberculous pericarditis.46 Pericarditis may also result from hematogenous dissemination.b0 Constrictive pericarditis develops in 10% of patients with tuberculous pericardial effusion and is associated with late pericardial calcification .46- 60

Pleural Effusion

Tuberculous pleuritis usually is considered a late sequelae of primary infection, typically

Figure 10. Primary TB in a 34-year-old woman. Posteroanterior chest radiograph shows right paratracheal and right hilar adenopathy and normal lungs.

Figure 11. Primary TB in a 26-year-old man. Posteroanterior chest radiograph shows bilateral mediastinal adenopathy and normal lungs.

8 McADAMS et al

Figure 12. TB in a 74-year-old woman. A, Chest CT (lung window) shows right lung consolidation and multifocal cavitation. There is evidence of both endobronchial and hematogenous spread to the left lung (suboptimally demon -strated due to motion artifact). B, Chest CT (mediastinal window) shows confluent, low attenuation mediastinal adenopathy. C, Contrast-enhanced abdominal CT (soft-tissue window) shows marked retroperitoneal adenopathy. The enlarged nodes have central low attenuation and thin enhancing rims (arrows).

manifesting 3 to 7 months after exposure9, 11,

23 (Figs. 13 and 14). Effusion is the sole radiographic manifestation of primary tuber-culosis in 38%95 to 63%9 of cases; however, CT often detects occult parenchymal disease or adenopathy when the chest radiograph is otherwise negative .33 Effusion is very uncommon in young children with primary TB .2. 43 It is much more common in adolescents and adults in whom frequencies of 6% to 38% (mean 10%) are reported.43, 47, 60, 81, 95 The effusion is most commonly unilateral '22, 95 freeflowing,53 and moderate to large in size.22, 95 True empyema, bronchopleural fistulae, rib or bone erosion, and pleurocutaneous fistulae (empyema necessitatis) are rare complications .33, 5s

Resolution of the effusion generally is prompt and complete with appropriate ther-apy60 (Fig. 14); however, residual pleural thickening or calcification can result. When

residual pleural thickening of 2 cm or greater is seen by chest radiograph, CT often will demonstrate persistent fluid that may contain viable bacilli .3-1, " Reactivation TB and bron-chopleural fistula may then develop as a late complication .33, _

5 3, 60

Miliary TBLimited, early hematogenous dissemina-

tion is common in primary TB, usually without clinical or radiographic manifestations .z, 25 Clinically significant, radiologically detectable miliary disease affects between 1% and 7% of patients with all forms of TB.53, 90, 95 The elderly, children under the age of 2, and immunocompromised hosts are most often affected .2. 12, 43 Miliary disease usually manifests within 6 months of primary infection .68.80 Chest radiographs typically are normal at onset of symptoms. Gallium-67 scintigraphy,


Figure 13. Tuberculous pleurisy in a 25-year-old woman. A, Posteroanterior chest radiograph reveals a large, partially loculated right pleural effusion and a fissural pseudotumor. There is right lower lobe consolidation and right hilar and right paratracheal adenopathy. 8, Follow-up radiograph 2 months later shows partial resolution of the effusion. Subcarinal adenopathy (arrow) is now seen.

Figure 14. Tuberculous pleurisy in a 48-year-old man. A, Posteroanterior chest radiograph shows complete opacification of the left hemithorax with contralateral mediastinal shift. 8, Contrast-enhanced chest CT (mediastinal window) reveals a large homogeneous pleural fluid collection with a smooth enhancing rim. C, Follow-up radiograph 10 months later shows complete resolution of pleural effusion without significant residual pleural thickening. There is a peripherally located left upper lobe opacity, which may reflect the healed primary focus.

10 McADAMS et

however, can show diffuse parenchymal up-take at this stage .z9 Hyperinflation can be the earliest radiographic manifestation, seen within 1 to 2 weeks.$° The classic radiographic finding of diffuse small (2-3 mm) nodular opacities may not appear until 6 weeks or more after hematogenous dissemination 2 (Fig. 15A and 15B). In 85% of cases, the nodules are evenly distributed with a slight lower lobe predominance. Asymmetric dissemination is seen in 15%65

(Fig. 16A and 16B). Associated lymphadenopathy is seen in 95% of children and 12% of adults with miliary disease .65 Associated parenchymal consolidation is also more common in children (42% to 12%) .65

High-resolution CT (HRCT) is more sensi-tive than chest radiography for the detection of miliary TB.32, 58 Miliary disease manifests on HRCT as discrete 1- to 2-mm nodules seen in a perivascular and

(Figs. 15C and 16C). Nodular thickening of the interlobular septa can result in a "beaded septum" appearance, similar to that of lymphangitic carcinomatosis89 (Fig. 16C).

