497

Update: The Radiographic Features

of Pulmonary Tuberculosis

John H. Woodring1H. Mac Vandiviere2

Andrew M. Fried1Marcus L. Dillon3

Terry D. Williams1Irene G. Melvin2

Received April 1 5, 1 985; accepted after revisionNovember 4, 1985.

1 Department of Diagnostic Radiology, Albert B.Chandler Medical Center, University of KentuckyCollege of Medicine, 800 Rose St., Lexington, KY40536-0084. Address reprint requests to J. H.Woodnng.

2Dep�ment of Pediatrics, Albert B. Chandler

Medical Center, University of Kentucky College ofMedicine, Lexington, KY 40536-0084.

3Department of Cardiovascular and ThoracicSurgery, Albert B. Chandler Medical Center, Uni-versity of Kentucky College of Medicine, Lexington,KY 40536-0084.

AJR 146:497-506, March 19860361 -803X/86/1 463-0497C American Roentgen Ray Society

Pulmonary tuberculosis produces a broad spectrum of radiographic abnormalities.During the primary phase of the disease these include pulmonary consolidation (50%),which often involves the middle or lower lobes or the anterior segment of an upper lobe;cavitation (29%) or pneumatocele formation(12%); segmental orlobar atelectasis(18%);pleural effusion (24%); hilar and mediastinal lymphadenopathy (35%); disseminatedmiliary disease (6%); and a normal chest radiograph (15%). During the postprimaryphase of the disease, common abnormalities include exudative and/or fibroproductiveparenchymal densities (100%), predominantly in the apical and posterior segments ofthe upper lobes (91%); cavitation (45%) with bronchogenic spread of disease (21%);marked fibrotic response in the lungs (29%); and pleural effusion, empyema, and fibrosis(18%, 4%, and 41%, respectively). Upper-lobe masslike lesions are seen occasionally(7%); spontaneous pneumothorax and intrathoracic lymphadenopathy are rare (5%each). Common causes of a missed diagnosis of tuberculosis are (1) failure to recognizehilar and mediastinal lymphadenopathy as a manifestation of primary disease in adults,(2) exclusion of tuberculosis because disease predominates in or is limited to theanterior segment of an upper lobe or the basilar segment of a lower lobe, (3) overlookingof minimal fibroproductive lesions or reporting them as inactive, (4) failure to recognizethat an upper-lobe mass surrounded by satellite fibroproductive lesions might betuberculous, and (5) failure to consider healed sequelae of primary disease or a positivepurified protein derivative skin test as contributory to identifying the patient’s pulmonarydisease.

During the last decade, various authors have enumerated the “unusual” manifes-tations of pulmonary tuberculosis in the adult population [1-6]. These unusualmanifestations usually have been implicated in the frequent failure of both radiolo-gist and clinician to recognize that tuberculosis could be the cause of an abnormalchest radiograph in patients who are subsequently, and rather surprisingly, provento have tuberculosis. As Choyke et al. [7] indicate, these so-called unusualmanifestations of tuberculosis in adults are actually typical of the disease: What isunusual is that they often represent primary disease occurring in the adult popula-tion.

Although physicians are more familiar with the radiographic manifestations ofpostprimary tuberculosis than with those of primary disease, problems in radi-ographic diagnosis do occur. Minimal exudative or fibroproductive tuberculosismay be overlooked or, commonly, fibroproductive lesions may be assumed to beinactive even though the patient subsequently proves to be sputum-positive forMycobacterium tuberculosis [1 , 5, 8]. Miller and MacGregor [1 ] reported severalcases of advanced postprimary tuberculosis with extensive upper-lobe cavitationin which tuberculosis was not even considered as a diagnostic possibility!

Because of the apparent widespread difficulty in recognizing the radiographicmanifestations of pulmonary tuberculosis, we thought it would be beneficial toreview the spectrum of radiographic abnormalities attributable to M. tuberculosisin a university medical center. We emphasize the radiographic features of primary

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498 WOODRING ET AL.

AGE IN YEARS

Fig. 2.-Primary lymphohematogenous dissemination with miliary pattern in43-year-old man.

