Technical Considerations

The views of the chest most frequently performed are the erect posteroanterior and lateral projections, taken with the patient’s breath held at total lung capacity. On a frontal (posteroanterior) chest radiograph, just under half of the lung is free from overlying structures, such as the ribs or diaphragm. Many technical factors determine how well the lungs are demonstrated. The characteristics of current digital imaging systems make it possible to adjust the final image and optimize exposure of the least and most dense parts of the chest in a single are image.

Because the coefficients of x-ray absorption for bone and for soft tissue approach one another at high kilovoltage, the skeletal structures do not obscure the lungs on a higher-kilovoltage radiograph to the same degree as on low-kilovoltage radiographs. The high-kilovoltage radiograph thus demonstrates much more of the lung. Improved penetration of the mediastinum also allows some of the central airways to be seen. Although high-kilovoltage radiographs are preferable for routine examinations of the lungs and mediastinum, low-kilovoltage radiographs provide good detail of unobscured lung because of the improved contrast between lung vessels and surrounding lung. Furthermore, dense lesions—for example, calcified pleural plaques—are particularly well demonstrated on low-kilovoltage films.

The past decade has seen a major change in plain film radiography with the development of digital imaging systems, which are now ubiquitous in modern radiology departments. Digital chest radiography, yielding images either stored on a phosphor plate and then digitally scanned or captured directly onto a detector plate, has been combined with computer-based picture archiving and communications systems (PACSs) for distribution of images around the hospital or over wider networks. The much wider latitude of digital systems also allows the image to be “postprocessed” to provide optimum visualization of the relevant structures

The frontal (posteroanterior) (Figure 7-1) and lateral (Figure 7-2) projections are sufficient for most purposes in chest radiography. Other radiographic views are less frequently required, but they should not be overlooked because they may solve a particular problem quickly and cheaply. The lateral decubitus view is not, as its name implies, a lateral view. It is a frontal view taken with use of a horizontal beam and the patient in a side-lying position. Its main purpose is to demonstrate the movement of fluid in the pleural space (Figure 7-3). An adaptation of this view is the “lateral shoot-through” sometimes used in bed-bound patients: A lateral radiograph of the supine patient is taken to show an anterior pneumothorax behind the sternum (not always visible on a frontal chest radiograph) (Figure 7-4). If a pleural effusion is not loculated, it gravitates, to some extent, to the dependent part of the pleural cavity. Thus, in a decubitus patient, the fluid will layer between the chest wall and the lung edge. This view also may be useful for demonstrating a small pneumothorax, because the visceral pleural edge of the lung falls away from the chest walls in the nondependent hemithorax.

Figure 7-1 A standard digital posteroanterior radiograph demonstrating the wide latitude that can be routinely achieved. This image provides good detail of both lung and mediastinal anatomy.

Figure 7-2 Standard lateral chest radiograph. The dorsal spine vertebral bodies are of progressively lower density toward the diaphragm. The metallic density over the cardiac silhouette is an atrial septal defect closure device.

Figure 7-3 Demonstration of small effusions. A, Posteroanterior chest radiograph obtained in a patient with a ventriculoperitoneal shunt. More soft tissue than usual is present between the gastric air bubble and the base of the lung because of a subpulmonic effusion. B, Decubitus view shows redistribution of fluid to the dependent part of the chest (arrows).

Figure 7-4 Lateral shoot-through digital radiograph of the chest obtained in a patient in the intensive care unit. The anterior pneumothorax (arrowheads indicate the visceral pleural edge) was not obvious on the anteroposterior portable radiograph.

For the lordotic view, now rarely performed, the x-ray beam is angled 15 degrees cranially, either by positioning the patient upright and directing the beam up or by leaving the beam horizontal and leaning the patient backward. On this view, the lung apices are demonstrated free from the superimposed clavicle and first rib. It may be useful to differentiate pulmonary shadows from incidental calcification of the costochondral junctions (Figure 7-5).

Figure 7-5 The value of lordotic views. A, Method of obtaining a lordotic view of the lung apices: The x-ray beam is angled upward. B, Selected area from a standard posteroanterior view of the upper lung zones in a patient who presented with hemoptysis, with a suggestion of a small opacity projected over the anterior end of the left first rib. C, A lordotic view confirms that the small opacity is intrapulmonary (rather than calcified costochondral cartilage).

Portable Chest Radiography

Portable or mobile chest radiography has the obvious advantage that the examination can be carried out without moving the patient from the ward. However, the portable radiograph has disadvantages. Use of the shorter-focus film distance results in undesirable magnification, and most portable machines are unable to deliver the power required for high-kilovoltage techniques. Furthermore, the maximum current is limited so that longer exposure times are needed, which potentially increases blurring of the image. Portable lateral radiographs are even less likely to be successful because of the extremely long exposure times required to obtain adequate penetration.

Patient positioning for portable radiography is difficult, and the resultant radiographs often are suboptimal. Even with use of the so-called erect position, in which the patient sits up, the chest is rarely as vertical as it is in a standing patient. Because many patients are unable to move to the radiography department for a formal radiograph, any method of improving the quality of a portable chest radiograph, such as digital radiography, represents a significant advance.

Digital Chest Radiography

The most widely employed systems use conventional radiographic equipment but use a reusable photostimulatable plate instead of conventional film. The reusable phosphor plate is housed in a cassette and stores some of the energy of the incident x ray as a latent image. On scanning the plate with a laser beam, the stored energy is emitted as light that is detected by a photomultiplier and converted into a digital signal. The digital information is then manipulated, displayed, and stored in whatever format is desired. The phosphor plate can be reused once the latent image has been erased by exposure to light. Most currently available computed radiography systems produce a digital radiograph with a resolution of more than 10 line pairs per millimeter. The fundamental requirement to segment the image into a finite number of pixels has resulted in much work to determine the relationship between pixel size, which affects spatial resolution, and the detectability of focal abnormalities. Although it might seem desirable to aim for an image composed of pixels of the smallest possible size, an inverse relationship occurs between pixel size and the cost and speed of data handling. Thus, pixel size is ultimately a compromise between image quality and ease of data processing and storage.

An unequivocal advantage of digital computed radiography over conventional film radiography is the linear photoluminescence-dose response, which is much greater than that of conventional film. This extremely wide latitude coupled with the facility for image processing produces diagnostic images over a wide range of exposures.

Observer performance studies have shown that computed radiography is just as useful as conventional film radiography for virtually any relevant application. However, postprocessing of the digital image has to be used to match the digital radiograph to the specific task. Enhancement of the image for one purpose often degrades it for another but is easily achieved in most PACS reporting systems.

Technical Considerations

The CT image is composed of a matrix of picture elements (pixels). A fixed number of pixels make up the matrix, so the size of each pixel varies according to the diameter of the circle to be scanned. A typical matrix in a modern CT system would be 512 by 512 pixels. The smaller the image field of view, the smaller the area represented by a pixel and the higher the spatial resolution of the image. In practical terms, the field of view size is adjusted to the size of the area of interest, usually the chest diameter.

Often, marked differences can be seen in the “look” of the images obtained on the various models of CT scanners. Such differences are largely the result of specific features of the software reconstruction algorithms used to smooth the image, to a greater or lesser extent, by averaging the density of neighboring pixels. The lung is a high-contrast environment, so less smoothing is needed than in other parts of the body. Higher-spatial-resolution algorithms (which make image “noise”—a granular appearance—more conspicuous) generally are more desirable for lung work.

Section Thickness

Although a CT section is viewed as a two-dimensional image, it has a third dimension of depth. The depth, or section thickness, is determined by a combination of factors, depending on the exact parameters utilized, including focal spot size, thickness of the individual detector elements, and width of the x-ray beam collimation. Because a section has a predetermined thickness, each pixel has a volume and this three-dimensional element is referred to as a voxel. The computer calculates the average radiographic density of tissue within each voxel, and the final CT image consists of a representation of the numerous voxels (not individually visible without magnification) in the section. The single attenuation value of a voxel represents the average of the attenuation values of all of the various structures within the voxel. The thicker the section, the greater the chance that different structures will be included within the voxel and the greater the signal averaging that occurs. This is known as the partial volume effect; the easiest way to reduce this effect is to use thinner sections (Figure 7-8).

Figure 7-8 The partial volume effect on computed tomography (CT) scan appearance. A, This 10-mm CT section shows a poorly defined opacity, adjacent to the left superior mediastinum, apparently within the lung. B, The 1.5-mm section through the same region reveals that the appearance in A results from a partial volume effect—that is, the aortic arch is partially included in the 10-mm-thick sections.

When the entire chest is examined, contiguous thin sections are reconstructed for analysis. If the study is undertaken on a multichannel system, the dataset may be reconstructed at thinner intervals predetermined by the thickness of the detector rows, and these thinner sections may be used for reporting or multiplanar reconstructions. Thinner sections also are used to study fine detail and complex areas of anatomy, such as the aortopulmonary window and subcarinal regions. Another specific example for which narrow sections may be useful is to display differential densities (which would otherwise be lost because of the partial volume effect) of the small foci of fat or calcium that are sometimes seen within a hamartoma.

If exposure factors are otherwise kept the same, the total patient radiation dose varies very little between different multichannel systems. Of note, however, a striking difference in the radiation dose to the patient is associated with use of contiguous sections versus interspaced fine sections. Thus, the effective dose to the patient with interspaced fine sections (e.g., 1 or 2 mm) every 10 mm, such as used for high-resolution CT of the lung parenchyma, is 5 to 10 times less than that imposed by single-channel or multichannel spiral CT of the entire chest volume. The disadvantage of interspaced sections is the inability to view the data in any plane, but for the purposes of assessment of the lung interstitium, this added refinement usually is not of sufficient added diagnostic value to warrant the increased radiation burden. This consideration is especially important in the relatively younger patient.