Without therapy, the miliary nodules typically enlarge to 5 mm in diameter at which time the patient may succumb to the disease. Occasionally, the nodules will coalesce into focal (Fig. 16D) or diffuse consolidations or progress to the adult respiratory distress syndrome (ARDS).18

Rarely, miliary disease can persist radiographically unchanged for months .2, 60,

75 With therapy, the nodules usually resolve in 2 to 6 months; resolution is faster in children than in adults." Miliary calcification is rarely, if ever, encountered.$°Progressive Primary

The radiologic features of progressive primary TB are similar to those of postprimary

Figure 15. Miliary TB in a 26-year-old man. Posteroanterior chest radiograph (A) and coned-down view of the right lower lobe (B) demonstrate innumerable fine nodular opacities diffusely distributed throughout the lungs. There is no evidence of focal consolidation, cavitation, adenopathy, or pleural effusion. C, HRCT of the right lung reveals fine discrete nodules in a peribronchiolar and perivascular distribution.


Figure 16. Miliary TB in a 40-year-old man. A, Posteroanterior chest radiograph demonstrates fine reticular opacities in both lungs. B, Follow-up film 2 weeks later demonstrates asymmetric progression with discrete nodules seen on the left. C, HRCT (lung window) demonstrates peribronchiolar and perivascular nodules. There is thickening of interlobular septa and cylindric bronchiectasis on the left. D, Follow-up film 2 months later shows further progression and coalescent opacification of the left upper lobe.

TB and are thought to be due to the same mechanisms (see below).$° It manifests as progressive parenchymal consolidation often involving the secondary foci within the upper lobes .58 Cavitation occurs with greater fre-quency than in primary disease; endobron-chial spread and miliary dissemination may results$- 8° (Fig. 17).

POSTPRIMARY TUBERCULOSIS

Pathologic Manifestations

Postprimary TB occurs in patients pre-viously sensitized to M. tuberculosis.'9 There is controversy concerning the pathogenesis of this chronic form of TB. Although some cases may be due to reinfection of a previously sensitized host, most cases in the United States are thought to result from reactivation of dormant bacilli.19, 31 Nevertheless, the term

postprimary TB is preferred to reactivation TB because an antecedent primary infection can-not be definitively established in many cases. 25

Reactivation of dormant bacilli occurs dur-ing periods of immunosuppression, malnutri-tion, and debilitation or as a result of aging.2s, 62 It happens in 5% to 15% of all infected patients and is most likely in the first 2 years after exposure .25 Pulmonary reactiva-tion usually occurs in the secondary foci in the apical and posterior segments of the upper lobes and the superior segments of the lower lobes .28, 31 Persistence of viable bacilli at these sites is thought to be due either to the high oxygen tension or the decreased lym-phatic clearance of these lung segments.19, 20,28

The pathologic manifestations of postpri-mary TB are the same as those of primary TB after cellular immunity and delayed hyper-sensitivity has developed 31 (see Fig. 1); how-ever, whereas primary TB usually is a self-

12 McADAMS

Figure 17. Progressive primary TB in a 14-year-old girl. A, CT scan (lung window) through the apices shows cavitary consolidation of the right upper lobe. There are clustered poorly marginated nodules in the left upper lobe (arrowhead). These suggest endobronchial spread. B, HRCT (lung window) of the right lung better demonstrates the characteristic "tree-in-bud" appearance (arrows) of endobronchial spread.

limited disease, postprimary TB may progress until arrested by surgical intervention, antituberculous chemotherapy, or the death of the host." Histologically, both proliferative and exudative lesions are seen .19, .19,31,11

Caseous necrosis occurs rapidly because of preexisting tissue hypersensitivity." If bacterial proliferation proceeds unchecked, the ensuing hypersensitivity response can rapidly destroy the entire lung." 25

Cavitation is the hallmark of postprimary TB and occurs after enlarging tubercles have eroded into the airways .64 Open cavitation also requires liquefaction of the caseous material, a process directly related to the intensity of the hypersensitivity response."