AJR:146, March 1986

o PRIMARY TB

� POST- PRIMARY TB

Fig. 1.-Prevalence of primary and postprimary tuberculosis by age in 90patients.

and postprimary disease, similarities and differences betweenthe two, and the recognition of certain patterns that shouldlead to suspicion of pulmonary tuberculosis. The pathogen-esis of pulmonary tuberculosis is also discussed.

Materials and Methods

The chest radiographs and medical records of patients diagnosed

as having clinically active M. tuberculosis were reviewed. Between1974 and 1984, 107 patients with active pulmonary tuberculosis weredocumented at the University of Kentucky Medical Center. Of these,17 patients had insufficient information in their medical records todetermine whether they had primary or postprimary disease with M.tuberculosis. These 17 patients were excluded from the study. TheCenters for Disease Control and American Thoracic Society criteriafor confirmation of tuberculosis were met in the 90 remaining cases,that is, (1) either bacteriologic confirmation of current disease or both

TABLE 1 : Location of Pulmonary Consolidation in 73 Patientswith Pulmonary Tuberculosis

Site of consoldabon

Type of Pul monary Tuberculosis

Primary

(n=17)

Postpnmary(n=56)

Right upper lobe:Anterior 4 18ApicalPosterior

01

4131

Right middle lobeRight lower lobe:

SuperiorBasal

2

13

10

1316

Left upper lobe:Anterior 2 16ApicalPosterior

12

3330

LingulaLeft lower lobe:

2 14

SuperiorBasal

Totals

24

1410

24 246

a significant skin reaction to the purified protein derivative (PPD) andclinical and/or radiographic evidence of current disease, and (2)radiographic improvement after administration of two or more anti-tuberculous drugs [9, 10].

Primary tuberculosis was documented in 34 (38%) of the 90patients on the basis ofthe following criteria: (1) recently documentedconversion of the PPD skin test coupled with a positive culture of M.tuberculosis from tissue or body fluids (24 patients); (2) recentlydocumented conversion of the PPD skin test coupled with clinicaland radiographic evidence of current disease although subsequentcultures for M. tuberculosis were negative (seven patients, all chil-dren); and (3) positive culture for M. tuberculosis with no prior historyof tuberculosis, a previously negative PPD skin test, and a previouslynormal chest radiograph (three patients). At the time of illness thesepatients were anergic and the PPD skin test was nonreactive. Of the34 patients with primary tuberculosis, 1 9 were female and 1 5 weremale; the patients were between 6 months and 87 years of age(average, 24 years) (fig. 1). Of these 34 patients, 19 (56%) were 18years of age or older. These 19 adults with primary tuberculosiscomprised 25% of the 75 adults with active pulmonary tuberculosisin our total study population of 90 individuals. As shown in figure 1,four of the patients with primary tuberculosis were over 71 years ofage. There was no evidence that these four patients had ever hadtuberculosis or a positive PPD skin test previously to suggest thatthe booster effect was the cause of the recent PPD conversion. Oneof these four elderly patients was quite debilitated with chroniclymphocytic leukemia. Two of the other adults with primary tubercu-losis had diabetes mellitus (one case each ofjuvenile-onset and adult-onset diabetes).

Postprimary tuberculosis was documented in 56 (62%) of the 90patients on the basis of the following criteria: (1) positive culture forM. tuberculosis obtained on one or more admissions to the hospital(all 56 patients), either from the sputum (53 cases), from materialobtained from fiberoptic bronchoscopy (two), orfrom gastric aspirates(one); and (2) evidence of previous primary infection with tuberculosis(all 56 patients) based on a documented positive PPD skin test beforethe episode of current disease (39 patients), radiographic evidenceof the previous primary infection (35), and/or a previously positiveculture for M. tuberculosis without antituberculous treatment before

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AJR:146, March 1986 PULMONARY TUBERCULOSIS 499

Fig. 3.-Primary tuberculosis in 26-year-old man. A, Consolidation of theanterior segment of left-upper-lobe cavitation, left paratracheal lymphadenop-athy (arrow), and enlarged cardiac silhouette from pericardial effusion. Recentlydocumented conversion of PPD skin test was believed to be noncontributory,and patient was treated with erythromycin for presumed Mycoplasma pneu-monia. B and C, 1 month later: spontaneous clearing of pericardial effusion.Cavitary disease in anterior segment of left upper lobe and left paratracheallymphadenopathy (B, arrow) are more clearly seen. Sputum cultures obtainedat this time grew Mycobacterium tuberculosis.

the time of diagnosis (1 1). Of the 56 patients with postprimarytuberculosis, 36 were men and 20 were women; the patients werebetween 20 and 87 years of age (average, 51) (fig. 1). Five of these56 patients had associated conditions that may have contributed tothe development of postprimary tuberculosis, including chronic renalfailure (two cases) and acute lymphocytic leukemia, chronic alcohol-ism, and pregnancy (one case each).

