High-Resolution Computed Tomography of the Lung: Normal and Abnormal Anatomy By W. Richard Webb
URING THE LAST few years, improvements in computed tomography (CT) scanner technology have aided in the development of high-resolution CT (HRCI’) techniques capable of imaging the lung with excellent spatial resolution and anatomic detail. HRCT is clearly superior to conventional CT in defining pulmonary anatomy, demonstrating both the normal and abnormal lung interstitium, and delineating morphological characteristics of localized and diffuse parenchymal processes,particularly interstitial lung diseases.Fundamental to an understanding of HRCT and its appropriate application in the diagnosis of lung pathology is an understanding of normal lung anatomy, as resolved using this technique, and alterations in normal anatomy that can be produced by different lung diseases. These will be the subject of this review.
NORMAL LUNG ANATOMY
With HRCT, it is particularly important to review the anatomy of the “secondary pulmonary lobule.” HRCT can show many features of the secondary pulmonary lobule in both normals and abnormals,‘-’ and many lung diseases, particularly interstitial lung diseases, produce characteristic HRCT findings at the lobular level. Normal HRCT lung anatomy relative to the subpleural interstitium and the parahilar bronchi and vessels will also be reviewed, as abnormalities are sometimes recognizable in these areas as well.
CT, computed tomography; HRm,
From ihe Department of Radio&, University of California, San Francisco, CA. Address reprint requeststo W. Richard Webb,MD, Profissor of Radio&v, Department of Radiology, University of California, San Francisco, CA 94143-0628. Copyright o 1991 by W B. *SaundersCompany 003%198X~91/2602-0005$5.00iQ 110
The Secondary Pulmonary Lobule
The secondary pulmonary lobule (or simply, pulmonary lobule) is a unit of lung structure made up of less than a dozen acini. To digress briefly, an “acinus” is defined as the portion of the pulmonary parenchyma arising distal to a single terminal bronchiole (the last purely conducting airway); it is the largest lung unit in which all airways participate in gas exchange and measures about 6 to 10 mm in diameter.‘S2A secondary pulmonary lobule, made up of several acini, is thus supplied by several terminal bronchioles. Lobules are irregularly polyhedral in shape, measuring approximately 1 to 2.5 cm on each side and are marginated by connective-tissue interlobular septa that are best developed in the peripheral lung and less well-developed centrally (Fig 1).3S4 Although lobules are somewhat variable in shape, in the lung periphery they are often shaped like truncated cones, with the basesof the cones located at the pleural surface and their apices directed centrally. Within the central lung, particularly at the lung base, lobules tend to be roughly hexagonal in shape. The individual anatomic components of the secondary pulmonary lobule are quite consistent. The central portion of the lobule (the lobular core) contains the pulmonary artery and bronchial branches supplying the lobule, as well as some supporting connective tissue (Fig l).l, Pulmonary veins and lymphatics lie within the connective tissue interlobular septa that marginate the lobule. The remaining lobule contains small branches of these structures, the alveoli, the pulmonary capillary bed, and a fine connective tissue (interstitial) network. High-Resolution Computed Tomography of the Secondary Lobule in Normals
On HRCT, interlobular septa are sometimes visible as very thin, straight lines of uniform thickness that are 1 to 2 cm in length and may contact the pleural surface (Fig 2); in most normal patients either the septa are hard to see or only a few are visible (Fig 3).3-7These are better seen within the peripheral lung than in Seminars
Vol XXVI, No 2 (April), 1991: pp 110-l 17
pulmonary artery and bronchiole in lobular core
pulmonary artery and bronchiole
inter IobuIarm I*=lcm Fig 1.
