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Turkish Society of Radiology 2009

Bronchopulmonary foregut malformations (BPFMs), also known ascongenital lung malformations or abnormalities, are a heteroge-neous group of disorders involving conducting airways, lung pa-

renchyma, and lung vasculature. Several malformations that present asmass lesions have been described, some of which include bronchogeniccyst (BC), pulmonary sequestration (PS), congenital cystic adenomatoidmalformation (CCAM) [currently named as congenital pulmonary air-way malformation (CPAM)], congenital lobar emphysema (CLA) [cur-rently named as congenital lobar overinflation (CLO)], bronchial atresia,and congenital pulmonary cyst (CPC) (14). Moreover, combinations ofthose malformations (hybrid malformations) have also been described(2, 57). These malformations can manifest in various ways from respi-ratory distress at birth to incidental findings on chest radiograph. Al-though malignancies have been described with BPFMs, the number ofreported cases is less than fifteen (8).

Etiopathogenetic concepts

BPFMs are characterized with defective budding, differentiation or

separation of the primitive foregut. Although most lesions have theirindividual histologic features, presence of histologically hybrid lesionssuggests that these entities have a common embryologic origin. In orderfor a common origin to reconcile with a variety of consequent lesions,several classifications, terminologies and theories relating to the etiologyof BPFM have been suggested (8, 9). Clements and Warner (9) proposedthat an interruption of relative growth and development of the pulmo-nary vessels is responsible in etiopathogenesis. For instance, an earlyinterruption in the development of the pulmonary arterial tree couldresult in continued development of the primitive capillary supply andsubsequent abnormal development of the arterial supply. Langston (8)has recently suggested a new concept where an in utero airway obstruc-tion represents the main pathogenetic mechanism for some lesions. Thelevel, degree and timing of obstruction may be responsible for differentpatterns of malformations.

Imaging evaluation

Lesions may be detected by prenatal ultrasonography (US) or by fetalmagnetic resonance imaging (MRI). In this scenario, a chest radiographwith cross-sectional imaging is recommended. When discovered inci-dentally on radiography, or for evaluation of non-specific chest signs orsymptoms, a follow-up radiograph should be obtained to document per-sistence since pneumonia (i.e., round pneumonia) can mimic these le-sions. If persistent, cross-sectional imaging is recommended. Computedtomography (CT) is generally recommended for parenchymal lesions, andCT or MRI is appropriate for mediastinal lesions. For CT evaluation, angi-

PEDIATRIC IMAGING

PICTORIAL ESSAY

Diagn Interv Radiol DOI 10.4261/1305-3825.DIR.2063-08.2

Bronchopulmonary foregut malformations presenting as masslesions in children: spectrum of imaging findings

Murat Kocaolu, Donald P. Frush, Mehmet S. Uurel, brahim Somuncu

From the Department of Radiology (M.K. kocaoglumurat@

yahoo.com, M.S.U., .S.), Glhane Military Medical School,Ankara, Turkey; and the Department of Radiology (D.P.F.), Duke

University Medical Center, Durham, North Carolina, USA.

Received 25 August 2008; revision requested 2 September 2008; revisionreceived 3 September 2008; accepted 8 September 2008.

Published online 9 October 2009DOI 10.4261/1305-3825.DIR.2063-08.2

ABSTRACTBronchopulmonary foregut malformations are a heterogene-ous but interrelated group of abnormalities that may containmore than one histologic feature. Familiarity with the pres-entation and imaging features of bronchopulmonary foregutmalformations presenting as a congenital mass or mass-like

lesion is important. Moreover, imaging plays a central rolein the evaluation of these lesions since, when symptomatic,clinical features are usually nonspecific. With imaging, thepresence of and features of the lesion can be determined, fa-cilitating appropriate management to prevent the potentialcomplications including infection, respiratory compromiseand, very rarely, malignancy.