The patients in our study were from central and eastern Kentucky.Although these patients are similar in many respects to those seenat other major medical centers, the majority came from small ruralcommunities (less than 10,000 population) rather than urban inner-city areas. In fact, Kentucky is unique in that the case rate oftuberculosis is significantly greater in the nonurban population.

The chest radiographs of the 90 patients were reviewed andevaluated for abnormalities of the lung parenchyma, airways, intra-thoracic lymph nodes, and pleura. Finally, the initial radiographic

report and clinical diagnosis in each patient’s medical record wasreviewed with attention directed to the degree of initial suspicion oftuberculous disease. The initial radiographic interpretations wereprepared in conjunction by a radiology resident and board-certifieddiagnostic radiologist in all cases. Specific historical information con-cerning the status of the PPD skin test or a high degree of clinicalsuspicion of active tuberculosis was provided to the initial interpretersin less than one-half of cases. Potential causes of a nondiagnosis oftuberculosis were evaluated.

Results

Primary Tuberculosis

A normal chest radiograph coupled with a positive culturefor M. tuberculosis was found in five (15%) of the 34 patients

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________� #{149}1

500 WOODRING ET AL. AJR:146, March 1986

Fig. 5.-Primary tuberculosis in 3-year-old boy. Right hilar lymphadenopathyand thin-walled pneumatocele (arrows) in right lower lobe.

Fig. 6.-Primary tuberculosis in 4-year-old girl. Right lower-lobe collapse(black arrow) and shift of upper mediastinum to right (white arrow).

with primary tuberculosis, who were clinically thought to have

endobronchial disease. Two patients presented with a diffusemiliary pattern (fig. 2). The remaining 27 patients had pulmo-nary parenchymal consolidation, atelectasis, intrathoracic

Fig. 4.-Primary tuberculosis in 24-year-old female diabetic with recentconversion of PPD skin test. Multiple cavities with air-fluid levels (arrowheads)in superior segment of right lower lobe.

lymphadenopathy, pleural effusion, and pericardial effusion aseither isolated or combined findings.

Pulmonary consolidation occurred in 1 7 patients (50%). In13 patients a single area of pulmonary consolidation wasencountered; in four patients multiple areas of parenchymalconsolidation were present. Overall, 24 areas of consolidationwere encountered in these 1 7 patients (table 1). The right andleft lungs were equally affected; the mid and lower parts ofthe lungs were involved slightly more often than the upperlung zones; however, when the upper lobes were involved,anterior segment involvement was more common than in-volvement of the apical or posterior segments (table 1 , fig. 3).

Cavitation had developed in five (29%) of the 1 7 patientswith pulmonary consolidation (figs. 3 and 4); in one case air-fluid levels were noted. In two patients pneumatoceles werepresent (fig. 5). In seven of these patients pulmonary consol-idation was an isolated finding; however, in 1 0 patients con-solidation was associated with other findings including lymph-adenopathy, pleural effusion, pericardial effusion, and lobaratelectasis.

Segmental or lobar atelectasis occurred in six patients(1 8%) (fig. 6). The anterior segment of the right upper lobewas involved in one case, the right middle lobe in two cases,and the right lower lobe in three cases.

Pleural effusion was present in eight (24%) of the 34patients (fig. 7). Effusion was unilateral in seven cases andbilateral in one. The size of the effusion was judged to besmall in two cases, medium in one, and large in six accordingto the criteria of Roper and Waring [1 1 ]. Three patientspresented with isolated pleural effusions; however, in fivepatients effusion was associated with parenchymal consoli-dation and/or lymphadenopathy. Pericardial effusion wasseen in only one case (fig. 3). Echocardiography was not

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Fig. 7.-Primary tuberculosis in 8-year-old girt. Large pleural effusion on Fig. 8.-Primary tuberculosis in 13-year-old boy. Bilateral hilar, right para-right. tracheal, and aortic-pulmonic window lymphadenopathy (arrows) resembles

sarcoidosis, lymphoma, or metastatic disease.