Window Settings

The average density of each voxel is measured in Hounsfield units (H); these units have been arbitrarily chosen so that zero is water density and −1000 is air density. The span of Hounsfield units reflecting density in the thorax is wider than in any other part of the body, ranging from that for aerated lung (approximately −800 H) to that for ribs (+700 H). Two variables are used that allow the operator to select the range of densities to be viewed—window width and window center (or level).

The window width determines the number of Hounsfield units to be displayed. Any densities greater than the upper limit of the window width are displayed as white, and any below the limit of the window are displayed as black. Between these two limits, the densities are displayed in shades of gray. The median density of the window chosen is the window center or level; this center can be moved higher or lower as desired, thus moving the window up or down through the range. The narrower the window width, the greater the contrast discrimination within the window. No single window setting can depict the wide range of densities encountered in the chest on a single image. For this reason, at least two sets of images are required to demonstrate the lung parenchyma and soft tissues of the mediastinum, respectively (Figure 7-9). Standard window widths and centers for thoracic CT vary between departments, but generally for the soft tissues of the mediastinum, a window width of 400 to 600 H and a center of +30 H is appropriate. For the lungs, a wide window of 1500 H and a center of approximately −500 H are usually satisfactory. For bones, the widest possible window setting at a center of +30 H is best.

Figure 7-9 The effect of window settings on computed tomography scan appearance. A 5-mm-thick computed tomography section is displayed on different window settings. A, On lung windows (center, 500 H; width, 1500 H), nodules in the lungs and pulmonary vessels are clearly visible. B, On soft tissue windows (center, 35 H; width, 400 H), the contrast-enhanced vessels in the mediastinum and the soft tissue structures are delineated, but the lung detail is lost.

Window settings have a profound influence on the size and conspicuity of normal and abnormal structures. Nonetheless, it is impossible to prescribe precise window settings because of the element of observer preference and also differences between machines. The most accurate representation of an object seems to be achieved if the value of the window level is halfway between the density of the structure to be measured and the density of the surrounding tissue. For example, the diameter of a pulmonary nodule, measured on soft tissue settings appropriate for the mediastinum, will be grossly underestimated. When inappropriate window settings are used, imaging of smaller structures (e.g., peripheral pulmonary vessels) will be affected proportionately much more than that of larger structures.

Intravenous Contrast Enhancement

Intravenous contrast enhancement is needed only in specific instances, because of the high contrast on CT between vessels and surrounding air in the lung and between vessels and surrounding fat within the mediastinum. One such instance is to aid the distinction between hilar vessels and a soft tissue mass. The exact timing of the injection of contrast material depends most on the time the CT scanner takes to scan the thorax. With multichannel CT scanners, the circulation time specific for the patient becomes an important factor.

Contrast medium rapidly diffuses out of the vascular space into the extravascular space, so that opacification of the vasculature after a bolus injection with a “power injector” quickly declines, and structures such as lymph nodes steadily increase in density over time. Such dynamics result in a point at which a solid structure may have exactly the same density as an adjacent vessel. The timing and duration of the contrast medium infusion must therefore be taken into account in interpreting images obtained in a contrast-enhanced CT study. Rapid scanning protocols with automated injectors tend to improve contrast enhancement of vascular structures at the expense of enhancement of solid lesions because of the rapidity of scanning. With spiral CT, it is possible to achieve good opacification of all of the thoracic vascular structures by using small volumes of contrast material. Optimal contrast enhancement is a prerequisite for the diagnosis of pulmonary embolism or aortic and great vessel abnormalities. To achieve optimal contrast enhancement, many CT systems now use an automated triggering system. Thus, in examining the pulmonary arteries, a low-dose repeating scan will monitor the density in the pulmonary outflow tract once every second. When a predetermined density threshold is reached as a result of the arrival of intravenous contrast, the preplanned examination is triggered. The couch rapidly moves the patient from the monitoring position to the start position, a prerecorded breath-hold instruction is given to the patient over a loudspeaker, and the data acquisition commences. The acquisition is timed to correspond with appropriate enhancement of anatomic structures if contrast has been administered.

For examining inflammatory lesions, such as the reaction around an empyema, it may be necessary to delay scanning by 30 seconds, to allow contrast to diffuse into the extravascular space. For examining the liver and adrenals in evaluation of a patient with suspected lung cancer, the optimal phase of contrast enhancement to maximize the conspicuity of hepatic metastases is during the portal venous phase of contrast enhancement, and this occurs 60 to 80 seconds after contrast injection.

Technical Considerations

Over the past two decades, the development of high-resolution computed tomography (HRCT) has had great impact on the approach to the imaging of diffuse interstitial lung disease and bronchiectasis. Images of the lung produced by HRCT correlate closely with the macroscopic appearance of pathologic specimens, so in the context of diffuse lung disease, HRCT represents a substantial improvement over chest radiography. Three factors associated with significantly improved spatial resolution of CT—hence the designation “high-resolution”—are narrow beam collimation, use of a high-spatial-frequency reconstruction algorithm, and a small field of view.

Narrow collimation of the x-ray beam reduces volume averaging within the section and so increases spatial resolution compared with standard 10-mm collimation. For routine HRCT scanning, 1.50-mm beam collimation generally is regarded as optimal. Narrow collimation has a marked effect on the appearance of the lungs, notably the vessels and bronchi—the branching vascular pattern seen particularly in the midzones on standard 10-mm sections has a more nodular appearance with narrow sections, because shorter segments of the obliquely running vessels are included in the section. In addition, parenchymal details become more clearly visualized (Figure 7-10).

Figure 7-10 The effect of computed tomography (CT) section thickness and edge enhancement on image appearance. A, A 10-mm-thick section reconstructed with edge enhancement from a multidetector CT (MDCT) dataset. B, A 1.5-mm-thick section with high edge enhancement from the same dataset, typical of a high-resolution CT (HRCT) lung image from a volume acquisition.

In HRCT lung imaging, a high-spatial-frequency algorithm is used to take advantage of the inherently high-contrast environment of the lung. The high-spatial-frequency algorithm (also known as the edge-enhancing, sharp, or formerly “bone” algorithm) reduces image smoothing and makes structures visibly sharper but at the same time makes image noise more obvious (see Figure 7-10).

Several artifacts are consistently identified on HRCT images, but they do not usually degrade the diagnostic content of the images. Nevertheless, it is useful to be able to recognize the more common ones. Probably the most frequently encountered is a streaking appearance, which arises from patient motion. Cardiac motion sometimes causes movement of the adjacent lung with consequent degradation of image quality. Some CT scanners are able to eliminate this artifact by triggering the acquisition of the slice from the electrocardiogram (ECG) tracing so that the data are collected during diastole, when cardiac motion is minimized. To optimize this technique, the scanner must have a short rotation time and also be capable of formatting a CT image from data from a partial rotation. This reduces the data acquisition time window to as little as 360 msec.

The size of the patient has a direct effect on the quality of the lung image—the larger the patient, the more conspicuous the noise, which is seen as granular streaks because of increased x-ray absorption by the patient. This artifact is particularly evident in the posterior lung adjacent to the vertebral column. The phenomenon of aliasing results in a fine, streaklike pattern radiating from sharp, high-contrast interfaces. The severity of the aliasing artifact is related to the geometry of the CT scanner, and, unlike quantum mottle, aliasing is independent of the radiation dose. These artifacts are exaggerated by the nonsmoothing, high spatial-resolution reconstruction algorithm but do not mimic normal anatomic structures and are rarely severe enough to obscure important detail in the lung parenchyma (Figure 7-11).

Figure 7-11 High-resolution computed tomography image demonstrating artifact caused by aliasing and quantum mottleing. Detail is obscured in the posterior parts of the lungs. The patchy parenchymal opacification results from desquamative interstitial pneumonitis.

The degree to which HRCT samples the lung depends primarily on the spacing between the thin sections. An HRCT examination also may vary in terms of the number of sections, the position of the patient, the phase in which respiration is suspended, the window settings at which the images are displayed, and the manipulation of the image by postprocessing. No single protocol can be recommended to cover every eventuality. However, the simplest protocol entails 1.5-mm collimation sections at 20-mm intervals from apex to lung bases. Any given scanning protocol may need to be modified—a patient referred with unexplained hemoptysis ideally is scanned with contiguous standard sections through the major airways (to show a small endobronchial abnormality) and interspaced narrow sections through the remainder of the lungs (to identify bronchiectasis).

When early interstitial disease is suspected, for example, in asbestos-exposed persons in whom the chest radiograph is normal in appearance, HRCT scans often are performed with the patient in the prone position, to prevent any confusion with the increased opacification seen in the dependent posterior basal segments in many normal subjects scanned in the usual supine position. The increased density seen in the posterior dependent lung with supine positioning disappears in normal persons when the scan is repeated at the same level with prone positioning. No advantage is gained by scanning a patient in the prone position if no obvious diffuse lung disease is found on a contemporary chest radiograph.

A limited number of scans taken at end expiration can reveal evidence of air trapping caused by small airway disease, which may not be detectable on routine inspiratory scans. Areas of air trapping range from a single secondary pulmonary lobule to a cluster of lobules that give a patchwork appearance of low attenuation areas adjacent to higher attenuation, normal lung parenchyma (Figure 7-12).

Figure 7-12 A, High-resolution computed tomography (CT) scan through the lower lung lobes of a patient with severe asthma. The inspiratory image through the upper zones is normal. B, A high-resolution CT image at end expiration emphasizes the regional air trapping due to small airways obstruction.

Alterations of the window settings of HRCT images sometimes make detection of parenchymal abnormalities impossible when there is a subtle increase or decrease in attenuation of the lung parenchyma. Uniformity of window settings from patient to patient aids consistent interpretation of the lung images. In general, a window level of −500 to −800 HU and a width of between 900 and 1500 HU are usually satisfactory. Modification of the window settings for particular tasks is often desirable; for example, in looking for pleuroparenchymal abnormalities in asbestos-exposed patients, a wider window of up to 2000 HU may be useful. Conversely, a narrower window of approximately 600 HU may emphasize the subtle density differences that characterize emphysema and small airway disease.

