Ebook Chest radiology - The esentials (3/E): Part 2

LEARNINGOBJECTIVES
 1. List an appropriate differential diagnosis for upper lung disease
seenonchestradiographyorcomputedtomography(CT).
 2. Describetheradiographicclassificationofsarcoidosis.
 3. State the three most common locations (Garland triad) for
adenopathytooccurinthechestofpatientswithsarcoidosis.
 4. Listfourcommonetiologiesof“eggshell”calcifiedlymphnodes
inthechest.
 5. Recognizeprogressivemassivefibrosissecondarytosilicosison
chestradiographyandCT.
 6. Recognize and describe the typical appearance of cystic fibrosis
onchestradiographyandCT.
 7. Describe the radiologic manifestations of primary pulmonary
tuberculosis.
 8. Name the most common segmental sites of involvement for
reactivationtuberculosisinthelung.
 9. Define a Ghon lesion (calcified pulmonary parenchymal
granuloma) and Ranke complex (calcified node and Ghon
lesion); recognize both on a chest radiograph and CT and
describetheirsignificance.
10. Suggestthepossibilityofradiationasacauseofnewupperlung
opacificationonachestradiographofapatientwithevidenceof
mastectomy and/or axillary node dissection or known head and
neckcancer.


11. Describe the acute and chronic phases of radiation-caused
changesinthelungs,includingthetimecourseandtypicalchest
radiographandCTappearances.
12. Recognizethetypicalappearanceofirregularlungcystsonchest
CTofapatientwithLangerhanscellhistiocytosis.

13. Name the major categories of disease that cause chest
radiographic or CT abnormalities in the immunocompromised
patient.
14. Other than typical bacterial infection, name two important
infections and two important neoplasms to consider in patients
with acquired immunodeficiency syndrome (AIDS) and chest
radiographicorCTabnormalities.
15. Describe the typical chest radiographic and CT appearances of
Kaposisarcoma.
16. Describe the chest radiographic and CT appearances of
Pneumocystisjirovecipneumonia.
17. Name four important etiologies of hilar and mediastinal
lymphadenopathyinpatientswithAIDS.
18. Describethetimecourseandchestradiographicappearanceofa
bloodtransfusionreaction.
19. DescribethechestradiographicandCTappearancesofamiliary
patternandprovideadifferentialdiagnosis.
20. NameanddescribethetypesofpulmonaryAspergillusdisease.
21. IdentifyanintracavitaryfungusballonchestradiographyandCT.
22. Name the most common pulmonary infections that occur after
solid organ (e.g., liver, renal, lung, cardiac) and bone marrow
transplantation.
23. DescribethechestradiographicandCTfindingsofposttransplant
lymphoproliferativedisorders.


Pulmonaryinfectionsareamajorcauseofmorbidityandmortality,especiallyin
immunocompromised patients. Immunocompromised patients have altered
immunemechanismsandarepredisposedtoopportunisticinfections.Numerous
factors are associated with an immunocompromised state, including but not

limited to diabetes; renal or liver failure; advanced age; bone marrow or solid
organ transplantation; acquired immunodeficiency syndrome (AIDS); presence
of access lines (e.g., intravenous lines, endotracheal tubes, chest tubes);
splenectomy, hospital environment (predisposing to nosocomial pneumonia);
underlyingmalignancy;drugtherapy(e.g.,steroids,chemotherapy);andimmune
deficiencies (e.g., hypogammaglobulinemia). Some of the clinically important
infections and other diseases seen in immunocompetent and
immunocompromised patients tend to have an upper lung–predominant
distribution (e.g., mycobacterial and fungal disease). Recognition of an upper
lungdistributionofdiseasehelpsthecliniciantoformanappropriatedifferential
diagnosis.Thischapterbeginswithadiscussionofupperlungdisease,including
infectiousandnoninfectiouscauses,andcontinueswithareviewofthedisorders
that occur in immunocompromised individuals and their radiographic
appearances.