Cavitation is the seminal event in the life cycle of M. tuberculosis because it results in bacillary proliferation outside the macro-phage's cytoplasm. This leads to an exponential increase in the bacterial population, endobronchial spread to previously unaffected areas of the lung, and expectoration of large numbers of bacilli.19

The cavity can rupture

into the pleural space, resulting in empyema and bronchopleural fistula. Tubercle erosion into a pulmonary artery leads to pseudoaneurysm formation (Rasmussen aneurysm) and potentially fatal hemoptysis.6' Erosion into smaller, systemic vessels or pulmonary veins results in symptomatic hematogenous dissemination zs (see Fig. 2). Lymphatic dissemination is rare in postprimary TB .64

Healing of postprimary TB typically occurs with fibrosis and calcification .64

Cavities usually heal with closure but are rarely completely obliterated by scar; encapsulated Gaseous material can persist for years .64 Open healing with progressive wall thinning and occasional squamous epithelization is rare.' Bronchial strictures, lobar or segmental collapse, and bronchiectasis can result from en-dobronchial disease .25 Tuberculomas also

Radiologic

Postprimary TB is almost exclusively a disease of adolescence and adulthood .z. 12

Although the radiographic findings of postprimary TB may overlap those of primary TB, distinguishing features include a predilection for the upper lobes, absence of lymphadenopathy, and a propensity for cavitation. Postprimary TB manifests radiographically as (1) parenchymal disease and cavitation, (2) airway disease, (3) pleural disease, and (4) other com-plications.

Parenchymal Disease

The earliest finding of postprimary TB is a heterogeneous, poorly marginated opacity

Figure 18. Active postprimary TB in a 51-year-old woman. Posteroanterior chest radiograph demonstrates bilateral ill-defined apical opacities typical of postprimary TB.


Figure 19. Active postprimary TB in a 60-year-old woman. A, Posteroanterior chest radiograph shows cavitary consolida -tion of the left lung with an air-fluid level (arrow) and volume loss. This is a typical "exudative" opacity of postprimary TB. Clumped linear and nodular ("fibroproductive" or "fibronodular") opacities are seen in the superior segment of the right lower lobe. The clustered poorly marginated nodules in the left base represent endobronchial spread of disease. 8, Follow-up radiograph after 6 months of antituberculous therapy reveals partial resolution of the parenchymal abnormalities. There is residual fibrosis within the left upper lobe, traction bronchiectasis, volume loss, and focal calcification.

("exudative" lesion) in the apical or posterior segment of an upper lobe or in the superior segment of a lower lobe 25, 25,60 (Fig. 18). Anterior or basal segment disease occurs in up to 75% of cases but only when the usual pulmonary segments are also diseased .95 Isolated anterior or basal segment disease are rare, seen in only 2%95 to 6%'9 of cases. In most cases (88%), more than one pulmonary segment is in-volved95; bilateral upper lobe disease is seen in 32%95 to 64%.15

If the infection is not adequately contained, progression to lobar (Fig. 19A) or complete lung opacification and destruction can be swiftz5, 6° (Fig. 20). In most cases, however, the initial heterogeneous opacities evolve into more well-defined medium-to-coarse reticular and nodular opacities (so-called "fibroproductive" or "fibroproliferative" lesions)25. 61 (Figs. 21 and 22). Mixed "exudative" and "fibroproductive" lesions are seen in 79% of cases; pure "exudative" or "fibroproductive" lesions are uncommon .95 With healing, these lesions may calcify and can be associated with lung architectural distortion, cicatricial atelectasis, and traction bronchiectasisz5 (Figs. 19B and 23). Severe fibrosis with upper lobe volume loss, hilar retraction, and secondary tracheomegaly is seen in up to 29% of cases 60, 95 (Fig. 24). In 41%, an apical opacity or "apical cap" results37, 95 (Fig. 24). These apical opacities have been shown by

tatic and fibrotic lung, and extrapleural fat deposition, which is indicative of the chronicity of the inflammatory process.37

Disease activity cannot be accurately as-sessed by chest radiography. Incorrect ap-praisal of disease activity is one of the most common causes of misdiagnosis in patients with TB .95 Although active infection is most often associated with "exudative" lesions or cavitation on chest radiographs,b° "fibropro

Figure 20. End-stage lung from postprimary TB. Pos-teroanterior chest radiograph demonstrates complete de-struction of the left lung with residual cavitation and bronchiectasis.