The relatively high radiation dose to the patient inherent in all CT scanning needs to be appreciated. The radiation burden to the patient is considerably less with HRCT than with conventional CT scanning. It has been estimated that the mean radiation dose delivered to the skin with HRCT by use of 1.5-mm sections at 20-mm intervals is 6% that of conventional 10-mm contiguous scanning protocols. A further method of reducing the radiation burden to the patient is to decrease the milliamperage; it is possible to reduce the milliamperage by up to 10-fold and still obtain comparably diagnostic images. Although continuous refinement in CT technology is reducing the radiation burden to patients, CT still delivers a relatively high radiation dose to patients, so this imaging modality must not be used indiscriminately.

Clinical Applications of High-Resolution Computed Tomography

Increasingly, HRCT is used to confirm or refute the impression of an abnormality seen on a chest radiograph. It may also be used to achieve a histospecific diagnosis in some patients who have obvious, but nonspecific, radiographic abnormalities.

It probably is impossible to determine the frequency with which HRCT will show significant parenchymal abnormalities when the chest radiograph appears normal. Studies of individual diseases show that HRCT demonstrates abnormalities despite normal chest radiographs in 29% of patients with systemic sclerosis and in up to 30% of those with asbestosis. For hypersensitivity pneumonitis, the proportion may be even higher. As indicated by the average sensitivity results of several studies, HRCT seems to have a sensitivity of approximately 94%, compared with 80% for chest radiography; this increased sensitivity does not seem to be achieved at the expense of decreased specificity.

In patients with clinical and lung function evidence of diffuse lung disease, HRCT is now central in the diagnostic workup, with clinical performance greatly exceeding that of plain chest radiography and may obviate the need for lung biopsy. In the original study that compared the diagnostic accuracy of chest radiography and CT in the prediction of specific histologic diagnosis in patients with diffuse lung disease, Mathieson and associates showed that three observers could make a confident diagnosis in 23% of cases on the basis of chest radiographs and in 49% of cases with use of CT; the correct diagnosis was made in 77% and 93% of these readings, respectively (Figure 7-13).

Figure 7-13 High-resolution computed tomography patterns in diffuse interstitial lung disease. A, Subpleural reticular pattern typical of established fibrosing alveolitis. B, Multiple irregularly shaped cystic spaces within the lungs in a young patient with preserved lung volumes. Images through the lung bases were more normal. This high-resolution computed tomography pattern and distribution combination is virtually pathognomonic for Langerhans cell histiocytosis.

A number of subsequent early HRCT studies acted as the forerunners of a large body of work that has established HRCT as a cornerstone in the assessment of patients suspected of having diffuse lung disease but for whom the clinical features and appearance on the chest radiograph do not allow a confident diagnosis to be made. A number of diffuse lung diseases can have a “diagnostic” appearance on HRCT when findings are interpreted by experienced chest radiologists; such diseases include fibrosing alveolitis, sarcoidosis, Langerhans cell histiocytosis, lymphangioleiomyomatosis, pneumoconiosis, and hypersensitivity pneumonitis (Figure 7-14). An intriguing observation is that the ability of HRCT to allow observers to provide correct histospecific diagnoses seems to be maintained in advanced end-stage disease.

Figure 7-14 High-resolution computed tomography scans of the chest in a patient with subacute hypersensitivity pneumonitis. A, Widespread nodular and ground glass patterns. B, The areas of decreased attenuation evident posteriorly are made more obvious on this scan obtained at end expiration.

However, HRCT is sometimes used indiscriminately for patients in whom the high certainty of diagnosis from clinical and radiographic findings does not justify the extra cost and radiation burden. No evidence shows that an HRCT examination adds anything of diagnostic value for a patient who has progressive shortness of breath, finger clubbing, crackles at the lung bases, and the typical radiographic pattern and lung function profile of fibrosing alveolitis. Nevertheless, the ability of HRCT to characterize disease, and often to deliver a definite and correct diagnosis in patients with nonspecific radiographic shadowing, frequently is helpful.

Much interest has been shown in defining the role of HRCT in staging disease activity, particularly for fibrosing alveolitis, in which cellular histology indicates disease activity and is used to predict both responses to treatment and prognosis. As shown by more recent evidence, a predominance of ground glass opacification in fibrosing alveolitis predicts a good response to treatment and increased actuarial survival compared with patients with a more reticular pattern, which denotes established fibrosis. Similar observations about the potential reversibility of disease can be made with use of HRCT in patients who have sarcoidosis, in whom a ground glass or a nodular pattern predominates. In other conditions, the identification of ground glass opacification on HRCT, although nonspecific, almost invariably indicates a potentially reversible disease—for example, extrinsic allergic alveolitis, diffuse pulmonary hemorrhage, and Pneumocystis jiroveci pneumonia (Box 7-1). An important exception is bronchoalveolar cell carcinoma, in which areas of ground glass opacification that merge into areas of frank consolidation or a more nodular pattern may be seen. Another caveat applies with the situation in which fine, intralobular fibrosis is seen on HRCT as widespread ground glass opacification; in this rare occurrence, evidence of traction bronchiectasis usually is present within the areas of ground-glass opacification.

The ability of CT to discriminate among various patterns of disease has clarified the basis for the sometimes complex mixed obstructive and restrictive functional deficits found in some diffuse lung diseases. A good example is hypersensitivity pneumonitis, in which both interstitial and small airway disease coexist; patterns caused by these different pathologic processes can be readily appreciated on HRCT. The extent of the various HRCT patterns correlates with the expected functional indices of restriction and obstruction, respectively. Other conditions in which CT is able to tease out the morphologic abnormalities responsible for complex functional deficits include fibrosing alveolitis with coexisting emphysema and sarcoidosis associated with a combination of interstitial fibrosis and small airway obstruction by peribronchiolar granulomata.

In patients for whom lung biopsy is deemed necessary, HRCT may be invaluable to indicate which type of biopsy procedure is likely to be successful in obtaining diagnostic material. The broad distinction between peripheral disease versus central and bronchocentric disease is easily made on HRCT. Thus, disease with a subpleural distribution, such as fibrosing alveolitis, is most unlikely to be sampled by transbronchial biopsy, whereas diseases with a bronchocentric distribution on HRCT, such as sarcoidosis and lymphangitis carcinomatosa, are consistently accessible to transbronchial biopsy. In patients for whom an open or thoracoscopic lung biopsy is contemplated, HRCT assists in determining the optimal biopsy site. Pathologic examination of a lung biopsy specimen can still justifiably be regarded as the final arbiter of the presence or absence of subtle interstitial lung disease. Because HRCT images provide a kind of “in vivo big picture,” many lung pathologists now combine the imaging and pathologic information before assigning a final diagnosis, and in many centers, the benefits of a team approach to the diagnosis of diffuse lung disease are recognized. The indications for HRCT that have been developed over the past 20 years are summarized in Box 7-2.

Mediastinal and Chest Wall Imaging

The most common indications for the use of MRI in respiratory disease are for investigation of neoplastic disease, most commonly bronchogenic carcinoma. In addition to the primary disease, secondary complications such as cerebral secondaries, spinal metastases, and retroperitoneal fibrosis all lend themselves to evaluation by MRI. MRI also permits assessment for invasion of mediastinal structures such as the major airways, heart and great vessels, chest wall, and diaphragm and allows differentiation among different forms of soft tissue, fluid, hemorrhage, local hematoma formation, and aneurysms (Figures 7-15 and 7-16). With modern multichannel CT techniques, MRI now holds relatively little advantage over CT in assessing chest wall invasion, except with superior sulcus tumors. However, MRI does provide superb anatomic detail without subjecting the patient to radiation exposure—an important consideration in the pediatric age group, in which a number of follow-up studies may be required (Figure 7-17). The disadvantage of MRI in the very young child is the necessity for general anesthesia in many cases.

Figure 7-15 Magnetic resonance imaging of a right upper zone lung mass in an 11-year-old boy. A, A coronal T1-weighted sequence demonstrates a high-signal-intensity apical mass. B, With the addition of fat saturation, reducing the signal returned from fat, the signal intensity in the mass falls significantly. This imaging feature confirms the fatty nature of the mass, which was a large pleural lipoma.

Figure 7-16 Chest wall invasion by tumor demonstrated with magnetic resonance imaging. Oblique sagittal T2-weighted image through the long axis of the left ventricle demonstrates an adjacent chest wall mass (arrows) extending through the interior chest wall into the overlying breast tissue. This was due to recurrent breast carcinoma.

Figure 7-17 Extralobar pulmonary sequestration. A, A coronal contrast-enhanced breath-hold image demonstrates the avidly enhancing pulmonary sequestration at the left lung base. Note the clear plane between the triangular sequestrated segment and the diaphragm and underlying spleen. B, Volume-rendered angiographic image demonstrating the same triangular sequestrated segment (asterisk) with two supplying branches from the aorta (arrowheads) and complex venous drainage. The largest vein drains subdiaphragmatically (arrows) into the left renal vein.

Lung Parenchymal Imaging

Use of magnetic resonance techniques for imaging the lungs has been limited by a number of significant technical challenges. First, the lungs are constantly moving because of respiratory and cardiac motion. Second, they have a low water content relative to other biologic tissues, so they have a low proton density and return relatively little signal. Third, because of the multiple interfaces between air and soft tissue, innumerable small disturbances arise in the magnetic field. This loss of homogeneity at air-tissue interfaces results in a phenomenon known as magnetic susceptibility artifact, further reducing signal and increasing noise. Thus, on standard sequences, normal lung exhibits little signal and often is obliterated by artifact. Attempts to tackle this problem are showing increasing promise—for example, in the area of suppurative lung disease in younger patients.