AJR:146, March 1986 PULMONARY TUBERCULOSIS 501

performed routinely and therefore was not evaluated in thisretrospective study.

Hilar and/or mediastinal lymphadenopathy was present in1 2 (35%) of the 34 patients (figs. 3, 5, and 8). Lymphadenop-athy was present in six of the 1 5 children and six of the 19adults. Lymphadenopathy was limited to the hilum in sixcases, involved both hilar and mediastinal nodes in three, andwas limited to the mediastinum in three. In two patientslymphadenopathy was an isolated finding; however, in 10instances lymphadenopathy was associated with pleural ef-fusion, consolidation, and/or atelectasis.

The radiographic diagnosis was initially correct in only 11(34%) of these patients with primary tuberculosis. Radi-ographic patterns most often diagnosed as tuberculosis in-

cluded a miliary pattern, parenchymal consolidation accom-panied by lymphadenopathy in a child, and cavitation. Pat-terns least likely to elicit a diagnosis of tuberculosis includeda normal chest radiograph, hilar and mediastinal lymphade-nopathy in an adult, and isolated findings of parenchymalconsolidation, atelectasis, or pleural effusion.

The clinical diagnosis was initially correct in 29 cases (85%)on the basis of the history and physical examination, chestradiograph report, and knowledge of a recent conversion ofthe PPD skin test. However, in five patients, all adults, tuber-culosis was initially excluded as a possible diagnosis becausethe chest radiograph was felt to be incompatible with thediagnosis of tuberculosis in an adult. Four of these patientsdemonstrated hilar and/or mediastinal lymphadenopathy andthe fifth had consolidation of the anterior segment of the rightupper lobe.

Postprimary Tuberculosis

Pulmonary parenchymal disease was present in all 56patients with postprimary tuberculosis. In seven patients asingle segment of lung was involved; in 49, two or more areasof the lungs were involved. Overall, 246 areas of pulmonarydisease were present in these 56 patients (table 1). The apicaland posterior segments of the upper lobes were the mostcommonly involved parts of the lungs (figs. 9 and 10).

Involvement of unusual parts of the lung was common inpostprimary tuberculosis (fig. 1 1). Twenty-four patients haddisease involving the anterior segment of an upper lobe; 18patients had involvement of the basilar segments of the lowerlobes. However, in the vast majority of these cases, diseasewas present in more typical parts of the lung as well, forexample, the apical and posterior parts of the upper lobes orsuperior segment of a lower lobe. In only one case each waspostprimary tuberculosis isolated to the anterior segment ofan upper lobe or basilar segment of a lower lobe.

The pulmonary parenchymal disease was characterized asbeing exudative, fibroproductive (fibronodular and/or fibrocal-cific), and nodular. The most common finding (79%) was thatof a mixture of exudative and fibroproductive lesions. In 18%the pulmonary disease was purely fibroproductive in nature,and in 3% the disease was purely exudative in nature. In 11patients virtually all parts of both lungs were involved, andthe disease was considered to be extensive. Lobar enlarge-ment was noted in one case. Large nodules or masslikedensities were seen in four patients. These always occurredin the upper lobes and were always accompanied by other

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502 WOODRING ET AL. AJR:146, March 1986

9

Fig. 9.-Postprimary tuberculosis. Fibroproductive (fibronodular) densi-ties in apical segment of left upper lobe (arrows), initially interpreted as old,inactive scarring. Sputum culture obtained 1 year later grew Mycobacteriumtuberculosis.

Fig. 1 0.-Postprimary tuberculosis in apical and posterior segments ofboth upper lobes in 36-year-old man. Blunting of right costophrenic angle(curved arrow) and calcified Ghon lesion in lingula (straight arrow) wereresidual findings from primary infection.