Key words: respiratory system abnormalities radiography computed tomography magnetic resonance imaging


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Kocaolu et al.iiDiagnostic and Interventional Radiology

on prenatal US. On chest radiograph,BC is a well-defined solitary mass inthe aforementioned areas. The cysts areusually homogeneous, and have fluidattenuation on CT scans; cysts are hy-perintense on T2-weighted MR images,

and are isointense to skeletal musclesignal intensity on T1-weighted MRimages (Fig. 1). Cyst content does notenhance; however, when infected, cystsmay demonstrate air-fluid levels andwall enhancement (Fig. 2). Presence of

ographic technique is recommended todetermine potential arterial supply andvenous drainage. Although the prenataldiagnosis has been largely facilitated

with the recent advancements on UStechniques, overlapping sonographicappearances render an accurate diag-nosis difficult. In this pictorial review,we mainly present postnatal imagingfindings of BPFMs with an emphasis onmass and mass-like lesions.

Bronchogenic cyst

Bronchogenic cyst (BC) is a result ofinsult at 45 weeks of embryonic life.The cyst is lined with respiratory epithe-lium associated with a wall containingmucous glands, cartilage, and smoothmuscle. The cyst fluid may be clear,serous, or may contain proteinaceousmaterial (10). They may be seen in anypart of the chest; however, two thirds ofBCs are located in the mediastinum andthe remainder is parenchymal (1012),most often perihilar. However, BC hasalso been reported in several other sitessuch as retroperitoneal locations andthe neck, as well as at the base of thetongue (8). BC is visualized as a singlecystic lesion with an imperceptible wall

ba

c

Figure 2.a, b. Infected bronchogenic cyst. Frontal chest radiograph(a) demonstrates a welldefined right lung mass with an airfluidlevel. Axial contrastenhanced CT image (b) through the rightatrium confirms the airfluid level, and shows enhancement within athickened cyst wall.

b

a

Figure 1.ac.

Bronchogenic cyst.Axial contrastenhancedCT image (a) throughthe subcarinal level

reveals a welldefined,round, homogeneous,predominantly fluidattenuation mass

(heterogeneity is likely

due to scan artifact).Axial T2-weighted (b)and T1-weighted (c)

MR images at the samelevel demonstrate themass as hyperintense tocerebrospinal fluid on

T2-weighted scan and isointense to myocardium on T1-weighted scanin accordance

with its proteinaceous content.


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Bronchopulmonary foregut malformationsiii

proteinaceous material in the cyst maycause increased density on CT, and in-creased intensity on T1-weighted MRimages (10).

BC and cystic esophageal duplica-tion (CED) are both foregut cysts (1).There are two forms of esophagealduplication, CED and complete tu-bular duplication. On esophagogram,the lumen of the esophagus maycommunicate with the cyst in com-plete tubular duplication. The imag-ing appearance of CED on CT andMRI is same with the BC; however,the cyst wall of CED may be thicker,and esophagogram demonstrates thedisplacement of the esophagus to thecontralateral site (1, 13) (Fig. 3). Be-cause of the potential complications,including infection, rupture, and he-morrhage, lesions are usually resected(11, 1417).

Imaging findings of round pneu-monia, arteriovenous malformation(AVM), and normal thymus maymimic BC. Round pneumonia is a bac-

terial pneumonia characterized by around, well-defined opacity on chestradiograms. Symptoms of pneumo-nia and characteristic radiographicfindings are adequate for the diagno-sis; however, if CT is obtained with asuspicion of mass, air bronchograminside the round density confirmsthe diagnosis of round pneumonia(18). On chest radiographs, the AVMmay be occult; but if relatively large,it appears as a well-defined lobulateddensity. Pulmonary CT-angiography(CTA) technique is recommended tomaximize the chance of identifyingthe malformations. Pulmonary CTAreveals the vascular nature of these le-sions, including the tubular and nod-ular areas consistent with feeding ar-teries, draining veins, and aneurysms(19, 20). Normal thymus decreases insize throughout the first decade of lifeand does not displace or compress theadjacent airways and vessels. Liver-like echotexture on US is consideredcharacteristic for thymus (21).