Ventilation Studies

Another area of intense interest has been the use of polarized gases (helium 3 and xenon 129) to show pulmonary ventilation. With this technique, a process of heating and irradiating with polarized light produces polarized gases. The gases (which have a short half-life) are inhaled and imaged using optimized sequences. The use of dual-frequency probes allows gas and proton images to be acquired and registered, enabling function and anatomy to be correlated.

Pulmonary Emboli and Infarction

At present, MRI is not routinely used in patients with suspected pulmonary embolism and infarction, but it has been the subject of much research: In a number of published series, breath-hold pulmonary MRA has been found to show fifth-order pulmonary vessels and to permit diagnosis of emboli to the segmental level. Presence of smaller pulmonary emboli can be inferred by lack of segmental and subsegmental perfusion. Three-dimensional MRA datasets can be acquired and displayed on workstations as moving projections to demonstrate areas of deficient perfusion.

Vascular Malformations and Congenital Anomalies

Increasing evidence suggests that MRI can clearly define a number of vascular and developmental anomalies of the lungs by combining anatomic and flow studies. Such anomalies include the scimitar syndrome, hypogenetic lung syndrome, pulmonary artery agenesis, bronchopulmonary sequestration, and vascular malformations (see Figure 7-17).

Cardiovascular Imaging

MRI is now a key technique for imaging the heart and great vessels and is widely used for the assessment of cardiac anatomy and function. Rapid and accurate assessment of wall motion, determination of ejection fraction, and stress testing for reversible ischemia, hibernating myocardium, and valvular disease are now routine. The ultimate challenge—namely, accurate imaging of the coronary arteries—is under intense investigation, although this application has not yet reached routine practice. Nevertheless, MRI is now able to provide comprehensive noninvasive cardiac assessment that is likely to challenge more established techniques such as nuclear medicine and echocardiography.

Mediastinum and Hilar Structures

The mediastinum is delineated by the lungs on either side, the thoracic inlet above, the diaphragm below, and the vertebral column posteriorly. In the context of radiographic anatomy, the various structures that make up the mediastinum are superimposed on each other, so they cannot be separately identified on a two-dimensional chest radiograph; for this reason, the normal anatomy of the individual components of the mediastinum is considered in more detail in the later section on CT of the mediastinum. Nevertheless, because a chest radiograph usually is the first imaging investigation, it is necessary to appreciate the normal appearances of the mediastinum and the considerable possible variations resulting from the patient’s body habitus and age.

The mediastinum is conventionally divided into superior, anterior, middle, and posterior compartments (Figure 7-21). The practical benefit of use of these arbitrary divisions is that specific mediastinal pathologies show a definite predilection for individual compartments (e.g., a superior mediastinal mass most frequently is caused by intrathoracic extension of the thyroid gland; a middle mediastinal mass usually results from enlarged lymph nodes). However, localization of a mass within one of these compartments does not normally allow a specific diagnosis to be made, and neither do the arbitrary boundaries preclude disease from involving more than one compartment.

Figure 7-21 The mediastinal compartmental divisions. A, Arbitrary division of the mediastinum into superior, anterior, middle, and posterior compartments. B, An alternative scheme omits the superior mediastinal compartment. The area posterior to the sternum and anterior to the heart and great vessels (blue arrows) defines the anterior mediastinum in both cases. Likewise, a line placed along the posterior aspect of the trachea and heart (yellow arrowheads) distinguishes the middle from the posterior mediastinum, which is bounded posteriorly by the vertebra (red asterisks).

Only the outline of the mediastinum and the air-containing trachea and bronchi (and sometimes esophagus) is clearly seen on a normal posteroanterior chest radiograph. On a chest radiograph, the right brachiocephalic vein and superior vena cava form the right superior mediastinal border. This border usually is vertical and straight (in contrast with the situation in which right paratracheal lymphadenopathy is present, when the right superior mediastinal border tends to be undulate), and it becomes less distinct as it reaches the thoracic inlet. The right side of the superior mediastinum can appear to be considerably widened in patients who have an abundance of mediastinal fat (Figure 7-22); such persons often have prominent cardiophrenic fat pads. The mediastinal border to the left of the trachea above the aortic arch is the result of summation of the left carotid and left subclavian arteries, together with the left brachiocephalic and jugular veins. The left cardiac border consists of the left atrial appendage, which merges inferiorly with the left ventricle. The silhouette of the heart should always be sharply outlined. Any blurring of the border results from loss of immediately adjacent aerated lung, usually by collapse or consolidation.

Figure 7-22 Widening of the superior mediastinum in this image is caused by abundance of mediastinal fat. In addition, bilateral cardiophrenic fat pads are present.

The density of the heart shadow to the left and right of the vertebral column should be identical—any difference indicates pathology (e.g., an area of consolidation or a mass in a lower lobe). On a well-penetrated film, a density with a convex lateral border frequently is seen through the right heart border—this apparent mass is caused by the confluence of the right pulmonary veins as they enter the left atrium and is of no clinical significance.

The trachea and main bronchi should be visible through the upper and middle mediastinum. The trachea is rarely straight and often is to the right of the midline at its midpoint. In older persons, the trachea may be markedly displaced by a dilated aortic arch below. In approximately 60% of normal subjects, the right wall of the trachea (the right paratracheal stripe) can be identified as a line of uniform thickness (less than 4 mm in width); when visible, it excludes the presence of any adjacent space-occupying lesion, most usually lymphadenopathy. The angle between the left and right main bronchi, which forms the carina, usually is somewhat less than 80 degrees. Splaying of the carina is a relatively crude sign of subcarinal disease, in the form of either a massive subcarinal lymphadenopathy or a markedly enlarged left atrium. A more sensitive sign of subcarinal disease is obscuration of the upper part of the azygoesophageal line, which usually is visible in its entirety on a chest radiograph with good penetration (Figure 7-23). The origins of the lobar bronchi, when they are projected over the mediastinal shadow, usually can be identified, but segmental bronchi within the lungs generally are not seen on plain radiography.

Figure 7-23 Chest radiograph made using the advanced multiple beam equalization radiography (AMBER) system. The normal azygoesophageal line is demonstrated (arrows).

The normal hilar shadows on a chest radiograph represent the summation of the pulmonary arteries and veins, with little contribution from the overlying bronchial walls or lymph nodes of normal size. The hila are of approximately the same size, and the left hilum normally lies between 0.5 and 1.5 cm above the level of the right hilum. The size and shape of the hila show remarkable variation in normal persons, making subtle abnormalities difficult to identify.

Pulmonary Fissures, Vessels, and Bronchi

The two lungs are separated by the four layers of pleura behind and in front of the mediastinum. The resultant posterior and anterior junction lines often are visible on frontal chest radiographs as nearly vertical stripes, the posterior junction line lying higher than the anterior (Figure 7-24). Because these junction lines are not invariably seen (their visibility is largely dependent on whether the pleural reflections are tangential to the x-ray beam), their presence or absence is not usually of significance.

Figure 7-24 Diagram showing some of the mediastinal lines and stripes frequently seen on a frontal chest radiograph.

The lobes of lung are surrounded by visceral pleura—the major (or oblique) fissure separates the upper and lower lobes of the left lung. The major (or oblique) fissure and the minor (horizontal or transverse) fissure separate the upper, middle, and lower lobes of the right lung. In the absence of abnormality, the minor fissure is visible in more than half of posteroanterior chest radiographs. In normal persons, the minor fissure is slightly bowed upward and runs horizontally; any deviation from this configuration usually is caused by loss of volume of a lobe. The major fissures are not visible on a frontal radiograph and are inconsistently identifiable on lateral radiographs. Inability to detect a fissure usually reflects that the fissure is not exactly in the line of the x-ray beam. Occasionally, however, fissures may be incompletely developed—a point familiar to thoracic surgeons, who sometimes encounter difficulty in performing a lobectomy because of incomplete cleavage between lobes. Accessory fissures are occasionally seen; for example, in the left lung a minor fissure can be present, which separates the lingula from the remainder of the upper lobe.

All of the branching structures seen within normal lungs on a chest radiograph represent pulmonary arteries or veins. The pulmonary veins may sometimes be differentiated from the pulmonary arteries—the superior pulmonary veins have a distinctly vertical course. Often, however, it is impossible to differentiate arteries from veins in the lung periphery. On a chest radiograph taken in the erect position, a gradual increase in the diameter of the vessels is seen, at equidistant points from the hilum, traveling from lung apex to base; this gravity-dependent effect disappears if the patient is supine or in cardiac failure.

The lobes of the lung are divided into segments, each of which is supplied by its own segmental pulmonary artery and accompanying bronchus. The walls of the segmental bronchi are rarely seen on the chest radiograph, except when lying parallel with the x-ray beam, in which case they are seen end on as ring shadows measuring up to 8 mm in diameter. The most frequently identified segmental airways are the anterior segmental bronchi of the upper lobes.

Diaphragm and Thoracic Cage

The interface between aerated lung and the hemidiaphragms is sharp, and the highest point of each dome normally is medial to the midclavicular line. The right dome of the diaphragm is higher than the left by up to 2 cm in the erect position, unless the left dome is elevated by air in the stomach. Laterally, the hemidiaphragm forms an acute angle with the chest wall. Filling in or blunting of these costophrenic angles usually represents pleural disease, either pleural thickening or an effusion. In elderly persons, localized humps on the dome of the diaphragm, particularly posteriorly (and therefore most obvious on a lateral radiograph), are common and represent minor weaknesses or defects of the diaphragm. Interposition of the colon in front of the right lobe of the liver is a frequently seen normal variant (so-called Chilaiditi syndrome).