the central lung because of the better development of septa in this location. Branching vessels seen in relation to the septa represent veins. A linear, branching, or dot-like density seen within a lobule or within a centimeter of the pleural surface represents the intralobular artery branch (Figs 2 and 3). The visible lobular arteries are not seen to extend to the pleural surface in the absence of atelectasis. The intralobular bronchi or bronchioles are not normally visible because their walls are too thin (Figs 2 and 3). Fissures and the Subpleural Interstitium
The peripheral interlobular septa are contiguous with an interstitial compartment that ex-
Fig 2. Normal lung anatomy on HRCT. HRCT of a fresh, iM lung obtained at autopsy from a normal subject. A normal secondary pulmonary lobule is marginated by thin interlobular septa (large anows) that are faintly visible. The artery branch in the center of the lobule is seen as e [email protected]
branching struc4ure (smell arrow). The intralobular bronchii is not visible. Septa along the mediaf lung surface lopn arrows) ara thkkanod by fluid. Note that tha walls of tfta large bronchi and vessels that ore viafble are smooth and sharply deffned. The pleural surface adjacant to the fissure is likewiaa smooth. (Reprinted with permission.‘)
tends over the surface of the lung, beneath the pleural membrane (the subpleural interstitium). Interstitial lung diseases that affect the interlobular septa also cause abnormalities of the subpleural interstitium, which can sometimes be recognized over the costal surfaces of the lung but are more easily seen in relation to the major fissures where two layers of the pleura along with the subpleural interstitium (from different lobes) come in contact. In all locations, the normal fissures and subpleural interstitium should appear smooth and of uniform thickness (Figs 2 and 3). In contrast to conventional CT, in which the obliquely oriented major fissures are usually poorly seen, the major fissures are consistently seen as continuous smooth thin lines on HRCT. Normal fissures are less than 1 mm thick, except laterally where a small amount of subpleural fat can appear as a triangular radioopacity at its point of contact with the chest wall. The minor fissure is variable in appearance and visibility, depending on its orientation relative to the scan plane. Because the fissure lies roughly parallel to the scan plane, it is not particularly useful in diagnosing lung disease. Parahilar Structures
Central bronchi and pulmonary arteries are surrounded by interstitial tissue, part of the so-called “axial” interstitium described by Wei-
Fig 3. Normal HRCT. In this subject, there is a small nodule in the anterior right lung, but the lungs are otherwise normal. No clearly deflned interlobular septa are visible. Vessels within 1 cm of the pleural surface (arrows) probably represent intralobular arteries. Note the smooth contours of central bronchi, large vessels, and fissures. Some streaky densities adjacent to the left heart border are artifacts commonly seen because of cardiac pulsation.
bel.* Some lung diseases produce thickening of the axial interstitium in the central or parahilar lung which can be recognized on HRCT (or for that matter plain radiographs) as “peribronchial cuffing.” Thus, it is important to be aware of the normal appearance of these structures. The central pulmonary arteries are normally visible as broad linear densities accompanied by uniformly thin-walled bronchi with the diameter of a vessel and bronchus being approximately equal. The parts of the walls of the pulmonary artery and adjacent bronchus that contact lung appear smooth and sharply defined (Figs 2 and 3). HIGH-RESOLUTION COMPUTED TOMOGRAPHY FINDINGS IN ABNORMALS
Septal Thickening Thickening of the interlobular septa can be seen in patients with a variety of interstitial lung diseases. Within the peripheral lung, one or more thickened septa (1 to 2 cm in length) may outline part of, or an entire lobule and are usually seen extending to the pleural surface.3 Often, thickened septa within the peripheral lung are associated with some overlying pleural (or subpleural interstitial) thickening or thickening of a fissure. Within the central lung, the thickened septa can outline an entire lobule (1 to 3 cm in diameter), which appears hexagonal or polygo-