/ � p

I r I

Fig. 1 1 .-Postprimary tuberculosis in 77-year-old man. Homogeneous con-solidation of right middle and lower lobes and mottled consolidation of left lowerlobe. Subtle fibroproductive lesions in apical segment of right upper lobe(straight arrow) and calcified Ghon lesion in left lower lobe (curved arrow).Bilateral apical pleural thickening.

Fig. 1 2.-Postprimary tuberculosis in 87-year-old woman. A 2-cm nonneo-plastic masslike density is seen associated with marked fibrosis of right upperlobe with upward retraction of right hilum and displacement of trachea to right.There is marked right apical pleural thickening. Fibroproductive lesions arepresent in basilar segments of right lower lobe and apical segment of left upperlobe. Calcified Ghon lesion in left lower lobe (arrowhead).

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Fig. 13.-Postprimary tuberculosis in 20-year-old man. A 5-cm thick-walledcavity in posterior segment of right upper lobe contains air-fluid level (blackarrow). Bronchogenic spread with acute tuberculous pneumonia involvingbasilar segments of right lower lobe, left upper lobe and lingula, and basilarsegments of left lower lobe. White arrow indicates calcified aortic-pulmonicwindow node from previous primary infection.

Fig. 1 4.-Postprimary tuberculosis. Extensive fibroproductive and exudativedensities with cavitation in apical and posterior segments of right upper lobe.Right hilar and paratracheal lymphadenopathy (straight arrows). Curved arrowindicates calcified Ghon lesion in right lower lobe.

AJR:146, March 1986 PULMONARY TUBERCULOSIS 503

areas of fibroproductive or exudative densities (satellite le-sions) (fig. 12).

Cavitation was common, being present in 25 (45%) of the56 patients (fig. 1 3). In six cases a single cavity was present;in 1 9 cases there were multiple cavities. The cavity wallsranged from very thin and smooth to very thick and nodular.Air-fluid levels were present in five cases. Pneumatoceleswere encountered in only one case. Bronchogenic spread oftuberculous material from upper-lobe cavities to other partsof the ipsilateral and/or contralateral lung was presumed tohave occurred in 1 2 of the 56 patients (fig. 13) and oftenresulted in extensive abnormalities on the chest radiograph.

A marked fibrotic response was evoked in the lungs of 16patients (29%) (fig. 1 2). This was manifested by lobar atelec-tasis in nine patients, upward hilar retraction in 1 0, downwardhilar retraction in one, tracheal deviation in seven, and ac-quired tracheomegaly in four.

Pleural effusion occurred in 1 0 (1 8%) of the 56 patientswith postprimary tuberculosis. Effusion was unilateral in eightcases and bilateral in two. The size of effusion was small inseven cases and medium in three. In two cases air-fluid levelswere present in the pleural space, indicating bronchopleuralfistula with empyema formation. Apical pleural thickening waspresent in 23 cases (41 %) (figs. 1 1 , 1 2, and 14); it wasunilateral in 14 cases and bilateral in nine. The extent of apicalpleural thickening was usually 1 cm or less; in only threecases was the apical pleura over 1 cm in thickness. Sponta-neous pneumothorax was noted in three of 56 patients and

was usually associated with extensive disease with multiplecavities.

Hilar and/or mediastinal lymphadenopathy was present inthree patients (5%) with postprimary tuberculosis (fig. 14).Lymph node groups involved included the right hilar, rightparatracheal, and subcarinal nodes. The presence of intra-thoracic lymphadenopathy in these three cases accompaniedrather extensive parenchymal disease with multiple areas ofcavitation. By comparison with the lung disease, lymphade-nopathy was not a prominent feature of postprimary tuber-culosis in these three cases.

Residual evidence of the original primary infection wasapparent in 35 cases (63%). This included calcified or non-calcified Ghon lesions in 24 patients, calcified hilar and/ormediastinal lymph nodes in nine, and blunting of the lateralcostophrenic angle in nine (figs. 10-14).