Apparent pleural thickening along the lateral chest wall in the middle zones is a frequent observation in obese patients; it is caused by subpleural fat bulging inward. Deformities of the thoracic cage may cause distortion of the normal mediastinum and so simulate disease. One of the most common deformities is pectus excavatum, which, by compressing the heart between the depressed sternum and vertebral column, causes displacement of the apparently enlarged heart to the left and blurring of the right heart border (Figure 7-25). A similar appearance may arise with an unusually straight thoracic spine, referred to as straight back syndrome.

Figure 7-25 A, Chest radiograph, posteroanterior view, obtained in a patient with marked pectus excavatum. The blurring of the right heart border and the apparent increase in heart size are a direct consequence of a depressed sternum. Note the 7 configuration of the ribs. B, Computed tomography scan shows the sternal depression.

Anatomy of the Lateral Chest Radiograph

Consistent viewing of lateral chest radiographs in the same orientation, whether a right or a left lateral projection, improves the ability to detect deviations from normal. In the lateral view, the trachea is angled slightly posteriorly as it runs toward the carina, and its posterior wall is always visible as a fine stripe (Figure 7-26). The posterior walls of the right main bronchus and the right intermediate bronchus are outlined by air and also are seen as a continuous stripe on the lateral radiograph. The overlying scapulae are invariably seen running almost vertically in the upper part of the lateral radiograph (and may be misinterpreted as intrathoracic structures). Further confusing shadows are formed by the soft tissues of the outstretched arms, which project over the upper mediastinum. The carina is not visible as such on the lateral radiograph, and the two transradiancies projected over the lower trachea represent the right main bronchus (superiorly) and the left main bronchus (inferiorly).

Figure 7-26 The lateral chest radiograph in a normal subject.

Overlying structures on a lateral radiograph obscure most of the lung. In normal persons, the unobscured lung in the retrosternal and retrocardiac regions should be of the same transradiancy. Furthermore, as the eye travels down the spine, a gradual increase in transradiancy should be apparent. The loss of this phenomenon suggests the presence of disease in the posterior-basal segments of the lower lobes (e.g., fibrosing alveolitis) (Figure 7-27).

Figure 7-27 Loss of the normal increase in transradiancy toward the lower part of the dorsal spine in a patient with interstitial lung disease.

The two major fissures are seen as diagonal lines, of a hair’s breadth, that run from the upper dorsal spine to the anterior surface of the diaphragm. Care must be taken not to confuse the obliquely running rib edges with fissures. The minor fissure extends horizontally from the middle right major fissure. It is often not possible to differentiate the right from the left major fissures with confidence. Similarly, although the two hemidiaphragms may be identified individually (especially if the gastric bubble is visible under the left dome of the diaphragm), differentiation between the right and the left hemidiaphragm is often impossible. A useful sign is the relative heights of the two domes—the dome farther from the film normally appears higher because of magnification.

The summation of both hilar on the lateral radiograph generates a complex shadow. However, one general point is useful in the interpretation of this difficult area—the right pulmonary artery lies anterior to the trachea and right main bronchus, whereas the left pulmonary artery arches over the left main bronchus so that a large part of it lies posterior to the major bronchi (Figure 7-28). A bandlike opacity often is seen along the lower third of the anterior chest wall behind the sternum. It represents a normal density and occurs because less aerated lung is in contact with the chest wall, because the space is occupied by the heart; it should not be confused with pleural disease.

Figure 7-28 Diagram showing the proximal pulmonary arteries seen on a lateral chest radiograph.

Radiographic Signs

Typically, the shadowing is ill-defined, except when it directly abuts a pleural surface (including the interlobar fissures), in which case it is sharply demarcated (Figure 7-29). Although consolidation respects lobar boundaries, there are no such barriers to spread into adjacent lung segments, which are frequently contiguously involved. Thus, an area of consolidation within a single lobe often enlarges in an irregular manner, and a discrete, well-defined opacity (so-called round pneumonia) is the exception and not the rule (Figure 7-30).

Figure 7-29 Patchy consolidation caused by tuberculosis. Where this area of involvement abuts the horizontal fissure, the inferior surface of the consolidation is sharply defined.

Figure 7-30 Well-defined, rounded opacity in the right middle lung zone, which fades out peripherally. This “round pneumonia” was caused by pneumococcal infection.

The vascular markings within an area of consolidation usually become obscured, because the contrast between the air-containing lung and the soft tissue density vascular markings is lost. By contrast, the bronchi, which usually are too thin-walled to be differentiated from the surrounding lung parenchyma, become apparent in negative contrast to the air space opacification, to produce the true hallmark of consolidation, the air bronchogram (Figure 7-31). A relatively uncommon but very suggestive radiologic sign of consolidation is the acinar shadow, in which an individual secondary pulmonary lobule becomes opacified but remains surrounded by normally aerated lung. The resultant soft tissue density nodule usually is on the periphery of a more confluent area of consolidation and normally measures 0.5 to 1 cm in diameter. These acinar opacities most commonly are seen in association with mycobacterial and varicella-zoster pneumonias but can occur with any other cause of consolidation (Figure 7-32). Occasionally, an acinus is left normally aerated but surrounded by opacified air spaces; this radiologic sign has been termed the air alveologram. When consolidation is not fully developed and has caused only partial filling of the air spaces, the resultant radiographic appearance is ground glass opacification (Figure 7-33). Again, a wide range of possible causes has been documented, and in addition to causes of consolidation, this pattern may result from interstitial lung infiltration.

Figure 7-31 Air bronchogram in consolidation. A, Plain radiograph of the left upper zone in a patient with tuberculosis shows an air bronchogram. B, Computed tomography scan through the left lower lobe in a different patient demonstrates an area of segmental pneumonia.

Figure 7-32 Acinar opacities seen at the periphery of confluent right upper lobe consolidation in a patient with tuberculosis. Note the elevation of the horizontal fissure.

Figure 7-33 Ground glass opacification in the middle and lower zones associated with Pneumocystis jiroveci pneumonia. A, Chest radiograph shows perihilar poorly defined, increased (ground glass) density. The patient was a young man who was seropositive for human immunodeficiency virus (HIV) infection. B, High-resolution computed tomography image from the same patient demonstrates variable lung attenuation with markedly black airways highlighted by the ground glass patchy infiltrate. C, Diffuse and severe ground glass and air space infiltrate is seen on a chest radiograph obtained in a different patient with P. jiroveci pneumonia.

(A, Courtesy Dr. M. Taylor.)

When an area of consolidation undergoes necrosis, because of either infection or infarction, liquefaction may result, and if either a gas-forming organism or communication with the bronchial tree is present, an air-fluid level may develop in addition to cavity formation (Figure 7-34). Consolidation frequently produces a silhouette sign, as described by Felson and Felson. Although this radiographic sign may be seen in association with a wide number of intrapulmonary pathologic processes, it is the relatively transitory nature of many forms of consolidation that best demonstrates the features of this finding. The original description stated that when an intrathoracic lesion touched a border of the heart, aorta, or diaphragm, it obliterated that border on the radiograph. Furthermore, a small area of consolidation may obliterate a normal air–soft tissue interface as effectively as a large area. This contingency is demonstrated well by the obliteration of the right heart border by subtle middle lobe consolidation that might otherwise be overlooked.

Figure 7-34 Large right lower lobe cavity in a patient with widespread pneumonic consolidation. In this radiograph obtained with the patient supine, an air-fluid level is not evident.

Understanding the significance of the silhouette sign allows the observer to localize an area of consolidation or other pulmonary opacity. Only if an area of consolidation lies in direct contact with a normal structure is the silhouette of that structure lost. If an area of consolidation and a normal structure–lung interface merely lie along the same x-ray path, they are superimposed on the radiograph but do not demonstrate the silhouette sign. Thus, lingular consolidation is likely to obscure the heart border, but left lower lobe consolidation usually does not (Figures 7-35 through 7-37). Several potential causes for a falsely positive silhouette sign are recognized. Some relatively common anatomic variants that result in a reduced anteroposterior diameter of the thorax, such as pectus excavatum or straight back syndrome, cause loss of the right heart border as the depressed sternum distorts the normal anatomy (see Figure 7-25). Occasionally, a scoliosis, usually concave to the left and often of relatively trivial clinical significance, causes the right heart border to be projected over the spine. It is only when the heart border is projected over the right lung that the silhouette sign can be elicited. Underexposed radiographs may appear to demonstrate the silhouette sign, so it is imperative that the technical quality of the radiograph be taken into account.

Figure 7-35 Radiographic appearance of lingular consolidation. A, Loss of the left heart border with a diffuse pulmonary infiltrate in the left middle and lower zones. The outer aspect of the left diaphragm is preserved. B, Lateral view in the same patient as in A, showing consolidation within the lingula, delineated posteriorly by the major fissure.

Figure 7-36 Middle and lower zone consolidation in the left lower lobe. A, On this posteroanterior view, radiographic features include preservation of the left heart border with loss of the left hemidiaphragm silouette. B, Lateral view shows the consolidation in the lower lobe delineated anteriorly by the major fissure.

Figure 7-37 Right lower lobe consolidation. The right heart border is clearly defined. Because the consolidation is not complete, the hemidiaphragm has not been effaced.

Collapse

Partial or complete volume loss in a lung or lobe is referred to as collapse or atelectasis. The two terms are essentially interchangeable, and both imply a diminished volume of air in the lung with associated reduction of lung volume. Any of several different mechanisms may be responsible for lung or lobar collapse.

Complete Lung Collapse

With complete collapse of an entire lung (in the absence of an accompanying pneumothorax, large pleural effusion, or extensive consolidation), complete opacification of that hemithorax is seen, with displacement of the mediastinum to the affected side and elevation of the hemidiaphragm. Compensatory hyperinflation of the contralateral lung occurs, often with herniation across the midline. Herniation most often is in the retrosternal space, anterior to the ascending aorta, but may occur posterior to the heart (Figure 7-38).