14 McADAMS et

Figure 21. Active postprimary TB in a middle-aged woman. Posteroanterior chest radiograph shows clumped nodular ("fibroproductive") opacities in both upper lobes, right greater than left. These are typical of active postprimary TB.

ductive" lesions also can indicate active dis-ease" (see Figs. 21-23). Patients can remain sputum culture positive for M. tuberculosis despite radiographic "healing" and calcifica-tion.'-' Radiographic stability for a period of at least 6 months and repeatedly negative sputum cultures is the best indicator of inactive disease.' 95 It also has been suggested that cases should be reported as being radiographically "stable" rather than "inactive" or "healed.""

Cavitation is seen by chest radiography in 40%30,15 to 87°%'5 (mean, 50%) of patients at sometime during the course of their disease (Figs. 19A, 25-27). Chest CT is more accurate in the detection of cavitation, particularly in cases complicated by extensive fibrosis and architectural distortion", ", 53 (see Figs. 12 and 17). The clinical relevance of this observation is unclear. Cavities are more frequently multi-ple (54°%3° to 76%95) than single and range in size from a few millimeters to several centi

Figure 22. Active postprimary TB in a 51-year-old woman. Chest CT (lung window) reveals coarse linear and nodular opacities in a peribronchiolar distribution.

Figure 23. Stable postprimary TB in a middle-aged man. Coned-down view of a posteroanterior chest radiograph shows multifocal calcifications in the right upper lobe and right hilum. Although this appearance suggests healing, disease activity cannot be definitively established by radi-ography as these lesions may harbor viable tubercle ba-cilli.

meters in diameter."' They typically occur within areas of consolidation (see Fig. 19A), although isolated cavities are sometimes seen" (Fig. 27). The walls of the cavities are initially thick and irregular',' (see Fig. 25). With healing, they can progressively thin (see Fig. 26) and balloon into large emphysematous spaces," although they usually resolve

Figure 24. Stable postprimary TB in a 44-year-old man. Posteroanterior chest radiograph shows severe upper lobe volume loss with bilateral hilar retraction. There are scattered parenchymal calcifications and "apical capping" on the right.


Figure 27. Active postprimary TB in a 50-year-old woman. Coned-down view of a posteroanterior chest radiograph demonstrates a well-defined cavity in the right upper lobe (arrows). The inner wall is smooth and there is minimal surrounding parenchymal opacity.

Figure 25. Active postprimary TB in a 67-year-old man. A, Coned-down view of a posteroanterior chest radiograph demonstrates a thick-walled cavity with an air-fluid level in the right upper lobe. Linear opacities extend from the inferior aspect of the cavity toward the right hilum. 8, Follow-up radiograph 5 months later demonstrates cavitation in the left upper lobe. Both cavities are thick-walled but have smooth inner margins.

with or without scarring. Persistent sterile cavitation is rare. Intracavitary air-fluid levels are thought to be an uncommon manifestation of tuberculosis, usually indicative of anaerobic abscess or superinfection30, 60; however, air-fluid levels in uncomplicated, active

Figure 26. Active postprimary TB in a middle-aged woman. Posteroanterior chest radiograph shows clumped linear and nodular opacities in the left upper lobe and a thin-walled cavity (arrowheads). Subtle nodules are seen in the right upper lobe. The poorly clustered marginated nodules in the left base are typical of endobronchial spread.

tuberculous cavities occurs in 9%30 to 22%'6- sl of cases (see Figs. 19A and 25A).

The most common complication of tuberculous cavitation is endobronchial spread, detected radiographically in 19%11

to 58%i5 of cases and by HRCT in up to 98%.35 HRCT is more sensitive than the chest radiograph in the detection of early endobronchial disease, 35, 58 although, again, the clinical relevance of this observation is not established. Endobronchial spread manifests as 5- to 10-mm, poorly defined nodules that cluster in dependent portions of the lungs (sometimes the contralateral lung )25, 35, 41 (see Fig. 26). Rapid coalescence into diffuse parenchymal consolidation (galloping consumption) can result2s (Fig. 28). HRCT demonstrates these nodules to be peribronchiolar and centrilobular in location. This pattern, termed the "tree