The radiographic diagnosis was initially correct in 33 (59%)of these 56 patients. In 1 2 patients the radiograph wasinterpreted as abnormal but tuberculosis was not consideredas a diagnosis, and in 1 1 patients the chest radiograph wasinterpreted as being normal (six cases) or as showing inactivelung scars (five cases). Common pitfalls in radiographic inter-pretation included the following: Fibroproductive lesions wereeither overlooked entirely or interpreted as being inactive;involvement of the anterior segments of the upper lobes orbasal parts of the lower lobes was used as evidence againstthe diagnosis of tuberculosis; and large nodular or masslikedensities were interpreted as being neoplastic. The clinical

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504 WOODRING ET AL. AJR:146, March 1986

diagnosis was initially correct in only 31 cases (55%). In 12patients the pulmonary symptoms were mild and nonspecific,and tuberculosis was not thought to be the cause; in addition,in several cases the chest radiographic abnormalities and

positive PPD skin test were considered to be noncontributoryto the present illness. In 13 patients the pulmonary symptomswere so slight that pulmonary disease was not clinicallysuspected. In all, there were 17 patients (30%) in whichneither the radiologist nor clinician initially suspected tuber-culosis, resulting in a delay of 1 -3 years in the diagnosis.

Discussion

Primary tuberculosis is an airborne infection. The site ofprimary tuberculosis in the lungs reflects areas of greatestventilation; the most common sites are the middle or lowerlung zones or the anterior segment of an upper lobe [1 2]. Theregional multiplication of organisms is followed by hilar and/or mediastinal lymphadenopathy and the lymphohematoge-nous dissemination of organisms diffusely to the lungs and tonumerous extrapulmonary sites [1 2]. During this time, mostpatients are either asymptomatic or develop mild to moderatesystemic symptoms [1 2]. Tuberculin conversion occurs in 4-8 weeks, at which time the patient will demonstrate a positivePPD skin test [12]. This corresponds to an activation ofmacrophage responsiveness, when activated macrophagesbecome capable of containing the primary infection [1 2]. In2%-6% of cases, the lymphohematogenous dissemination ofmassive numbers of viable organisms results in clinical andradiographic evidence of miliary tuberculosis [7, 1 2, 1 3]. Thisevent is life-threatening and is characterized clinically by fever,weight loss, prostration, and, if untreated, death from respi-ratory failure and disseminated intravascular coagulation[12]. In about 10% of primary infections, acquired immunityis inadequate to contain the primary infection, and regionalmultiplication is followed by chronic, progressive parenchymaldisease [1 2]. This phenomenon is distinguishable from post-primary disease only by documentation of a recent conversionof the PPD skin test [1 4]. In the remainder of cases theprimary infection is contained but remains a significant riskfor postprimary tuberculosis unless preventive treatment isgiven [1 5, 1 6]; memory lymphocytes become immunologicallycommitted, and patients with primary infection generally retainboth tuberculin reactivity and immunity from primary reinfec-tion for life [12].

Primary tuberculosis was once thought to be strictly adisease of childhood. During this century there has been amarked decrease in the incidence of tuberculosis in the UnitedStates as a result of careful public health measures and theadvent of antituberculous chemotherapy. Because of this,only a small percentage of American adults have a positivePPD skin test, indicating that most adults today are suscep-tible to the development of primary tuberculosis [1 , 7]. Wecan be reasonably certain that 25% of the adults with pul-monary tuberculosis in our series had the primary form of thedisease. Figure 1 shows three age-related peaks of highestprevalence. The highest prevalence of primary tuberculosiswas noted in the 0-5-year age group; a second peak was

noted in the 21 -30-year age group; and a third peak wasnoted in patients 71 years of age or older. The high prevalence

of primary tuberculosis in young adults may be related tomobile, healthy, susceptible individuals living or working incrowded environments or under poor socioeconomic condi-tions [5]; primary tuberculosis in the elderly may be related topoor or crowded living conditions in addition to chronic ordebilitating disease and immunosuppression [5]. Because ofthe recent increased prevalence of primary tuberculosis in

adults, the term “childhood” tuberculosis to describe primarytuberculosis should be abandoned.

Postprimary tuberculosis is the name given to a clinical andradiographic pattern of disease that correlates pathogeneti-cally with acquired hypersensitivity and immunity [1 3]. Thecareful observations and retrospective analyses of Stead [14,17] and others [1 2] have led to the understanding that in 90%of cases, postprimary tuberculosis results from reactivationof a previously dormant primary i�J#{231}n; a minority of casesrepresent a continuation of the pnThary disease [13, 14].Rarely, postprimary tuberculosis ‘is exogenous superinfectionon an inactive or even active original infection-true reinfec-tion [13].