Figure 7-38 Collapse of the left lung. A proximal obstructing tumor is evident within the left main bronchus, with complete collapse of the left lung and a mediastinal shift to the left.

Individual Lobar Collapse

The descriptions that follow apply to collapse of individual lobes, uncomplicated by preexisting pulmonary or pleural disease. The alterations in the positions of the fissures, mediastinal structures, and diaphragms are shown in Figures 7-39 to 7-43.

Figure 7-39 Right upper lobe collapse caused by a right hilum tumor. A, On the chest radiograph, the horizontal fissure takes on an S configuration, known as the S sign of Golden (arrows). B, Line diagram of pathoanatomic changes: left, frontal view; right, lateral view.

Figure 7-40 Middle lobe collapse. A, Loss of the right heart border is seen on the anteroposterior radiograph. B, A well-defined wedge-shaped opacity on the lateral radiograph is delineated by the horizontal and oblique fissures.

Figure 7-41 Left lower lobe collapse due to occlusion of the left lower lobe bronchus. A, The left hemithorax is of reduced volume, and there is loss of the normal silhouette of the left lower lobe pulmonary artery. The left lower lobe has contracted behind the cardiac silhouette (arrowheads). B, Line diagram of pathoanatomic changes: left, frontal view; right, lateral view.

Figure 7-42 Right lower lobe collapse in a patient with asthma. A, Radiographic features include preservation of the right heart border with reduction in volume of the right hemithorax and shift of the trachea to the right side. B, Line diagram of pathoanatomic changes: left, frontal view; right, lateral view.

Figure 7-43 Left upper lobe collapse with shift of the mediastinum to the left and loss of definition of the mediastinal structures. A, In this patient, a large tumor (arrow) is causing left upper lobe and lingula collapse. The opacification fades out more inferiorly. B, Line diagram of pathoanatomic changes: left, frontal view; right, lateral view. C, In another patient, very tight left upper lobe collapse was due to a small tumor. The appearances are different, but volume loss is marked in both instances.

Right Upper Lobe Collapse

As the right upper lobe collapses (see Figure 7-39), the horizontal fissure rotates around the hilum and the lateral end moves upward and medially toward the superior mediastinum. The anterior end moves upward, toward the apex. The upper half of the oblique fissure moves anteriorly. The two fissures become concave superiorly. In severe collapse, the lobe may be flattened against the superior mediastinum and may obscure the upper pole of the hilum. The hilum is elevated, and its lower pole may be prominent. Deviation of the trachea to the right is usual, and compensatory hyperinflation of the right middle and lower lobes may be apparent.

Middle Lobe Collapse

In right middle lobe collapse (see Figure 7-40), the horizontal fissure and lower half of the oblique fissure move toward each other, a feature best seen on the lateral projection. Because the horizontal fissure tends to be more mobile, it usually shows greater displacement. On the frontal (anteroposterior) radiograph, changes associated with middle lobe collapse may be subtle, because the horizontal fissure may not be visible, and increased opacity does not become apparent until collapse is almost complete. Critical analysis of the radiograph sometimes reveals obscuration of the right heart border as the only clue. The lordotic anteroposterior projection is rarely required but may be used to bring the displaced fissure into the line of the x-ray beam and occasionally may elegantly demonstrate middle lobe collapse. Because the volume of this lobe is relatively small, indirect signs of volume loss are rarely obvious.

Left Lower Lobe Collapse

In left lower lobe collapse (see Figure 7-41), the normal oblique fissures extend from the level of the fourth thoracic vertebra posteriorly to the diaphragm, close to the sternum anteriorly. The position of these fissures on the lateral projection is the best index of lower lobe volumes. When a lower lobe collapses, the oblique fissure moves posteriorly but maintains its normal slope. In addition to posterior movement, the collapsing lower lobe causes medial displacement of the oblique fissure, which may become visible in places on the frontal projection.

Right Lower Lobe Collapse

Right lower lobe collapse (see Figure 7-42) causes partial depression of the horizontal fissure, which may be apparent on the frontal projection. Increased opacity of a collapsed lower lobe is usually visible on the frontal projection also. A completely collapsed lower lobe may be so small that it flattens and merges with the mediastinum to produce a thin, wedge-shaped shadow. In left lower lobe collapse, the heart may obscure this opacity, and a penetrated view may be required to demonstrate it. Mediastinal structures and parts of the diaphragm adjacent to the nonaerated lobe are obscured. When significant lower lobe collapse occurs, especially when the collapsed lobe is so small as to be invisible as a separate opacity, confirmatory evidence usually is apparent from close inspection of the relevant hilum. This area typically is depressed and rotated medially, with loss of the normal hilar vascular structures, which is made all the more obvious if a previous film is available for comparison. In addition, indirect signs of collapse, such as upper lobe hyperinflation, are present. Diaphragmatic elevation is unusual.

Lingula Collapse

The lingula often is involved in collapse of the left upper lobe, but occasionally it may collapse individually, in which case the radiographic features are similar to those of middle lobe collapse. With absence of a horizontal fissure on the left, however, anterior displacement of the lower half of the oblique fissure and increased opacity anterior to it become important signs. On the frontal projection, the left heart border becomes obscured.

Left Upper Lobe Collapse

The pattern of upper lobe collapse is different in the two lungs. Left upper lobe collapse (see Figure 7-43) is apparent on the lateral projection as anterior displacement of the entire oblique fissure, which becomes oriented almost parallel to the anterior chest wall. With increasing collapse, the upper lobe retracts posteriorly and loses contact with the anterior chest wall. With complete collapse, the left upper lobe may lose contact with the chest wall and diaphragm and retract medially against the mediastinum. On a lateral film, therefore, left upper lobe collapse is seen as an elongated opacity that extends from the apex and reaches, or almost reaches, the diaphragm; it is anterior to the hilum and is bounded by the displaced oblique fissure posteriorly and by the hyperinflated lower lobe.

A collapsed left upper lobe does not produce a sharp outline on the frontal view. An ill-defined, hazy opacity is present in the upper, middle, and sometimes lower zones, the opacity being densest near the hilum. Pulmonary vessels in the hyperinflated lower lobe usually are visible through the haze. The aortic knuckle typically is obscured, unless the upper lobe has collapsed anterior to it, in which case hyperexpansion of the lower lobe apical segment may occur, separating the collapsed upper lobe from the mediastinal silhouette and aortic knuckle. This separation produces an unusual-looking but characteristic medial crescent of lucency termed the Luftsichel sign. If the lingula is involved, the left heart border is obscured. The hilum often is elevated, and the trachea is deviated to the left.

Combined Lobar Collapses

Right Lower and Middle Lobe Collapse

Because the right lower and middle lobes take their origin from the bronchus intermedius, an extensive lesion involving those sites may cause combined collapse. The radiographic appearance is similar to that in right lower lobe collapse (Figure 7-44), except that the horizontal fissure is not apparent, and the opacification reaches the lateral chest wall on the frontal view and similarly extends to the anterior chest wall on the lateral view.

Figure 7-44 Right middle and lower lobe collapse caused by an obstructing lesion in the bronchus intermedius. A bronchial cutoff sign is visible (arrows). A separate pulmonary mass is present in the right upper lobe.

Right Upper and Middle Lobe Collapse

Combined collapse of the right upper and middle lobes is unusual because of the distance between the origins of their bronchi; it generally can be taken to imply the presence of more than one lesion. This combination produces appearances almost identical to those of left upper lobe collapse (Figure 7-45). On occasion, isolated right upper lobe collapse also produces appearances that are identical to those with left upper lobe collapse.

Figure 7-45 Occasionally, the combination of right middle and upper lobe collapse mimics left upper lobe and lingular collapse on the chest radiograph. Both posteroanterior (A) and lateral (B) views demonstrate changes similar to those seen on the opposite side. The major fissure shifts anteriorly and extends from the lung apex to the anterior costophrenic recess.

Rounded Atelectasis

Rounded atelectasis is an unusual form of pulmonary collapse that may be misdiagnosed as a pulmonary tumor. The plain film will show an opacity that may be several centimeters in diameter, frequently with ill-defined edges. Rounded atelectasis is always pleura-based and associated with pleural thickening. Vascular shadows may radiate from part of the opacity, said to resemble a comet’s tail (Figure 7-46). The appearance is caused by peripheral lung tissue folding in on itself. Rounded atelectasis usually is related to previous asbestos exposure but also may be secondary to any exudative pleural effusion. It is not of any other pathologic significance, although when present often raises the question of a malignancy. The CT appearance usually is sufficiently diagnostic to allow differentiation from other pulmonary masses.

Figure 7-46 Rounded atelectasis. A, A poorly defined opacity is visible on the frontal radiograph (arrows). B, Coronal reformatted image from computed tomography scan reveals the characteristic pleurally based mass with radiating bronchovascular strands.

Unilateral Increased Transradiancy

The most common causes of increased unilateral transradiancy are technical factors, such as patient rotation, poor beam centering, or an offset grid. Usually, hypertransradiancy caused by technical factors can be identified by comparison of the soft tissues around the shoulder girdle and particularly over the axillae. Nevertheless, a number of pathologic causes of unilateral increased transradiancy are recognized.

Chest Wall

A hemithorax may appear of increased transradiancy (blacker) if the x rays are less attenuated because of a reduction in the amount of overlying soft tissue. The most common cause for this appearance is a mastectomy. Rarely, the same phenomenon may be seen in patients who have congenital unilateral absence of pectoral muscles in Poland syndrome (Figure 7-47). This defect may be accompanied by associated skeletal abnormalities in the ipsilateral ribs but may be recognized by loss of the normal axillary skin fold.

Figure 7-47 Congenital absence of the left pectoralis major muscle in Poland syndrome. In this patient, the muscle deficit was an incidental finding on a chest radiograph. Note the alteration in the left axillary skin fold compared with the right (arrows).