Figure 28. Active postprimary TB in a middle-aged woman. Coned-down view of a posteroanterior chest ra-diograph shows right lower lobe consolidation and an air bronchogram. This was due to progressive endobronchial spread.

endobronchial

16 McADAMS et al

in-bud" appearance ,35 is indicative of active tuberculosis35, s9 (see Fig. 17). Healing with parenchymal scarring, residual nodules, and parenchymal or endobronchial calcification is reported in 30%.25 Localized areas of hypoat-tenuation on CT also can result35 (Figs. 29 and 30). When not associated with parenchymal distortion, this finding is due to air-trapping from residual bronchiolar stenosis (Fig. 29); when architectural distortion is also seen, it usually reflects paracicatricial emphysema 3-1 (Fig. 30).

Spontaneous pneumothorax is uncommon, occurring in less than 5% of patients with severe cavitary disease .93 Mycetomas, which manifest as intracavitary masses (air-crescent sign), can also complicate the course of patients with open cavities .93 Pulmonary gangrene, a very rare and frequently (75%) fatal form of cavitary TB, also may manifest with the air-crescent sign. 40

Miliary TB is thought to occur less com-monly in postprimary than in primary or progressive primary TB .53 There is a type of (?post-primary) miliary disease known as late generalized TB (LGT), which presents in el-derly or otherwise debilitated patients, is of-ten cryptic in origin, and is insidious in on-set.'-1 In this form of miliary disease, dissemination can occur not only from a pul-monary source but also from reactivated sys-temic foci.75 LGT often is not diagnosed in life and has a high mortality rate .75 The initial chest radiograph may be nondiagnostic and the typical miliary pattern may not be evident until late in the course of the disease .75 Radiographic evidence of coexistent chronic pulmo

nary tuberculosis is seen in only 19% to 32%'S of cases.

Hilar and mediastinal lymphadenopathy is a rare manifestation of postprimary disease. 14, 15, 95 It is seen in only 5% to 6% of patients with active disease and usually is associated with extensive parenchymal disease and cavi-tation95 (see Fig. 12). Tuberculomas also may result from postprimary disease e° (see Figs. 7 and 8).

Airway TB

Bronchial stenosis occurs in 10% to 40% of patients with active TB.13, as It develops in several ways: by direct extension from tuber-culous adenitis, from endobronchial spread of infection, or by lymphatic dissemination to the airway. 13, 4s Radiologic manifestations of tuberculous bronchostenosis include persis-tent segmental or lobar collapse, lobar hyper-inflation, obstructive pneumonia, and mucoid impaction." CT is a useful adjunct to direct endoscopic visualization, particularly when performed at 5-mm intervals with 5-mm slice collimation through the hila.45 CT accurately depicts the bronchial abnormality in 93%13 to 100%45 of cases. CT findings include isolated long segment bronchial narrowing with con-centric wall thickening (41% to 43%) (Fig. 31), complete endobronchial obstruction (32%), and extrinsic obstruction by adjacent adenop-athy (23% to 50%).13, 4s Erosion of calcified hilar nodes into adjacent bronchi, known as broncholithiasis, also can result in segmental collapse or overinflation.13

Bronchiectasis is also a common complica

Figure 29. Stable postprimary TB in a 52-year-old woman. A, HRCT (lung window) shows a branching calcified endobronchial or peribronchial opac-ity (arrowheads) and segmental hy-perlucency (arrows) in the right lower lobe. There is also calcified subcarinal adenopathy. 8, HRCT (lung window) at a lower level shows another focal peribronchiolar opacity (arrow) and "mosaic" perfusion defects, which likely reflect distal bronchiolar stenosis. These findings are sugges-tive of prior endobronchial spread.


Figure 30. End-stage lung from postprimary TB. A, HRCT (lung window) of the right upper lobe shows numerous peribronchial stellate scars and paracicatricial emphysema. This finding is typical of healed endobronchial TB. 8, HRCT (lung window) shows destruction of the right lower lobe with volume loss and residual cavitation. Traction bronchiectasis and paracicatricial emphysema is seen.

tion of endobronchial tuberculosis .25 It most commonly develops as a paracicatricial pro-cess, secondary to pulmonary destruction and fibrosis (traction bronchiectasis) (Figs. 30 and 32). It also may result from central bronchostenosis and distal bronchial dilatation. It is typically asymptomatic and usually occurs in the upper lobes .25 When symptomatic, hemoptysis is the most common complaint.