UPPERLUNGDISEASE
Upperlungreferstotheupperone-thirdofthelung,whichincludesthemajority
of the upper lobes and the uppermost portion of the superior segments of the
lowerlobes.Inthenormaluprightlung,bloodflowandventilationpredominate
in the lung base; in many lung disorders however, the greatest degree of
abnormality occurs in the upper lung. Alterations in ventilation–perfusion,
lymphaticflow,metabolism,andmechanicsareproposedaspathogenicfactors
inupperlunglocalizationoflungdisease(1).Twomnemonics,“SHRIMP”and
“CASSET,”canbeusedtorecallcommonanduncommondisordersoccurringin
the upper lungs (Table 10.1). Because it may be difficult to appreciate a
predominantly upper lung distribution of disease on chest radiography, it is
useful to consider the differential diagnoses given in Table 10.1, even if the
disease appears diffuse, any time the upper lungs are as affected as much or
morethanthemiddleandlowerlungs.

SARCOIDOSIS


Sarcoidosisisacommonsystemicdiseaseofunknownetiologycharacterizedby
widespread development of noncaseating granulomas. These granulomas are
nonspecificandresemblethoseinmanyothergranulomatousprocesses,except
for tuberculosis (TB), a disease in which caseous necrosis of granulomas is
usuallyseen.Sarcoidosisis10timesmorecommoninAfrican-Americansthan
inCaucasians(2). Most patients who present with sarcoidosis are between the
ages of 20 and 40, but the disease occurs as early as 1 year and as late as 80
yearsofage(3).Thediseaseis2to3timesmorecommoninAfrican-American
women than in African-American men (3). The lung is the most commonly
involved organ in patients with sarcoidosis and accounts for most of the
morbidityandmortality,withanoverallmortalityratebetween2.2%and7.6%
(3).

Table10.1 UPPERLUNGDISEASE
“SHRIMP”
Sarcoidosis
Histiocytosis,Langerhanscell
Radiationpneumonitis(cancersofhead/neckandbreast)
Infection(tuberculous,fungal)
Metastasesa
Pneumoconiosesb(silicosis,coalminer’s)
“CASSET”
Cysticfibrosis
Ankylosingspondylitis
Silicosis
Sarcoidosis
Eosinophilicgranulomatosis(Langerhanscellhistiocytosis)

Tuberculous,fungalinfection
a

SeeChapter7.
SeeChapter3.

b


Table10.2 CLASSIFICATIONOFSARCOIDOSISONCHEST
RADIOGRAPHY
0
I
II
III
IV

Normalchestradiograph
Hilarormediastinalnodalenlargementonly
Nodalenlargementandparenchymaldisease
Parenchymaldiseaseonly
End-stagelung(pulmonaryfibrosis)

Sarcoidosis can be classified according to its appearance on the chest
radiograph (Table 10.2) (4). Patients commonly, but not necessarily, progress
through each class, and the class at presentation can, but does not always,
correlatewithprognosis(5).Forty-fivepercentto65%ofpatientsareclassIat
the time of presentation. Lymphadenopathy is the most common intrathoracic
manifestationofsarcoidosisandoccursin75%to80%ofpatientsatsomepoint
intheirillness(6).Theclassicpatternoflymphadenopathyisbilateralhilarand

right paratracheal nodal enlargement, the so-called Garland triad or 1-2-3 sign
(Figs.10.1and10.2),althoughanymediastinalnodescanbeandfrequentlyare
involved.Thehilarlymphnodesareusuallysymmetricinappearanceandcanbe
massivelyenlarged(“potatonodes”)butareusuallyclearofthecardiacborders,
a feature that helps distinguish sarcoidosis from lymphomatous
lymphadenopathy, as the latter usually abuts the cardiac margins. Of patients
with class I disease at initial examination, about 60% go on to complete
resolution (7), with parenchymal disease occurring in the remaining patients.
Nodalcalcificationisseeninupto20%ofcases(8),andinsomeofthesecases
(approximately5%),thecalcificationisofaperipheral“eggshell”pattern(Figs.
10.3 and 10.4). Eggshell calcification is largely limited to sarcoidosis and
silicosis,butitcanbeseeninotherdisorders(Table10.3)(9).


FIG.10.1•Sarcoidosis.Posteroanterior(PA)chestradiographofa31-year-old
woman with class I sarcoidosis shows right paratracheal (arrowheads) and
bilateral hilar (arrows) lymphadenopathy. This pattern of lymphadenopathy is
classicforsarcoidosisandisreferredtoasthe1-2-3signorGarlandtriad.