nal in shape and commonly contains a visible, central artery branch. Longer septa, several centimeters in length, that marginate more than one lobule, can also be seen on HRCT and may give the appearance of “parenchymal bands.“’ Areas of subsegmental or disc atelectasis or coarse scarring can have a similar appearance. Septal thickening can be seen as a result of edema fluid (Fig 2), tumor infiltration (ie, lymphangitic spread of carcinoma) (Fig 4), or fibrosis (Figs 5 and 6). In lymphangitic spread of carcinoma, the septal thickening is usually smooth or sometimes nodular (Fig 4).l”-12In patients with fibrosis, septal thickening is often very irregular (Fig 5).3,6*9,‘2,13 Intralobular Lines Interstitial disease associated with interlobular septal thickening, regardless of its cause, is often associated with thickening of the intralobular interstitial network. This can result in the presence of a fine network of lines within the lobule, sometimes seen in relation to small arterial or bronchiolar branches.3,‘f10*13 The presence of these lines gives the intralobular artery a spiderlike appearance that is not normally seen (Fig 5). The intralobular lines extend peripherally from the centrilobular vessel to join the thickened septa surrounding the lobule. When thickening of the intralobular intersti-
ening of interlobular aepta (black arrows)whk9lhcharacteristkof this disease. lhkkenlng of the fissure (white arrowe) rdects involvement of the subpleural interstltlum. The thlckenhrg of the septa and flsaurar is smooth or nodular in appearance. Bronchi (open arrow) in the right upper lobe appear thkk-wafled because of peribronchial cuffing. (Reprinted with permission.“)
tium is generalized, it gives the lung a fine netlike appearance.” Centrilobular Abnormalities
Visibility of the (normally invisible) intralobular bronchiole or prominence of the centrilobular vessel (dot) are often seen in patients with interstitial thickening because of thickening of
the peribronchial and perivascular interstitium (Fig 5); usually other findings of interstitial thickening (eg, septal thickening) will also be visible.3,5 It is analogous to “peribronchial cuffing” described below. Occasionally, diseases involving small bronchi such as cystic fibrosis14~1S also result in visibility of the intralobular bronchiole (Fig 7) or prominence of the centrilobu-
flbrosls and hone-. Findfngs of Fig 5. Findings of pulmonary flbrosii. An bdlated lung in a patient wltb puhomry pulmonary fibros&~ lnaMa irregular sef~tal thickening (black arrows), IntmWMar bandc of ffbrosb aausing a netflke or Wderweb bromdMefdWa-)~ ap~rsnteth~hvkgk~lhekrkrbindi~dbythe~~om.~d~~r inter&M thickening, irregular inar(acas at the adgas of vessels and brombl, pa#@mWM eufflng, of dllatatlon and swmwbWg and traction bro&WW& (open arrow). Gross honeycomb cysts having thick walls are visible within ti posterior lung (on the left of the image). (Reprinted with permission.‘)
Fig 6. Pulmonary fibrosis. Findings of fibrosis in a patient with sarcoidosis include septal thickening, some intralobular lines, and irregularity of the left major fissure and at the edges of vessels and bronchi. Central bronchi appear thick-walled because of peribronchial cuffing.
lar vessel, but other findings of interstitial thickening will usually be absent. Znte$ace Signs
If thick septa or intralobular lines contact pulmonary vessels,bronchi, fissures, or the pleural surface, they result in irregular interfaces between these structures and the adjacent airfilled lung. Such irregular edges have been termed “interface signs” and are a clue to the presence of interstitial thickening (Figs 5 and
many diseasesthat cause generalized interstitial thickening. This can result in a “nodular” appearance of the pulmonary vessels,” or apparent bronchial wall thickening (Figs 4-6)>l” equivcuffing” on plain alent to “peribronchial radiographs. This finding is particularly common in patients with lymphangitic spread of carcinoma. In patients with pulmonary fibrosis, peribronchial cuffing can be associated with dilatation of bronchi called “traction bronchiectasis” (Fig 5).