Reduced Vascularity

Interruption or significant reduction in the blood supply to one lung, either congenital or acquired, has increased transradiancy (Figure 7-48).

Figure 7-48 Increased transradiancy in the right lower lung zone. A large emphysematous bulla occupies the lower half of the right lung, and the apical changes are in keeping with previous tuberculosis.

Lung Hyperexpansion

If a lung is overexpanded because of either air trapping secondary to the presence of a foreign body or asymmetric emphysema, that hemithorax may demonstrate increased transradiancy. When the entire lung is affected, the hemithorax usually is relatively larger than the opposite side. However, the same phenomenon may occur with compensatory emphysema due to collapse or removal of an ipsilateral lobe. In this instance, the transradiant hemithorax may be of normal volume, and the presence of the increased transradiancy should prompt a search for other evidence of collapse or previous surgery.

A relatively increased transradiancy of one hemithorax with no obvious cause suggests the possibility of a generalized increase in radiopacity of the opposite side (for example, the posterior layering of a pleural effusion in a supine patient) (Figure 7-49).

Figure 7-49 Supine radiographic view of a large right pleural effusion. The generalized increase in radiopacity of the right side is caused by posterior layering of a pleural effusion.

The Pulmonary Mass

The finding of a solitary pulmonary nodule on the chest radiograph requires careful analysis, because the diagnostic possibilities are numerous. Once a pulmonary mass has been identified, the observer must decide first, if the lesion is genuine and second, whether the lesion is truly intrapulmonary. The possibility of a cutaneous lesion should not be overlooked, especially if only a part of the nodule is well defined. If doubt remains, repeat radiographs are obtained, with a lateral view and, if relevant, use of nipple markers. What appears at first glance to represent a solitary pulmonary mass may, on closer inspection, actually represent the most obvious of a number of pulmonary nodules. The radiology of multiple pulmonary nodules is discussed later.

When a pulmonary mass is clearly defined around its entire circumference and is projected over the lung on frontal and lateral projections, the mass is truly intrapulmonary (Figure 7-50). If a surface is in contact with another soft tissue structure, however, the possibility of an extrapulmonary mass projecting into the lung must be considered. Analysis of the breadth of the base of the lesion, the angle made with the adjacent structure, and the presence of bone destruction often allows the observer to differentiate an extrapulmonary mass that extends into the adjacent lung from an intrapulmonary mass that has grown to contact the mediastinum, diaphragm, or chest wall.

Figure 7-50 A rounded pulmonary mass. A, Posteroanterior chest radiograph obtained in a patient with a well-defined left upper lobe pulmonary mass. The entire circumference is visualized on the film, which shows minimal contact of the lesion with adjacent structures. B, Image obtained at computed tomography–guided needle biopsy demonstrates that the mass is largely surrounded by aerated lung.

The analysis of a solitary pulmonary mass relies on a number of radiologic and clinical factors. The latter include patient age, geographic and ethnic origins, smoking history, and medical history. The likelihood that a pulmonary nodule represents a malignancy in a young nonsmoker who comes from an area in which histoplasmosis is endemic clearly is different from that for an elderly patient with a lifetime history of smoking.

Radiographic features of a pulmonary nodule that should be analyzed include size, density, margins, vascular markings, and growth rate.

Density

Most pulmonary masses are of soft tissue density. However, careful inspection must be made for the presence of calcification, because certain patterns of calcification are typical of benign lesions that may be safely observed rather than resected (Figure 7-51). A completely or centrally calcified nodule is diagnostic of a tuberculoma or histoplasmoma. Often, CT is required to confirm this pattern of calcification. Likewise, concentric rings of calcification are typical of healed histoplasmosis infection. Popcorn calcification, within the matrix of a pulmonary nodule, is highly suggestive of a hamartoma (Figure 7-52). Other forms of calcification do not reliably indicate whether a nodule is benign or malignant, and dystrophic calcification within a pulmonary malignancy is relatively common.

Figure 7-51 Fat and calcium density in a small endobronchial mass seen on computed tomography. A small lesion in the left lower lobe bronchus is evident on both axial (A) and coronal (B) reformatted images. This density (arrow in B) confirms that the lesion is a hamartoma.

Figure 7-52 Pulmonary mass calcification. Posteroanterior chest radiograph shows a mass that projects over the left hilum. This is smoothly marginated and contains central popcorn calcification; it is unusually large but otherwise is a typical pulmonary hamartoma.

Growth Rate

Review of previous radiographs, when available, may establish whether a lesion is static or increasing in size. It is usual practice to express the growth of a pulmonary tumor in terms of the time taken for it to double in volume, which equates to an increase in diameter of 25%, assuming that the tumor is roughly spherical, as is usually the case. Tumors with a doubling time of less than 30 days or more than 2 years are very unlikely to result from malignancy. Often, however, no previous films are available, so the use of growth rate as a diagnostic aid is limited. Modern CT allows small pulmonary lesions to be followed over increasing intervals to confirm lack of growth. This is facilitated by the use of automated software that allows volumetric information to be derived from the CT dataset (Figure 7-53).

Figure 7-53 Nodule growth assessment. Computed tomography workstation volumetric assessment allows accurate follow-up imaging of small pulmonary nodules to detect interval growth.

Reticular Shadowing

Reticular or linear shadowing (Figure 7-61) is made up of multiple, short, irregular linear densities, usually randomly oriented and often overlapping to produce a netlike pattern. When profuse, they may summate to form ring shadows or sometimes a nodular pattern. Occasionally, the linear shadows may be oriented at right angles to the pleural surface, so-called Kerley B lines (Figure 7-62)—a feature that indicates thickening of the interlobular septa. When the linear opacities are extremely profuse or coarse, the impression of a ring or honeycomb pattern is typical.

Figure 7-61 Extensive reticular infiltrate in lungs of normal volume. The patient had Langerhans cell histiocytosis.

Figure 7-62 Kerley B lines in a patient with heart failure. Of note, the reticular opacities are oriented at right angles to the pleural surface.

Nodular Opacities

Nodules may be well or poorly defined and of varying density, ranging from soft tissue to calcific (Figure 7-63). They may be discrete or coalescent, with areas of confluence producing consolidation. When the nodules are greater than a few millimeters in diameter, the differential diagnosis changes. Larger discrete nodules were discussed previously.

Figure 7-63 Very profuse nodular shadowing. The individual nodules are of high density. The patient had alveolar microlithiasis.

Reticulonodular Shadowing

Often, it is impossible to confidently assign a pattern of diffuse shadowing to one of the two previously described categories, because they overlap. The reticulonodular pattern probably is the most common form of diffuse lung shadowing.

Ground Glass Shadowing

Ground glass shadowing (see Figure 7-33) refers to a generalized increase in density of the lung, which may be diffuse or patchy but most commonly is bilateral and in a middle and lower zone or perihilar location. The underlying vascular branching pattern is not totally obscured as it is in consolidation, but the vessels become less distinct; likewise, the hila and hemidiaphragms may appear less sharp. This subtle abnormality is considerably easier to appreciate with the benefit of a previous normal film for comparison.

In addition to determining the radiographic pattern of diffuse abnormality, a number of other features must be sought, including whether the distribution of disease is central or peripheral, in the upper, middle, or lower zone, and whether distortion of the lung architecture is present. Additional important features include signs of cardiac failure or fluid overload, such as increased heart size, equalization of upper and lower lobe vein size, and pleural effusions. Hilar or mediastinal enlargement caused by lymph node or vascular enlargement also should be specifically sought. In addition, the bones and soft tissues of the chest wall may provide important clues, such as evidence of previous breast surgery or an erosive arthritis. The accuracy of radiographic analysis is reduced in the absence of appropriate clinical information. For example, ascertaining whether the patient is well, acutely or chronically unwell, of normal immune status, or immunocompromised can dramatically narrow a wide range of possibilities in the radiologic differential diagnosis.

Tracheal Narrowing

Tracheal narrowing may be caused by an extrinsic mass, mediastinal fibrosis, or an intrinsic abnormality of the tracheal wall. Chronic inflammatory causes include fibrosing mediastinitis, sarcoidosis, chronic relapsing polychondritis, infection (Figure 7-64), and Wegener’s granulomatosis. Primary tumors of the trachea are rare. Benign tumors manifest as small, well-defined, intraluminal nodules that are difficult or impossible to visualize on the chest radiograph. Malignant tumors of the trachea tend to occur close to the carina (Figure 7-65), although they may be quite extensive and cause a long stricture. Tracheal wall thickening and tracheal luminal narrowing can be detected on the plain chest radiograph, especially when specifically sought, but are best appreciated on CT (Figure 7-66). The right lateral wall of the trachea (the right paratracheal stripe) above the level of the azygos vein, typically is a 2-mm-thick soft tissue stripe, and tracheal wall thickening can be detected on the plain radiograph if this portion of the airway is involved.

Figure 7-64 A, Diffuse wall thickening is present in the left and right main bronchi, just below the level of the carina. B, Diffuse tracheal wall thickening is evident at the high level, where a silicone stent is in place.

Figure 7-65 Adenoid cystic carcinoma—extensive tracheal tumor. A, Circumferential soft tissue tumor of the trachea at the level of the great vessels. B, Coronal reformatted image showing extensive tracheal wall thickening measuring, on the left, almost 2 cm (arrow).

Figure 7-66 Coronal reformatted images from computed tomography scan of the chest. A, An extensive mediastinal lymph node mass is the cause of tracheal narrowing. B, After stent insertion, airway caliber is restored.

Tracheal Widening

The normal dimensions of the trachea have been assessed by use of a variety of techniques, most recently CT. The trachea becomes slightly larger with increasing age. On CT scanning, the maximal coronal diameter of the trachea is 23 mm in a man and 20 mm in a woman. Dilatation of the trachea is rare and may result from a generalized defect of connective tissue.