FIG. 10.2 • Sarcoidosis. A: CT of a 23-year-old woman shows ill-defined
nodulesinabronchovasculardistribution(arrow)intherightupperlobe.B:CT
withmediastinalwindowingshowsrighthilarlymphadenopathy(arrow).C:CT
at the level of the inferior pulmonary veins shows left hilar lymphadenopathy
(arrow). D: CT at the level of the lower lobe pulmonary arteries shows
subcarinallymphadenopathy(arrow).
Parenchymaldiseaseisseenonchestradiographyatthetimeofpresentation
in approximately half of patients with sarcoidosis. Radiographic patterns of
parenchymaldiseaseincludereticulonodularopacities,ill-definedopacitiesthat
have an appearance of alveolar filling, large nodules, and lung fibrosis.

Reticulonodularopacitiesarethemostcommonpattern,seenin75%to90%of
patients with parenchymal disease; the opacities are usually bilaterally
symmetricwithadistributionpredominantlyinthemiddleandupperlungs(10)
(Figs.10.5and10.6).In10%to20%ofpatients,opacitieswithairspacefeatures
develop,whichcanbeill-definedorfocal,nodular,andwell-defined.Theterm
alveolarsarcoidreferstothispattern,althoughthe“airspace”diseaserepresents
an interstitial process that compresses and obliterates alveoli. Alveolar sarcoid
generally consists of bilateral, multifocal, poorly defined opacities showing a
predilectionfortheperipherallungs(11)(Fig.10.7).Theperipheraldistribution
isparticularlywellseenwithcomputedtomography(CT).


FIG. 10.3 • Sarcoidosis. CT shows precarinal lymphadenopathy with rim
calcification (arrow). This pattern of calcification is referred to as “eggshell”
calcificationandisseeninapproximately5%ofpatientswithsarcoidosis.
Sarcoidgranulomasmayresolvecompletelyorhealbyfibrosis.Pulmonary
fibrosis occurs in approximately 20% of patients with sarcoidosis, and the
radiologicfeaturesareconsideredbysomeauthorstobealmostpathognomonic.
The findings consist of permanent, coarse, linear opacities radiating laterally
from the hilum into adjacent upper and middle lungs. Bullae can form in the
upper lungs. The hila are pulled upward and outward, and vessels and fissures
are distorted. The fibrosis is occasionally so severe that massive parahilar
opacitiesinthemiddleandupperlungs,resemblingthoseofprogressivemassive
fibrosisofsilicosis,areseen(Fig.10.8).
CT can define the anatomic location of parenchymal sarcoid granulomas
muchmoreaccurately(12–14).ThemostcommonfindingofsarcoidosisonCT
is multiple, 1- to 5-mm nodules, usually with irregular margins, in a
perilymphatic distribution (bronchovascular margins, along interlobular septa,
subpleurally, and in the center of secondary pulmonary lobules) (Fig. 10.9).
Septalthickeningfromsarcoidosishasabeadedappearance,afeaturethathelps

distinguishitfrompulmonaryedema,inwhichtheseptalthickeningistypically
smooth. Patchy ground-glass opacities are seen in about 50% of patients with
sarcoidosisandrarelymaybetheonlyCTabnormality(Fig.10.10).Fibrosisis


bettercharacterizedonCTthanonchestradiography.CTcanshowfindingsof
sarcoidosiswhenthechestradiographisnormal,andpatientscanhaveanormal
CTstudyyethavesarcoidosisprovedbylungbiopsy(13).

FIG.10.4•Sarcoidosis.A: PA chest radiograph of a 37-year-old man shows
bilateral upper lobe nodular disease and hilar enlargement (class II). B: CT
shows nodules of varying size along the fissures (straight solid arrow) and
bronchovascular bundles (dashed arrow) and in a subpleural location (curved
solidarrow).C:CTwithmediastinalwindowingshowscentralcalcificationof
right paratracheal lymph nodes (arrow). D: CT at a lower level shows
calcificationofrighthilarnodes(arrow).