Tracheal and laryngeal tuberculosis are less common than endobronchial tuberculosis" (Fig. 33). Laryngeal tuberculosis, the most infectious form of the disease, results either from pooling of infected secretions in the posterior larynx or hematogenous dissemination to the anterior larynx .48, 85 Most patients with laryngeal disease also have active pulmonary

Figure 31. Tuberculous bronchostenosis in a 39-year-old woman. Chest CT (lung window) reveals collapse of the left upper lobe. There is a long-segment stricture of the distal left main stem bronchus (arrows) and a focal proximal stricture (open arrow).

disease, although it can be mild and go unrecognized.", 115 A laryngeal mass is uncommonly the presenting manifestation of postprimary TB .85

Pleural Disease

Pleural effusions most often are a manifestation of primary TB 53 but occur in 6%15 to 18%95 of patients with postprimary disease. Unlike those seen in primary disease, these effusions usually are sma1195

and are associated with parenchymal disease .22 Frank tuberculous empyema is less common (1%93 to 4%95). It typically manifests as a loculated pleural fluid collection in association with extensive parenchymal disease and cavitation.93

Figure 32. Active postprimary TB in a 65-year-old woman with hemoptysis. HRCT (lung window) of the left lung reveals heterogeneous opacities in the left upper lobe, pleural thickening, and cylindric bronchiectasis.

18 McADAMS et al

Figure 33. Laryngeal TB in a 49-year-old man. A and B, Contrast-enhanced CT scans of the neck show asymmetric thickening of the epiglottis with a focal hypoat-tenuating region of the right (ar-rowhead). The aryepiglottic folds and the glossoepiglottic fold are thickened (arrows). (From Swallow CE, McAdams HP, Colon E: Tuberculosis manifested by laryn-geal mass on CT scans. AJR Am J Roentgenol 163:179-180, 1994; with permission.)

Air-fluid levels indicate bronchopleural fistula '2 (Fig. 34). Spontaneous pleurocutaneous fistula (empyema necessitatis), chest wall mass, and rib and vertebra destruction can result from untreated empyema.27, 61, 93 Rib and costal cartilage involvement is unusual except in drug addicts24 (Fig. 35). Residual pleural thickening and calcification, either plaquelike or peripheral, also occurs33

(see Fig. 34).

Other Complications

Hemoptysis occurs in up to one third of patients with postprimary TB.86, 93 Significant pulmonary bleeding occurs in 8% and is fatal in 1% to 5% .57 Bleeding is most commonly from hypertrophied bronchial arteries due to bronchiectasis (see Fig. 32), ongoing chronic inflammation, or intracavitary mycetomas.57, 93 It less commonly occurs in patients with active cavitary disease and associated granulo-matous vasculitis.93 Surgery or transcatheter embolization may be required to treat cases of massive bleeding. 57

Pseudoaneurysms of small- to medium-sized pulmonary arteries (Rasmussen s aneu-rysms), although rarely encountered clini-cally, are reported in up to 4% to 5% of autopsies of patients with chronic tuberculosis .5° They present with catastrophic hemorrhage and are associated with a high mortality (84%) .25 They occur almost exclusively in chronic fibrocaseous TB, are usually single, and are typically located in the upper lobes.50, 69 Chest radiographs may reveal an enlarging mass or a rapidly appearing parenchymal consolidation due to pulmonary hemorrhage.69Emergent embolization can be lifesaving.50, 67,69

Other unusual intrathoracic complications of postprimary TB include vertebral osteomy-elitis, paraspinal, and prevertebral abscess 4z, 91 The chest radiograph is abnormal in up to 75% of patients with spinal tuberculosis.42

Most have evidence of pulmonary disease and half have evidence of spinal disease on plain radiographs .42 Late calcification of indolent paraspinal abscesses can be seen .42

Lung Cancer

The relationship between TB and lung can-cer is controversial. The frequency of coexis-tent lung cancer and tuberculosis is as high as 5% .87 Patients with prior TB may have a lifetime risk of lung cancer that is 5 to 10 times greater than that of the general popula-tion.84 This phenomenon is often attributed to the putative oncogenic effects of chronic inflammation and fibrosis (so-called scar car-cinoma).25 Also, lung cancer can cause reacti-vation of TB either by eroding previously en-capsulated foci or by suppressing the cellular immune system .76 Thus, sputum acid-fast bacilli should not delay investigation of a sus-pected lung cancer .25, 76