The early parenchymal infiltrate of postprimary tuberculosisresults from the intensive inflammatory reaction in the hyper-sensitive host [1 8]. This may lead to caseous necrosis, whichover time is apt to slough into a bronchus, leaving a cavity[1 8]. The most commonly involved parts of the lungs inpostprimary disease are the apical and posterior segments ofan upper lobe [1 , 5, 8, 1 3, 1 8-20]. Two main factors havebeen postulated to explain this common location of postpri-mary tuberculosis. The higher regional oxygen tensions of theapical and subapical parts of the upright lung (1 14 to 132 mmHg) have been highly touted as being responsible for apicallocalization of postprimary disease. It is suggested that thedemonstrated higher oxygen tensions in the apex of theupright lung produce increased mycobacterial virulence; thelower parts of lung where alveolar oxygen tension is 1 08 mmHg or less are theorized to be quite resistant to the develop-ment of postprimary tuberculosis [1 8]. This concept may bestbe put to the test by observing populations dwelling at highaltitude. Above 1 0,000 feet (3048 m) of elevation, alveolaroxygen tension is substantially less than 1 00 mm Hg; above1 5,000 feet (4570 m), alveolar oxygen tension is well below80 mm Hg, even in the extreme apex of the lung [181.Nevertheless, native permanent residents of the Peruvianhighlands (1 0,300-1 4,300 feet [31 38-4357 m]) seem to beespecially disposed to tuberculosis as compared to lowlandnatives (sea level) [1 8, 21].

A more likely explanation of the apical localization of post-primary tuberculosis is related to impaired clearance mech-anisms from poor lymph flow [1 8]. Pulmonary lymph flow isrelated to two factors: microvascular pressure and respiratorymotion. In the erect lung, owing to gravitational effect, pul-monary perfusion and microvascular pressure are reduced inthe apex relative to the middle and lower lung zones; as aresult, apical lymph flow is also relatively deficient comparedto the more dependent parts of the lung [1 8]. In addition,lymph flow in small lymphatic channels is directly related to

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AJR:146, March 1986 PULMONARY TUBERCULOSIS 505

respiratory excursion. Since the anterior rib cage moves withrespiration but the posterior rib cage is relatively fixed, lymphflow is also restricted in the posterior parts of the lung [18].In primary tuberculosis, lymphohematogenous disseminationresults in the seeding of mycobacterial organisms to many orall parts of the lungs; the decreased lymph flow in the apicaland posterior parts of the lungs would result in decreasedclearance of organisms from these parts of the lung andwould favor the development of postprimary tuberculosis inthese locations [18].

Our study reveals a broad spectrum of radiographic abnor-malities in primary and postprimary tuberculosis not unlikethose demonstrated in other reports on this subject. It alsoprovides helpful insights into common causes for a misdi-agnosis of tuberculosis.

In children, a clinical diagnosis of primary tuberculosis usu-ally is made when an abnormal chest radiograph is coupledwith clinical evidence of pulmonary disease and a documentedconversion of the PPD skin test. Certain radiographic pat-terns, such as parenchymal consolidation associated withhilar and/or mediastinal lymphadenopathy, or isolated hilarand/or mediastinal lymphadenopathy, in children elicit a fre-quent diagnosis of primary tuberculosis on the basis of thechest radiograph alone.

In adults, these same findings often are viewed as unusual,atypical, or even incompatible with tuberculosis, and tuber-culin conversion may be viewed as a coincidental and unre-lated phenomenon. Four adults in our 34 cases of primarytuberculosis escaped initial radiographic and clinical diagnosisbecause hilar and/or mediastinal lymphadenopathy were con-sidered by the clinician and radiologist alike to be incompatiblewith “adult” tuberculosis. Hilar and mediastinal lymphadenop-

athy are nonspecific findings that occur in bronchogenic car-cinoma, metastatic neoplasm, sarcoidosis, lymphoma, andfungal disease. But if the lymphadenopathy in these adultshad been recognized as a possible manifestation of primary

tuberculosis, the conversion of the PPD skin test might havebeen viewed as related to the patient’s illness, and a correctdiagnosis of primary tuberculosis might have been made. Inanother adult patient, tuberculosis was excluded as a possi-bility because parenchymal consolidation was limited to theanterior segment of an upper lobe. While disease limited tothe anterior segment of an upper lobe or basilar segment ofa lower lobe is rare in postprimary tuberculosis and commonin nontuberculous pneumonia, it should be remembered that

these findings are rather common in primary tuberculosis.Postprimary disease in adults is often misdiagnosed also.