Table10.3 COMMONCAUSESOF“EGGSHELL”
CALCIFICATIONOFLYMPHNODESINTHE
CHEST
“SIT”
Sarcoidosis
Silicosis
Infection(tuberculous,fungal)


Treatedlymphoma
Fungus balls (mycetomas) can develop in cystic areas that develop from
sarcoidosis,andsarcoidosisisthesecondmostcommonpredisposingcondition
(afterTB) leading to the development of mycetoma (15). Hemoptysis resulting

frommycetomaformationcanbelife-threatening.Mycetomasoccurintheupper
lobesandshouldbesuspectedwhennewopacitiesareseeninanareaofchronic
cysticorbullousdisease,especiallywhentheyareaccompaniedbynewapical
pleural or extrapleural opacity on chest radiography. There are myriad other
atypical features of sarcoidosis, including pleural effusions, pleural thickening,
cavitary nodules, bronchostenosis, pulmonary artery hypertension from
periarterialgranulomatosis(Fig.10.11),corpulmonale,andpneumothoraxfrom
chronicfibrosis.


FIG. 10.5 • Sarcoidosis. PA chest radiograph shows reticulonodular opacities
scattered throughout the upper and middle lungs. Parenchymal disease without
lymphadenopathyindicatesclassIIIsarcoidosis.

FIG. 10.6 • Sarcoidosis. Coronal CT shows multiple small nodules in a
predominantlyupperandmiddlelungdistribution.


FIG.10.7•Sarcoidosis.A:PAchestradiographofa28-year-oldmanwithmild
shortnessofbreathshowsrightparatrachealandbilateralhilarlymphadenopathy
andbilateralperipheralareasofconsolidation(arrows).B:CTshowsmultifocal
opacitiesintheperipheryoftheleftlung(arrows).Thispatternofsarcoidosisis
referred to as alveolar sarcoid, although pathologically it is seen to be an
interstitialprocess.


FIG.10.8•Sarcoidosis. Coronal CT shows bilateral upper lung–predominant
fibrosis (class IV) with associated traction bronchiectasis, architectural
distortion,upwardretractionofthehila,andmultiplecalcifiedlymphnodes.

FIG.10.9•Sarcoidosis.CTofa40-year-oldmanshowsill-definednodulesina
bronchovasculardistribution(arrows).

FIG. 10.10 • Sarcoidosis. CT image of a 46-year-old woman with mild
shortness of breath shows bilateral areas of abnormal opacification distributed
along the central and peripheral bronchovascular bundles (straight arrows).
Someoftheopacitiesareofground-glassattenuation,allowingvisualizationof
underlying bronchial and vascular markings. Note the small nodules along the
rightmajorfissure(arrowheads),inthecenterofsecondarypulmonarylobules
(curved arrows), and in a peripheral subpleural location (open arrow). All of
these findings illustrate a perilymphatic distribution, which is typical of
sarcoidosis.


FIG.10.11•Sarcoidosis.PA(A)andlateral(B)chestradiographsofa69-yearold man with class IV sarcoidosis show enlarged pulmonary arteries (arrows)
secondarytopulmonaryarterialhypertension.Notethediffuseupperandmiddle
lungreticulonodularopacities,andnotealsotheupwardretractionofthehila.C:
CT shows bilateral central areas of pulmonary fibrosis with thickening of
bronchovascular bundles and traction bronchiectasis. Note the parenchymal
bandsontheright(arrows).

SILICOSIS
Silicosisisadiseaseofthelungscausedbyinhalationofdustcontainingsilicon
dioxide,orsilica,thepredominantconstituentoftheearth’scrust.Silicadustis
prevalentinmining,quarrying,andtunnelingoperations.Occupationsassociated
with the development of silicosis include mining of heavy metals, the pottery
industry, sandblasting, foundry work, and stonemasonry. When silica particles
are inhaled, they are deposited in the alveoli and engulfed by alveolar
macrophages, where they are acted on by lysosomal enzymes. The affected

macrophage dies and liberates mediators (leading to stimulation of collagen
production)andthesilicaparticles.Thesilicaparticlesarethenfreetobetaken
up by other macrophages, and the cycle continues, leading to progressive lung