Congenital pulmonary airwaymalformation

Congenital pulmonary airway mal-formation (CPAM) has been suggestedas a preferred term to CCAM, becauseonly type III is adenomatoid, and notall types are cystic. CPAM is solid, cysticor mixed mass of pulmonary tissue (3,22). The embryonic insult occurs dur-

ing 5-8 weeks of gestation. Histopatho-logically, CPAM is a result of bronchialovergrowth with almost complete sup-pression of alveolar development (23).CPAM can occur in any portion of thelung. Typically, CPAM is restricted topart of one lung, which can commu-nicate normally with the bronchialtree, and tends to rapidly inflate withair at birth. The traditional classifi-cation was by Stocker, consisting ofthree histopathologic types; however,further classifications such as type 0and type IV have been described bysome authors (24, 25). Type I CPAMs(65%) have macroscopic cysts, at leastone larger than 2 cm and lined withmucine secreting epithelium, and cancontain cartilage plates. Type II CPAMs(25%) also have macroscopic cysts, butsmaller than 1 cm. They are lined byciliated columnar epithelium. Type IIICPAMs have solid-like content with amultiplicity of bronchial membranesand bronchiole-resembling histology,without cartilage content. They arelined by cuboidal epithelium and have

poor prognosis, as they tend to causenon-immune hydrops fetalis and pul-monary hypoplasia. In type IV CPAM, alarge cyst is lined by predominantly al-veolar type cells. Finally, type 0 CPAMsoriginate from tracheobronchial struc-tures. Currently, a more simplifiedclassification consisting of microcystic(cysts less than 1 cm) or macrocystictypes has also been suggested (8).

Depending on its type, CPAM canbe seen as a hyperechoic solid lesion,a cystic lesion or a mixed cystic/sol-id mass on prenatal US (Fig. 4). Thepostnatal radiological appearance ofCPAM depends on histologic type,presence of residual fetal fluid, orsuperimposed infection (2630). Onplain radiography and CT, mixedair filled (often with air-fluid levels)cystic and solid components are seen(Figs. 5, 6). A normal subdiaphrag-matic bowel gas pattern helps to dif-ferentiate this anomaly from a con-genital diaphragmatic hernia (CDH).However, change of appearances in

Figure 3. Cystic esophagealduplication. Axial T1-weightedMR image through the aorticarch demonstrates a well-defined low signal intensitymediastinal mass.

Figure 4. Congenitalpulmonary airwaymalformation. Fetal USimage through the righthemithorax in parasagittalplane shows a lung masswith solid and cystic areas(arrowheads).


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Kocaolu et al.ivDiagnostic and Interventional Radiology

position and paucity of bowel gas inthe abdomen with CDH are helpful indiagnosis. Moreover, US can show thediaphragmatic defect. Large-cyst type

CPAM should be differentiated fromlow-grade pleuropulmonary blastomaand pneumatocele (Fig. 7) (31, 32). In-flammatory findings of air spaces and

pleural fluid may be present with su-perimposed infection (3034). Associ-ated abnormalities such as BC can alsobe disclosed by CT (Fig. 8).

baFigure 5.a, b. Congenitalpulmonary airway malformation.Frontal chest radiograph (a)demonstrates a heterogeneousbubbly mass in the left lungdisplacing the mediastinal structuresto the opposite site. Axial CTimage (b) through lung basesshows multiple airfilled cysts withheterogeneous soft tissue density.

ba

Figure 6.a, b. Type I (macrocystic) congenital pulmonary airwaymalformation. Frontal chest radiograph (a) shows a right lung mass with airfluid levels. Corresponding axial CT image (b) through the hilar level confirms

the multiple airfluid levels within cysts larger than 2 cm in diameter.

ba

Figure 7.a, b. Congenital pulmonary airway malformation. Frontal chestradiograph (a) shows increased lucency of the right lung with mediastinal shift.Axial CT image (b) demonstrates a huge right lung cyst.


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Bronchopulmonary foregut malformationsv

Pulmonary sequestration

Pulmonary sequestration (PS) is aportion of lung, which loses its nor-mal communication with the tra-cheobronchial tree and is suppliedby a systemic artery (or arteries), fre-quently originating either from the

thoracic and abdominal aorta or fromtheir major branches. Sequestrationsclassically have been divided intointralobar (ILS) and extralobar (ELS)types, in which the former accountsfor 75% of all PS.

ILS is contained within the vis-ceral pleura of the remainder of thelobe, typically the posterior lateralsegment of the lower lobe, and hasa systemic arterial blood supply (thethoracic or abdominal aorta or one ofits primary branches). ILS usually hasnormal pulmonary venous drainage(rarely systemic venous drainage to

the hemiazygos). Langston suggestedthat ILSs can no longer be consideredacquired lesions (8). In some diseases,such as tuberculosis, bronchiectasisand pulmonary tromboembolism,hypertrophied normal systemic arter-ies may provide collateral supply tothe lung. Referring to these condi-tions as pseudosequestration may bemore accurate. Moreover, prenatal di-agnoses of ILS support its congenitalorigin.