More recent analyses of the available data suggest that the relationship between lung cancer and TB may be purely coincidenta125; however, when lung cancer does coexist with TB, the diagnosis is typically delayed .72, 87 The radiographic manifestations of cancer often are misinterpreted as progression of tuberculosis.'6, 87 Certain radiologic findings suggest a coexistent pulmonary malignancy in patients with postprimary disease: (1) progressive disease despite appropriate antituberculous chemotherapy, (2) hilar or mediastinal adenopathy, (3) a focal mass greater than 3 cm in


Figure 34. Tuberculous empyema in a 75-year-old woman. A, Posteroanterior chest radiograph shows a calcified fibrothorax on the right, typical of old tuberculous empyema or prior plombage. 8, Follow-up radiograph 2 years later demonstrates an air-fluid level within the right hemithorax indicative of bronchopleural fistula. This was due to reactivation tuberculosis in this patient. C, Chest CT (mediastinal window) shows that the calcification is confined to the wall of the fibrothorax.

Figure 35. Tuberculous osteomyelitis in a middle-aged woman. Chest CT (mediastinal window) shows destruction of the first costochondral junction by tuberculous osteomy-elitis. There is a soft-tissue mass with subpectoral and mediastinal extension.

20 McADAMS et

Figure 36. Tuberculosis and lung cancer in a 71-yearold man. Coned-down view of a posteroanterior chest radiograph demonstrates volume loss within the left upper lobe. The coarse linear opacities in both lung apices are typical of postprimary TB. The right hilar mass is an atypical finding and in this patient represented lung can-cer.

diameter, and (4) cavities with nodular walls11' (Fig. 36).

Unusual FeaturesIn the 1970s and early 1980s there were a number of reports concerning so-called un-usual radiographic manifestations of adult TB .8,30,49 Up to one third of adult cases were reported to have atypical findings such as mediastinal adenopathy, lower lung consolidation, and miliary disease 4, s. 39, 49, 5z; however, as was pointed out by Woodring et a1,95 Choyke et al, '4 and Hadlock and colleagues,30 these "unusual" manifestations in most instances are but "usual" manifestations of primary TB. The only unusual aspect is the increasing incidence of primary TB in adults. 14

Hadlock et a130 suggest that only the following constitute "unusual" manifestations of primary TB in adults: (1) adenopathy without parenchymal consolidation, (2) lower lobe disease without adenopathy, (3) solitary tuberculoma, or (4) primary disease in patients older than 40. Postprimary TB should be considered atypical only if (1) it is confined to the basal segments of the lower lobes or the anterior segment of the upper lobes or (2) if it manifests as bronchopleural fistula without other radiographic abnormalities .30 Using these criteria, the frequency of unusual manifestations is only 8% .30

The Postoperative Chest

Various forms of pulmonary collapse therapy were used in the treatment of cavitary

TB prior to the development of effective che-motherapy.34, 54, 93 These included plombage, phrenic nerve injury, artificial pneumothorax, and thoracoplasty.'3 Plombage was performed by the insertion of plastic (polystan) packs, methyl methacrylate (lucite) balls, or drilled polythene spheres into the extrapleural space.'-, 93 It was also accomplished by the extrapleural injection of oil or paraffin (oleothorax).93 Complications of this form of therapy include plomb migration, infection, plomb expectoration, and malignant degeneration.73 Plomb migration can result in superior vena caval obstruction, plomb extrusion, and erosion into the brachial plexus or the aorta .5,1,'4, 94 Bronchopleural, bronchoesophageal, and pleurocutaneous fistula formation are also complications of long-standing plombage therapy.34, 70 Surgical removal of the plomb with decortication or thoracoplasty may be required in these cases .55

The radiographic appearance of plombage depends upon the material (plomb) used. Because the lucite balls are hollow, this form manifests as multiple well-defined spherical lucencies" (Fig. 37). With time and infection, these balls may lose their original shape and develop air-fluid levels .73 Although this ap-pearance can be confused with pulmonary cavitation, the uniform size of the "cavities" and cavity walls suggests the correct diagno-sis" (Fig. 38). Polystan packs, drilled spheres, and oleothorax manifest as well marginated extraparenchymal masses in the upper hemithorax34, 54, 73 (Fig. 39). These opacities, al