The clinical symptoms often are minimal and the patient mayreport only a nonspecific “smoker’s cough” or no symptomsat all. In our series, 1 7 (30%) of 56 cases of active postprimarytuberculosis were missed by both the clinician and the radiol-ogist, resulting in a 1 -3-year delay in diagnosis on one ormore hospital admissions.

Incorrect appraisal of disease activity was the most com-mon cause of misdiagnosis. In local fibroproductive (fibro-nodular, fibrocalcific) tuberculosis the exudative lesion is grad-ually replaced by one or more sharply circumscribed shadows,which are often irregular and angular in contour [13]. Strand-

ing toward the hilum occurs, and calcification in one or moreof the nodules often appears [1 3]. This pattern of pulmonaryabnormality is characteristic of granulomatous disease and isseldom, if ever, found in other bacterial infections. However,we found that it was this characteristic pattern fo parenchymaltuberculosis that caused the greatest difficulty in diagnosis. Itis this stage of postprimary tuberculosis that is often over-looked entirely or is reported as “old scarring” or “no activedisease.” This is incorrect, since many of these patients maybe sputum-positive. Without films dating back at least 6months, an accurate statement about the stability of a fibro-productive lesion cannot be made; all of these lesions shouldbe reported as “possible tuberculosis or fungal disease, activ-ity indeterminant” [1 0, 22]. Even in patients with unchangingtuberculous scars, active tuberculous infection can still bepresent on sputum culture [1 ]. Therefore, these patientsshould be reported as “radiographically stable” rather than“inactive” [1 0, 22]. The term fibrotic, often used to describethis pattern of disease, is not recommended [1 0] because itimplies inactivity.

The second most common cause for a misdiagnosis ofpostprimary tuberculosis was involvement of an anterior seg-ment of an upper lobe or basilar segment of a lower lobe byparenchymal disease. It is a common misconception thatinvolvement of these areas excludes tuberculosis. This iscertainly not true of primary disease; moreover, in postprimary

disease we found the anterior segments of the upper lobesto be involved in 46% of cases and the basilar segments ofthe lower lobes to be involved in 32% of cases. In most ofthese cases cavitary or fibroproductive disease was presentin typical locations; many of these patients also showed

residual radiographic evidence of the previous primary dis-ease-subtle but helpful adjunctive findings in arriving at acorrect diagnosis.

The third most common cause for misdiagnosis of postpri-mary disease was the presence of large nodular or masslike

densities that were considered to be neoplastic. Typically,these were upper-lobe-predominant, rather than basilar, andwere associated with fibroproductive lesions in typical loca-tions.

As Palmer [1 9] states, “pulmonary tuberculosis continuesto keep the physician humble.” Since the advent of antituber-culous chemotherapy 30 years ago, there has been a dramaticdrop in the incidence of tuberculosis in this country. This hascreated a generation of American physicians who have littleexperience with it. Although the case rate of tuberculosis isrelatively stable in many areas of the country, some areas areexperiencing a marked increase in incidence. In addition, therecent increased prevalence of primary tuberculosis in adultshas produced a confusing spectrum of disease seldom en-countered in adults in the past. Because of the infectiousnature of tuberculosis, the morbidity and mortality of thenatural course of the disease, and the excellent therapeuticresults of antituberculous chemotherapy in most cases, thereis good reason for all physicians to be sensitive to the contin-ued existence of this disease. The presence of healed Se-quelae of primary disease or a positive PPD should suggestthat almost any radiographic abnormality could represent

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506 WOODRING ET AL. AJR:146, March 1986

active tuberculosis. The recognition of primary disease in theadult and close scrutiny for and proper reporting of fibropro-ductive lesions could further improve the detection and diag-nosis of active tuberculosis.

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