diseaseevenwithoutcontinuedoccupationalexposuretosilica.Silicosiscanbe
classified as simple silicosis, complicated silicosis, acute silicosis, or Caplan
syndrome.Coalworker’spneumoconiosis,causedbyinhalationofcoaldust,is
different pathologically from silicosis, but it produces chest radiographic
findingssimilartoandoftenindistinguishablefromthoseofsilicosis.
Patientswithsimplesilicosisareusuallyasymptomatic.Between10and20
years’ exposure is usually necessary before the chest radiograph becomes
abnormal (16). The chest radiograph shows multiple nodules, 1 to 10 mm in
diameter, with a diffuse but upper lung–predominant distribution (Fig. 10.12).
Occasionally, the nodules may calcify. Enlargement of mediastinal and hilar
nodes is common and is occasionally associated with eggshell calcification
similartothatseenwithsarcoidosis.
Complicated silicosis refers to progression of simple silicosis, where the
nodules become confluent and larger than 1 cm. On chest radiography, these
opacitiesareseenpredominantlyintheperipheryoftheupperlungs,which,over
time, tend to migrate or retract toward the hilum as the fibrotic process
progresses.Theseconglomeratemasses,whichcanreachseveralcentimetersin
size and contain obliterated blood vessels and bronchi, are referred to as
progressivemassivefibrosis(Figs.10.13and10.14).Theconglomeratemasses
areoftensurroundedbyparacicatricialemphysema,whichisbestappreciatedon
chest CT. As conglomeration of the nodules occurs, the lungs gradually lose
volume,andcavitationofthemassescanoccur.Patientswhohaveadvancedto
this stage are at increased risk of active TB, and this diagnosis should be
suspectedwhenanewareaofcavitationisseenonchestradiography.

FIG. 10.12 • Simple silicosis. A: PA chest radiograph of a foundry worker
showsnumerousbilateralill-definedtinynodules,creatinganoverallincreasein
lung opacity. B: On CT, the nodules are much better appreciated. C: CT with
mediastinal windowing shows densely calcified hilar (solid arrows) and
subcarinal(dashedarrow)lymphnodes.

FIG. 10.13 • Complicated silicosis. A: CT of a 52-year-old man who spent
manyyearsworkinginasandpitshowscalcificationofhilar(longarrows)and
subcarinal (short arrows) nodes. B: CT with lung windowing shows
“progressivemassivefibrosis”intherightupperlobe(longstraightarrows)and
early conglomeration of nodules in the superior segments of the lower lobes
(curved arrows). Multiple parenchymal bands are seen on the right (short
straightarrows).


FIG. 10.14 • Complicated silicosis. Coronal CT shows bilateral upper lung–
predominant fibrosis (“progressive massive fibrosis”), traction bronchiectasis,
peripheral bullae, and parenchymal calcifications. The appearance is similar to
thatofclassIVsarcoidosis.
Acutesilicosisisarareconditionrelatedtoheavyacuteexposuretosilicain
enclosedspaceswithminimalornoprotection.Histologically,theappearanceis
identical to that of pulmonary alveolar proteinosis; hence the term
silicoproteinosis is used. The disease is rapidly progressive, often leading to
deathasaresultofrespiratoryfailure.Thechestradiographicpatternisthatof
nonspecific diffuse airspace disease or ground-glass opacities, with a perihilar
distribution and air bronchograms identical to the radiographic findings of
pulmonaryedema.
Caplan syndrome consists of the presence of large necrobiotic rheumatoid
nodules superimposed on a background of simple silicosis. The syndrome is a

manifestation of rheumatoid lung disease and is seen in both coal worker’s


pneumoconiosisandsilicosis.

LANGERHANSCELLHISTIOCYTOSIS
Langerhans cell histiocytosis (LCH), also referred to as histiocytosis X or
eosinophilic granuloma, is a granulomatous disorder of unknown cause
characterized by the presence within the granulomas of a histiocyte, the
Langerhanscell.Thediseaseisequallyprevalentinmaleandfemalepatients,is
unusual in African-Americans (17), and 95% of adult patients are cigarette
smokers(17).In mostpatients,symptomsappearin thethird or fourth decade,
butthediseasecanoccurinteenagersandthoseoverage60.Thediagnosiscan
be made in asymptomatic patients with abnormal chest radiographs.
Pneumothorax is a classic manifestation of LCH, and the frequency of
pneumothorax as the initial manifestation is as high as 14% (18). The
pneumothoraces are commonly recurrent and may be bilateral. Approximately
one-thirdofpatientswithLCHimprove,one-thirdremainstable,andone-third
deteriorate(18).
The chest radiograph of patients with LCH shows a diffuse, symmetric,
reticulonodularpatternor,lesscommonly,asolelynodularpattern.Bothpatterns
have a predominantly middle and upper lung distribution. The nodules are
usuallyill-defined,varyinsizefrom1to15mm,andareofteninnumerablebut
can be few in number. Large nodules can mimic metastases. With time, small
cysticairspacesdevelop,andlargerairspacesupto5cmindiameterwillform
only rarely. Because of the development of these abnormal airspaces, lung
volume does not decrease with time but often increases. Pleural effusion and
hilarormediastinalnodalenlargementareuncommon.
CTofthelungsshowscystsandnodules,oftenincombination(19,20)(Figs.
10.15and10.16).Cystsrangeindiameterfrom1to30mmormoreand,unlike