ELS is less frequent than ILS. It iscommonly located in posterior lowerchest and enveloped by a separatepleura. The lung tissue disconnectedfrom the bronchial tree has a system-ic arterial supply with multiple feed-ers in 20% of cases (the aorta or a pri-mary branch of it), 15% of which areinfradiaphragmatic. Venous drainageis mostly systemic (azygos, hemiazy-gos, portal) as opposed to ILS. Patentconnections with foregut are muchmore common in the ELS. Intra-ab-dominal location is noted in at least5% of ELS. Ipsilateral CDH and other

associated congenital anomalies canbe seen in up to 50%.

PS presents with hyperechoic tho-racic lesions on prenatal US. DopplerUS can demonstrate systemic bloodsupply to the lesion (Fig. 9a, b). Plainradiographic appearances are vari-able, and most commonly as a well-defined, homogenous opacity in thelung base. PS may rarely be seen as anarea of hyperlucency, when aerationoccurs through existing collateralpathways. IPS may mimic malignan-cies when it has irregular margins. CTappearance is also variable, demon-strating a solid mass with or withoutcystic changes (Fig. 9c). Emphyse-matous changes around the mass areconsidered one of the characteristicCT findings of PS, which occur sec-ondary to collateral air entry (12, 35),or sometimes with coexistent bron-chial atresia or congenital lobar over-inflation (so-called hybrid lesions)(Figs. 10, 11). CT angiography can il-lustrate the aberrant artery, which is

b

a

c

Figure 8.ac. Bronchogenic cyst and type II congenital pulmonary airway malformation(CPAM). Axial contrastenhanced CT image through the azygoesophageal recess inmediastinal window setting (a) demonstrates a welldefined fluid density mass (arrow) in themiddle mediastinum. Axial CT images at the lung base in lung algorithm (b, c) demonstratethe airfilled cystic components of the CPAM.


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Kocaolu et al.viDiagnostic and Interventional Radiology

important in surgical planning. MRIcan also show the systemic arteriali-zation and venous drainage. Cath-eter angiography has mostly beenreplaced by CT angiography and MRangiography except in case of preop-erative embolization.

Congenital lobar overinflation

Congenital lobar overinflation(CLO) is characterized by progres-sive hyperexpansion of a lung lobe,almost exclusively an upper lobe orthe right middle lobe. Because of theoverdistension of otherwise normalalveoli without alveolar wall destruc-tion, the term CLO has been preferredto congenital lobar emphysema inthe description of this entity (4, 36).It is thought to occur due to check-valve mechanism or hypertrophy atthe bronchi that result in progressivehyperinflation of the lung. In half of

the cases, the etiology is unknown;however, the areas of malacia or ste-nosis of bronchial cartilage were de-tected (7, 37). In approximately 50%of cases no cause of bronchial obstruc-tion is identified, suggesting a diffuseprocess in those, such as decreasedelastic recoil of the lung parenchyma.Congenital cardiovascular anomaliesare commonly associated with CLO.Other causes of bronchial obstructionleading to lobar emphysema must beseparated out from CLO, and includebronchial stenosis or cysts, mucousplugs, lymph nodes, foreign bodies,Cytomegalovirus infection, redun-dant bronchial mucosa flaps andkinking of the bronchus caused byherniation into mediastinum.

On initial radiography, during firstfew days of life, an opaque mass maybe seen in the affected lung becauseof the delayed clearance of fetal lung

fluid. Later in life, radiography dem-onstrates hyperlucent expanded up-per or middle lobe, which can causemediastinal shift and compressionof unaffected lobes (38). CT dem-onstrates hyperexpansion with de-creased CT attenuation of the in-volved lobe, helping to differentiateCLO from CPAM type I or other cystic

lung lesions such as pneumatoceles,or persistent pulmonary interstitialemphysema (Fig. 12) (39). CT virtualbronchoscopy or multiplanar refor-matted images can demonstrate en-dobronchial pathologies, which canmimic CLO (40).