6)? Peribronchial Cufing
Thickening of the interstitium surrounding the parahilar vessels and bronchi occurs in
Small or miliary nodules, 1 to 2 mm in diameter, can be detected on HRCT in patients
Fig 7. Cystic fibrosis with bronchial abnormalities. HRCT in a young girl with cystic fibrosis shows branching intralobular bronchioles (arrow) that are filled with mucus or pus. Central bronchi are abnormally thick-walled. (Reprinted with permission.“)
Fig 8. Inter&M nodules in sarcoidosic. In a patlent with blopsyproven swcokkk, smelt wdules (arrows) 8m visible wltbln tbe hang [email protected]
su&ae end fissure. Compere the abnormal left side wltb the normal right side. (Fkprinted with permission.“)
with granulomatous diseasessuch as sarcoidosis (Fig g),“.” silicosis,” tuberculosis,’ and eosinophilic granuloma, and in patients with metastatic tumor. They can represent active granulomas in patients with sarcoidosis or nodular areas of fibrosis.16In patients with lymphangitic spread, nodules of tumor can be seen involving interlobular septa.” Small nodules can also be seen in patients with air-space consolidation,20 evidently representing peribronchiolar areas of airspace filling. This appearance is not uncommon in patients
with so-called lobular pneumonia.’ We have also seen it in patients with organizing pneumonia with bronchiolitis obliterans (BOOP). Honeycombing
Fibrosis associated with areas of lung destruction and disorganization of lung architecture (honeycombing) results in a characteristic cystic appearance on HRCT (Figs 6 and 9)“335,6213 Honeycombing results in cystic spaces several millimeters to several centimeters in diameter that are often peripheral in location and are charac-
In a pa-
ti=t*idioprthicptdmonHy flbro&onMapy,rmcTsbows -*ofhoneycombirrg. Small thi&-w8lled cystetb8t8wew8&8mvwbla illtM#M#@?&~.~l t#dek~Plrllrhlnt8se~md afees. &?eprinted with permission.“)
Fig 10. Ground-glass density. in a patient with idiopathic puimonary fibrosis, hazy increased density involves the lung with a patchy distribution. This represented active disease when biopsy was performed. Over the next year, the lung disease progressed to honeycombing.
terized by thick, clearly definable walls. Honeycombing is often associated with septal thickening, intralobular bands, interface signs, and thickening of the fissures. Also, intralobular bronchioles are often visible on HRCT in patients with honeycombing because of a combination of bronchiolectasis and thickening of the peribronchiolar interstitium. In patients with septal thickening, the presence of honeycombing can help distinguish fibrosis from other causes of septal thickening (eg, lymphangitic spread of tumor and pulmonary edema). The Subpleural Line A curvilinear density less than 1 cm from the pleural surface and paralleling the pleura was
Fii 11. Emphysema. Cystic areas do not have visible wails except where margineted by interlobular septa.
first described in patients with asbestosis,” and it was suggested that this line represented fibrosis. Indeed, this is the case in some patients. However, in other patients this finding simply reflects atelectasis.5 “Ground-Glass” Density In some patients with minimal airspace consolidation or minimal alveolar wall thickening as a result of interstitial disease, a hazy and often geographic increase in density can be observed on HRCT (Fig 10),5v8affecting some areas of lung and sparing others. This appearante is nonspecific but often indicates an ongoing, and potentially treatable, process such as
pulmonary edema, alveolitis,2’ pneumonia, desquamative interstitial pneumonitis,5 alveolar proteinosis,23or pneumocystis carinii pneumonia. Cystic Lung Destruction
Emphysema is the most common cause of lung destruction, but other diseases produce this appearance as well. Emphysema results in
focal areas of very low density that can be easily contrasted with surrounding, higher density, normal lung parenchyma if sufficiently low window means ( < -600 Hounsfield units [HI) are used.3,5,24 Emphysema is distinguishable from honeycombing in that the cystic areas lack visible walls (Fig 11). Honeycombing and emphysema can coexist in the same patient.