centrilobular emphysema, usually have very thin discrete walls and no
centrilobular core structure. Some cysts have bizarre shapes, which along with
an upper lung–predominant distribution can help to distinguish them from the
uniformly round cysts that are typical of lymphangioleiomyomatosis. Nodules
aretypically1to5mmindiameter,haveirregularmargins,andmaybecavitary.
The disease is thought to progress from solid nodules to cavitary nodules to
cysts, although this is controversial. End-stage disease can resemble that of
generalized centrilobular pulmonary emphysema. In addition, as this disease is
common in smokers, there is often superimposed centrilobular pulmonary


emphysema.

RADIATIONPNEUMONITIS
Radiation injury tothe lungis mostcommonly seenafterradiation therapyfor
breast cancer, lung cancer, and Hodgkin disease. On the chest radiograph, the
changes of radiation pneumonitis are almost always confined to the field of
irradiation. The first change is a diffuse haze in the irradiated region, with
obscuration of the normal vascular markings. Patchy opacities appear, which
maycoalesceintoanonanatomicbutgeometricareaofpulmonaryopacification.
These radiographic changes usually appear about 8 weeks after treatment,
dependingontheradiationdoseanddosinginterval(21);peakreactionoccursat
3 to 4 months. With time, the opacities become more linear or reticular, and
fibrous contraction and distortion of lung architecture occurs. The fibrosis and
contractioncontinueovera12-to18-monthperiod.Whenonlytheapicesofthe
lung are affected by radiation, such as with treatment for head and neck
neoplasms,theradiographicchangesdonotappeargeometricbutill-definedand
patchy (Fig. 10.17). When bilateral apical airspace opacities are seen on chest
radiography, radiation pneumonitis should be considered in the appropriate
patient population. Radiation of the axilla, an adjuvant treatment for patients

withbreastcancerwhohaveundergonelumpectomyormastectomy,canresult
inipsilateralperipheralupperlungpatchyairspaceopacities(Fig.10.18).

TUBERCULOSIS
Once a disease of childhood, more than half of cases of initial infection with
Mycobacterium tuberculosis, or primary TB, are now seen in the adult
population (22). In primary tuberculous infections, the pulmonary focus and
lymphadenopathy may resolve without a trace, or they may leave a focus of
caseousnecrosis,scarring,orcalcification.Severaltermsareusedtodescribethe
form of TB that develops after a primary infection under the influence of
established hypersensitivity including reactivation TB, postprimary TB, and
secondaryTB.
ThepredominantradiographicfeatureofprimaryTBisthepresenceofhilar
lymphadenopathy (usually unilateral) and mediastinal lymphadenopathy
contiguoustotheaffectedhilum.Lymphadenopathyislesscommonandmilder
in adults than in children, with the exception of immunocompromised adults,


especially those with AIDS. On CT, the enlarged nodes typically have a lowdensity center with rim enhancement (Fig. 10.19) (23). The pulmonary foci of
primaryTBarerandomlydistributedthroughoutthelungs,andtheyrangefrom
small, occasionally imperceptible, ill-defined parenchymal opacities to
segmental or lobar consolidation, often with an appearance similar to that of
otherbacterialpneumonias(Figs.10.20and10.21).Theincidenceofcavitation
variesbetween10%and30%(22).Hilarormediastinallymphnodecalcification
is observed in 35% of cases (24). Pleural effusions are not uncommon, are
generally unilateral, and are usually, but not always, associated with some
identifiable pulmonary parenchymal disease (Fig. 10.22). Bronchial stenosis,
bronchial occlusions, and polypoid endobronchial tuberculous lesions may be
seenonCT.Itshouldbenotedthatinsomeimmunocompromisedpatients,their
“reactivation”TBpresentsclinicallyandradiographicallylikeprimaryinfection

seeninimmunocompetentpatients.