Figure 37. Collapse therapy in a middle-aged patient with postprimary TB. Posteroanterior chest radiograph reveals the typical changes of left-sided thoracoplasty and rightsided lucite ball plombage.


or sterile exudation around the plomb.31, 'o Giant cysts around the plomb may occur.74

Thoracoplasty was a more radical form of therapy accomplished by staged chest wall resection and pulmonary collapse.44 Radio-logic (plain film and CT) evaluation of prior thoracoplasty may reveal diffuse pleural thickening (100%), focal pleural thickening (19%, often calcified), bronchiectasis (14%), bullae in the operated lung (33%), and skele-tal deformity (97%)54 (see Fig. 37). CT also may demonstrate residual, encapsulated pleural fluid collections; 3, 54 which are associ-ated with active TB or viable intrapleural tu-bercle bacilli .13, 54 Late onset respiratory insufficiency related to the degree of thoracic deformity, fibrothorax, and severity of underlying parenchymal abnormality has been reported.93

SUMMARYFigure 38. Plombage therapy in a 42-year-old woman. Posteroanterior chest radiograph shows evidence of right sided plombage. There is thinning and disorganization of the overlying ribs, characteristic of long-term plombage. Air-fluid levels in the lucite balls and ball rim calcification (arrow) also are seen. Air-fluid levels in the plomb suggest bronchopleural fistula and infection, either bacterial or tuberculous in origin.

though typically stable in size, can expand and cause significant respiratory symp-toms.'°,'3 Expansion is due to secondary bac-terial infection (empyema), reactivation TB,

Figure 39. Oleothorax in a 71-year-old man with prior TB. Posteroanterior chest radiograph shows near complete opacification of the right hemithorax by a rim-calcified mass. This appearance is typical of plombage therapy accomplished either with polystan packs or oleothorax.

In summary, the following points are re-emphasized:

1. The chest film is the mainstay in the radiologic evaluation of suspected or proven pulmonary TB. CT is occasion-ally useful for clarifying confusing findings but has not been conclusively shown to have a significant impact on patient management.

2. Primary TB is increasingly a disease of adults.

3. Primary TB usually manifests as a pa-renchymal consolidation in any pulmo-nary lobe or segment. Distinguishing features from typical bacterial pneumonia include associated adenopathy, lack of systemic toxicity, failure to respond to conventional antibacterial therapy, and recent PPD conversion.

4. Associated ipsilateral hilar and/or me-diastinal adenopathy is almost univer-sal in children with primary TB but is less common in adults. Adenopathy without parenchymal disease is an un-usual but well-reported manifestation.

5. Many of the so-called unusual manifes-tations of adult TB are the usual mani-festations of primary disease. The

terms adult and childhood TB should be discarded.

6. Postprimary TB typically manifests as a heterogeneous, often cavitary opacity in the apical and posterior segments of the upper lobes and the superior seg-

22 McADAMS et al

ments of the lower lobes. Lymphade-nopathy is rare.

7. Activity of postprimary disease cannot be accurately assessed by chest radiography. Radiographic stability for 6 months and negative sputum cultures is the best indicator of inactive disease. The descriptive terms inactive or old TB should be discarded in favor of radiographically stable TB, as viable bacilli may persist despite adequate therapy.

8. Cavitation is the most important radio-logic finding in postprimary disease. Cavitation implies a high bacillary bur-den, high infectivity, and is associated with numerous complications including endobronchial spread, tuberculous empyema, hematogenous dissemina-tion, pulmonary artery pseudoaneu-rysm, and so forth.

9. Tuberculous pleurisy is more common in primary than postprimary disease. It is a common presenting manifestation in young adults. The effusions are uni-lateral, large, and self-limited. The pleural fluid usually is a serous exudate with a marked lymphocytosis. Fluid cultures are frequently negative. Cor-rect diagnosis and therapy is important, as untreated patients are at high risk for subsequent pulmonary reactivation. 10. Miliary disease is also more common in primary than postprimary disease; however, its frequency in elderly patients with postprimary TB is increasing. This form, known as late generalized TB, is apt to be misdiagnosed or not diagnosed in life and has a high mortality.

ACKNOWLEDGMENTS

The authors wish to thank Drs. Philip Goodman, Edward Patz, and George Bisset, all of the Department of Radiology, Duke University Medical Center, for their generous contributions of case material for this article.

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