REFERENCES 1. Osborne DRS, Effmann EL, Hedlung LW: Postnatal growth and size of the pulmonary acinus and secondary lobule in man. AJR 140:449-454,1983 2. Raskin SP: The pulmonary acinus. Radiology 144:3134,1982 3. Webb WR, Stein MG, Finkbeiner WE, et al: Normal and diseased isolated lungs: High resolution CT. Radiology 16681~87,1988 4. Bergin C, Roggli V, Coblentz C, et al: The secondary pulmonary lobule: Normal and abnormal CT appearances. AJR 151:21-251988 5. Webb WR: High-resolution CT of the lung parenchyma. Radio1 Clin North Am 27:1085-1097,1989 6. Meziane MA, Hruban RH, Zerhouni EA, et al: High resolution CT of the lung parenchyma with pathologic correlation. Radiographics 8:27-54,1988 7. Murata K, Itoh H, Todo G, et al: Centrilobular lesions of the lung: Demonstration by high-resolution CT and pathologic correlation. Radiology 161:641-645,1986 8. Weibel ER: Looking at the lung: What can it tell us? AJR 133:1021-1031,1979 9. Aberle DR, Gamsu G, Ray CS, et al: Asbestos-related pleural and parenchymal fibrosis: Detection with highresolution CT. Radiology 166:729-734,1988 10. Stein MG, Mayo J, Miiller N, et al: Pulmonaty lymphangitic spread of carcinoma: Appearance on CT scans.Radiology 162:371-3751987 11. Munk PL, Miiller NL, Miller RR, et al: Pulmonary lymphangitic carcinomatosis: CT and pathologic findings. Radiology 166:705-709,1988 12. Zerhouni EA, Naidich DP, Stitik FP, et al: Computed tomography of the pulmonary parenchyma. Part 2: Interstitial disease. J Thorac Imaging 1:54-64, 1985 13. Miiller NL, Miller RR, Webb WR, et al: Fibrosing alveolitis: CT-pathologic correlation. Radiology 160:585588,1986
14. Akira M, Kitatani F, Yong-Sik L, et al: D&se panbronchiolitis: Evaluation with high-resolution CT. Radiology 168:433-438,1988 15. Lynch DA, Brasch RC, Hardy KA, et al: Pediatric pulmonary disease: Assessment with high-resolution ultrafast CT. Radiology 176:243-248,199O 16. Lynch DA, Webb WR, Gamsu G, et al: Computed tomography in Sarcoidosis. J Comput Assist Tomogr 13:405410,1989 17. Brauner MW, Grenier P, Mompoint D, et al: Pulmonaty sarcoidosis: Evaluation with high resolution CT. Radiology 172:467-471,1989 18. Miiller NL, Kullnig P, Miller RR: The CT findings of pulmonary sarcoidosis: Analysis of 25 patients. AJR 152: 1179-1182,1989 19. Bergin Cl, Muller NL, Vedal S, et al: CT in silicosis: Correlation with plain films and pulmonary function tests. AJR 146:477-483,1986 20. Naidich DP, Zerhouni EA, Hutchins GM, et al: Computed tomography of the pulmonaty parenchyma. Part 1: Distal air-space disease. J Thorac Imaging 1:39-53,1985 21. Yoshimura H, Hatakeyama M, Otsuji H, et al: Pulmonary asbestosis: CT study of subpleural curvilinear shadow. Radiology 158:653-658,1986 22. Miiller NL, Staples CA, Miller RR, et al: Disease activity in idiopathic pulmonary fibrosis: CT and pathologic correlation. Radiology 165:731-734,1987 23. Godwin JD, Miiller NL, Takasugi JE: Pulmonary alveolar proteinosis: CT findings. Radiology 169:609-613, 1988 24. Hruban RH, Meziane MA, Zerhouni EA, et al: High resolution computed tomography of inflation-fixed lungs: Pathologic-radiographic correlation of centrilobular emphysema. Am Rev Respir Dis 136:935-940,1987 25. Webb WR, Klein JS: High-resolution CT of the lung parenchyma: A primer. Perspect Radio1 3:1-24, 1990