FIG. 10.15 • Langerhans cell histiocytosis. PA (A) and lateral (B) chest
radiographs of a 32-year-old male cigarette smoker show bilateral reticular
interstitial opacities and thin-walled cysts (arrows). Note the increased lung
volumes. C: CT shows bilateral thin-walled cysts, with rounded and irregular


shapes(straightarrows),andill-definednodules(curvedarrows).

FIG.10.16•Langerhanscellhistiocytosis.CoronalCTshowsnumeroussmall,
irregularcystswithdefinedwallsinanupperlung–predominantdistribution.
TheearliestchestradiographicfindingsofreactivationTBconsistofoneor
more ill-defined patchy opacities, with or without small satellite foci in the
adjacent lung, occurring in the posterior segments of the upper lobes in the
majorityofpatientsandinthesuperiorsegmentofthelowerlobesinmostofthe
remainderofpatients.Thisdistributionofdiseaseisveryhelpfulinsuggesting
thediagnosisofreactivationTB.Cavitationwithorwithoutthepresenceofair–
fluidlevelsisadistinctfeatureofreactivationTBandindicatesahighlikelihood
ofactiveinfection(Figs.10.23to10.27).Endobronchialspreadofdisease,with
“tree-in-bud”opacities,bestseenwithCT,alsosuggestsactiveinfection.Inthe
proper clinical setting, the presence of cavitation and endobronchial spread
impliesthatthediseaseishighlycontagious,andpatientswithcavitarydisease
should be placed under immediate infective precautions (respiratory isolation)


on the basis of radiographic findings alone. With healing, the chest radiograph
shows gradually increasing definition of the lung opacities, development of
fibrosis in the surrounding lung, contraction and volume loss of the affected
segment or lobe with fissural displacement or distortion of the vascular

structures in the hilum, bronchiectasis, and calcification (Fig. 10.28). Fluid
levels in cavities disappear, and the cavities either disappear or persist with a
smoothinnerwall.ItshouldbenotedthatpatientscanrarelystillhavesputumpositiveTBandanormalchestradiograph.

FIG.10.17•Radiationpneumonitis.A:PAchestradiographofa60-year-old
woman 3 months after radiation treatment to the neck for a piriform sinus
carcinomashowssubtleareasofabnormalopacificationinbothapices(arrows).
B: PA chest radiograph obtained 2 months later shows progression of apical
opacities (arrows). C: CT shows bilateral apical airspace disease without
anatomicorgeographicdistribution.


FIG.10.18•Radiationpneumonitis.A:NormalbaselinePAchestradiograph
ofa71-year-oldwoman.B:PAchestradiographobtained11monthslatershows
interval right mastectomy for treatment of breast cancer (note the hyperlucent
rightlowerhemithorax)andsurgicalclipsintherightaxilla.Notenewabnormal
areas of nonsegmental opacification in the periphery of the right upper lobe
(arrows)fromrecentradiationtotheaxilla.

FIG. 10.19 • Primary tuberculosis. CT shows low-density subcarinal nodes
withpartialrimenhancement(arrow).


FIG.10.20•Primarytuberculosis.PAchestradiographshowsdiffusenodular
airspacedisease.
Other patterns of reactivation TB include lobar pneumonia, diffuse
bronchopneumonia,endobronchialTB,tuberculomaformation,miliaryTB,and
tuberculous pleuritis (Fig. 10.29). A calcified lymph node may erode into an
adjacentairway,becomingabroncholith,andbeassociatedwithhemoptysisor
postobstructiveatelectasisorpneumonia.Broncholithscanbesuggestedwhena

previouslydocumentednodalcalcificationonchestradiographyhasdisappeared
or changed position. On rare occasion, a patient can cough up pieces of a
calcifiedbroncholith,aphenomenonreferredtoaslithoptysis.Tuberculomasare
discrete tumorlike foci of TB in which there is a fine balance between
inflammation and healing. The margins of a tuberculoma are usually wellcircumscribed. Tuberculomas may be single or multiple, are occasionally as
largeas5cmindiameter,andmaygrowslowlyoveranextendedperiodoftime.