Congenital pulmonary cyst

Congenital pulmonary cysts (CPC)are very rare lesions that appear dur-ing alveolar development followingthe formation of terminal alveoli (41,42). Because of the communicationwith the tracheobronchial tree, 75%of them are air-filled; however, theymay also be fluid-filled and mass-likein appearance. CPC is normally sin-gular, located peripherally and affectsonly one lobe with a cyst diameterusually greater than 1 cm.

Unlike the BC, CPC is usually symp-tomatic. Air trapping secondary toball-valve mechanism within the cystresults in expansion and respiratorydistress in neonatal period (43). Ex-panded cysts also cause compression

of the ipsilateral lung and diaphragmwith a mediastinal shift, which resultin contralateral lung atelectasis. Thelatter worsen the respiratory compro-mise. CPC may manifest with infec-tion secondary to poor ventilation.

On plain radiography, CPC presentsas a well-defined, round, air densitymass (Fig. 13). Complicated cystscause mass effect, depressing the ip-silateral diaphragm and causing apronounced mediastinal shift (41,42). CT may be required to differenti-ate CPC from CLO. Surgical resectionis generally recommended, as mostCPCs are symptomatic.

Bronchial atresia

Bronchial atresia is an uncommoncondition secondary to focal oblitera-tion of a segmental or subsegmentalbronchus (44, 45). The alveoli distalto stenosis are ventilated by collat-eral airways and may demonstrateair trapping manifesting itself ashyperinflation around the stenosis.

ba

c Figure 9.ac. Pulmonarysequestration. PrenatalUS image at the level ofleft lung base (a) showsa hyperechoic solid lesion(arrowheads). Postnatalcolor Doppler US (b)reveals the mass (arrows)and its systemic vessels(arrowheads) originatingfrom the descendingaorta (stars: skin). Coronalreformatted postcontrastCT image (c) shows a softtissue mass with a feedingsystemic artery (arrowhead)and a draining vein (arrow)at the left lung base.


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The post-stenotic bronchus is filledby mucus to form a bronchocele. Inhalf of the cases, bronchial atresia isasymptomatic. In the neonatal pe-riod, bronchial atresia reveals fluiddensity secondary to entrapped fetalliquid. Then, the fetal liquid is re-

placed by air. Mucus accumulates indistal bronchi and bronchocele de-velops. In adults mucus plugs appearas solitary pulmonary nodule.

On plain radiography bronchoceleappears as rounded arborizing opaci-ties with or without air-fluid level.

Distal lung is hyperlucent due to airtrapping. CT better demonstratesthese features (46).

In conclusion BPFMs are heteroge-neous interrelated abnormalities thatmay contain more than one histolog-ic feature. Familiarity with the pres-

ba

c Figure 10.ac. Intralobar pulmonary sequestration with type I (macrocystic)congenital pulmonary airway malformation (CPAM). Axial, non-contrastenhanced CT image at the level of the lung bases (a) demonstrates a soft tissuemass in the posterior aspect of the left lower lobe. On axial contrastenhancedCT image (b) systemic arterial supply (arrows) to the mass from the descendingaorta is noted. Axial CT scan at a higher level (c) reveals accompanying type I(macrocystic) CPAM with large airfilled cysts.

b

a

Figure 11.a, b. Intralobar pulmonary sequestration (IPS) with type I (macrocystic) congenital pulmonary airway malformation

(CPAM) (hybrid lesion). Axial, contrastenhanced CT image (a) demonstrates a type I CPAM at a superior level to the IPSshown on (b). Coronal reformatted CT image (b) demonstrates an IPS in the posterior aspect of the left lower lobe with itsarterial supply (thin arrow) from the descending aorta and a draining vein (thick arrow).


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Kocaolu et al.viiiDiagnostic and Interventional Radiology

entation and imaging features of BP-FMs presenting as a mass-like lesionis important in management. Imag-ing plays a central role in the evalua-tion of these lesions. Selection of theappropriate modality and techniqueis fundamental in this evaluation andin differentiation from their mimick-ers. With the appropriate imagingstrategy, the presence and type of le-sion can be defined and appropriatemanagement be determined to pre-vent complications including infec-tion and respiratory compromise.

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ba

Figure 12.a, b. Congenital lobar overinflation (CLO). Frontal chestradiograph (a) shows a radiolucent area in the right hemithoraxwith mild shift of the heart to the left. Axial noncontrast enhancedCT image through the hila (b) demonstrates lung hyperinflationrepresenting CLO. Note also leftward shift of the heart.

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