Mounier-Kuhn syndrome is the condition that causes the most dramatic tracheal dilatation (Figure 7-67). It is extremely rare and was first described in 1932. On the plain radiograph, shift of the right paratracheal stripe to the right often is the only sign of tracheal widening, and because the trachea frequently is not central in location, tracheal widening can be recognized only if the left wall of the trachea also is identified. The Mounier-Kuhn syndrome is underreported because it may go undiagnosed—clinical signs and symptoms are similar to those of chronic bronchitis, COPD, or bronchiectasis. Other features include marked dilatation of the trachea and major bronchi associated with repeated respiratory infections and copious sputum production. CT scans demonstrate tracheobronchial dilatation; some will often reveal parenchymal scarring secondary to chronic infection. Bronchoscopy demonstrates dilated central airways with thickened walls. Dilatation results in ineffective mucociliary expectoration, and the subsequent chronic inflammation contributes to the cycle of infection and continued inflammation, leading to bronchiectasis and recurrent pneumonia and the development of emphysema.

Figure 7-67 Tracheobronchomegaly. Computed tomography scans showing diffuse moderate dilatation of the trachea and main bronchi in association with cystic bronchiectasis: A, At the level of the trachea. B, At the level of the carina.

Histopathologic inspection reveals loss of cartilage and muscle within the airway walls associated with dilatation and saccular diverticulosis. There may be associated connective tissue diseases such as Ehlers-Danlos syndrome in adults and cutis laxa in children. Airways usually return to normal caliber at the fourth or fifth bronchial generation. In some cases, the disease may be acquired, because a complete absence of symptoms until the third or fourth decade of life has been described.

The chest radiograph often is reported to be normal even when extensive disease is evident on CT. Management options are limited, because the central airway involvement prevents extensive surgical intervention. Postural drainage and antibiotic therapy are necessary, in parallel with other forms of bronchiectasis. In some reported cases, bronchoscopy was used to clear secretions, tracheostomy has been necessary, and transplantation has been attempted.

Another unusual form of airway dilatation was described by Williams and Campbell. All patients presented in early childhood with symptoms of cough and wheezing and recurrent pulmonary infections. On examination, the chest was barrel-shaped, and inspiratory and expiratory wheezes and clubbing were noted. In this original cohort, plain radiography and bronchography demonstrated thin-walled cystic bronchiectasis and ballooning of more peripheral airways on inspiration with collapse on expiration. Inspiratory and expiratory CT images have proved useful in the diagnosis of this syndrome in more recent reports.

Bronchiectasis

The chest radiograph is relatively insensitive for the detection of bronchiectasis, and in most series, a significant proportion of plain radiographs obtained in patients with clinical bronchiectasis are judged to be normal (Figure 7-68). The use of HRCT is discussed later on; this modality is now the investigation of choice for bronchiectasis. Abnormalities present on the chest radiograph are as follows.

Figure 7-68 Bronchiectasis. A, The chest radiograph of a patient with primary ciliary dyskinesia. Dextrocardia is obvious. Some questionable bronchial wall thickening adjacent to the left heart border is obscured. B, The changes of bronchiectasis are much more convincingly demonstrated on high-resolution computed tomography.

Bronchial wall thickening is evident as parallel, linear opacities radiating from the hilum, with lack of the normal convergence more peripherally. Ring shadows occur when the dilated airway is seen end on, may be thick- or thin-walled, and may contain secretions that produce an air-fluid level. Bronchiectatic airways that become plugged with secretions may produce tubular, soft tissue density opacities radiating from the hilum, more commonly in the lower lobes.

Distortion of the lobar anatomy with volume loss and crowding together of bronchovascular structures may be an associated finding. However, patients who have cystic fibrosis, also characterized by bronchiectasis, may have significant air trapping, which results in overexpansion. Even severe bronchiectasis may be invisible within a completely collapsed lobe.

Cylindrical (or tubular) bronchiectasis produces a dilated bronchus with parallel walls, in varicose bronchiectasis the walls are irregular, and in saccular (or cystic) bronchiectasis the airways terminate as round cysts. In an individual patient, presence of more than one pattern is typical. Bronchiectasis usually involves the peripheral bronchi more severely than the central bronchi. Although it has long been held that in allergic bronchopulmonary aspergillosis, this pattern may be reversed, overall the distribution and morphology demonstrated by CT give no more than a clue to the underlying etiology.

Mediastinal Lymphadenopathy

Lymph nodes are present in all compartments of the mediastinum but are visible on the chest radiograph only when they are calcified or enlarged. Causes of mediastinal nodal enlargement are discussed elsewhere. The chest radiograph is a relatively insensitive indicator of lymphadenopathy. Enlargement of right paratracheal nodes is identified more easily than that of left paratracheal nodes, aortic-pulmonary nodes, and subcarinal lymphadenopathies (Figure 7-70). Barium swallow is a simple method of identifying some cases of subcarinal lymphadenopathy, but CT is the most comprehensive and accurate method of assessing mediastinal nodes.

Figure 7-70 Right paratracheal lymph node enlargement caused by bronchogenic carcinoma. A, A right phrenic nerve palsy results in elevation of the right hemidiaphragm. B, Coronal volume-rendered slab image from a multidetector computed tomography machine obtained in a different patient. As in A, right paratracheal lymph node enlargement (arrows) abuts but does not distort the right brachiocephalic vein and superior vena cava.

Abnormalities of the Thoracic Aorta

The thoracic aorta arises in the middle mediastinum and then arches through the anterior, middle, and posterior mediastinal compartments. The greater vessels arise from the aortic arch in the superior mediastinum (Figure 7-71). Dilatation or tortuosity of the aortic arch or its branches may cause widening of the mediastinal shadow. So-called unfolding of the aorta is a common chest radiographic finding in elderly or hypertensive patients. Aneurysm of the aorta most often results from atherosclerosis (Figure 7-72). Cystic medial necrosis (Marfan syndrome), infection (mycotic aneurysm), syphilitic aortitis, and a history of trauma are less common causes. Most aortic aneurysms are asymptomatic and manifest as mediastinal opacities on the radiograph, sometimes with curvilinear calcification visible in the wall. Aneurysms of the ascending aorta are best appreciated on the lateral radiograph as a filling in of the retrosternal window. Aneurysms of the arch and descending aorta frequently are evident on the frontal radiograph, but a lateral view often is required for more accurate localization, and cross-sectional imaging may be warranted to confirm that the mediastinal abnormality in question is of vascular origin.

Figure 7-71 Digital subtraction arch aortogram. Two vessels can be seen arising from the arch—a common variant of the normal three-vessel anatomy. The image was obtained with the patient in a 30-degree left anterior oblique position.

Figure 7-72 Thoracic aortic aneurysm. A, On the posteroanterior radiographic view, marked dilatation and tortuosity of the descending thoracic aorta are present. Of note, the left heart border is still evident, indicating the abnormality is likely to lie in the posterior thorax. B, Lateral view in the same patient demonstrates that the aneurysm involves the posterior arch and descending thoracic aorta. Note calcification within the ascending aorta. C, Computed tomography scan demonstrating extensive mural thrombus.

In the acutely injured patient, traumatic aortic rupture may be suspected from the appearance on the chest radiograph, and confirmation of injury usually requires angiography (Figure 7-73). When the chest radiographic findings are equivocal, however, in concert with a degree of trauma less than that usually associated with aortic injury, a spiral CT scan may be performed in the stable patient to exclude a mediastinal hematoma. If any doubt remains, the patient should proceed to angiography. If the aortic injury remains undetected and the patient survives, an aneurysm secondary to the trauma may develop subsequently. Such lesions almost always are confined to the junction of the aortic arch and descending aorta. Aortic abnormalities may produce remodeling due to chronic pressure in adjacent skeletal structures.

Figure 7-73 Traumatic aortic aneurysm. A, On the posteroanterior radiographic view, a soft tissue density mass projects over the left hilum. Of note, the left lower lobe artery is still visible through this mass, indicating that it is separate from the hilum. The medial surface blends smoothly with the mediastinal structures, indicating that it is likely to be extrapulmonary. B, The lateral view confirms presence of an aneurysm secondary to previous trauma at the typical site, the junction of the posterior arch and descending thoracic aorta (arrows).

Aneurysm of the ascending aorta may be associated with erosion of the posterior surface of the sternum, and descending aortic aneurysms may cause scalloping of the spine. Tortuosity of the innominate artery is a common cause of widening of the superior mediastinum in elderly persons. Right-sided aortic arch (Figure 7-74) and pseudocoarctation of the aorta are two anomalies that may alter the appearance of the mediastinum, suggestive of a mass.

Figure 7-74 Tetralogy of Fallot. A right-sided aortic arch can be seen, in addition to elevation of the ventricular apex secondary to developing ventricular hypertrophy. Note the relatively oligemic lungs.

Abnormalities of the Esophagus

Abnormalities of the esophagus are relatively common. They include infection and inflammation, trauma and perforation, and benign and malignant neoplastic processes. Esophageal abnormalities may be associated with diseases that also involve the lungs. Such conditions are best exemplified by achalasia of the cardia (Figure 7-75) or systemic sclerosis (Figure 7-76), in which esophageal motility disorders resulting in significant dilatation and reflux may be encountered in conjunction with pulmonary fibrosis and the sequelae of recurrent aspiration.

Figure 7-75 Esophageal and gastric intrathoracic abnormalities. A, Achalasia of the cardia. The esophagus is empty, but its lateral walls are seen running up the mediastinum. B, Chest radiograph obtained in a patient who had a gastric pull-up subsequent to esophagectomy. The wall of the stomach is seen near the right chest wall margin. The stomach contains solid matter in its lower part and mainly air in its upper part. The missing rib was resected for the necessary surgery. C, Large hiatal hernia with fluid level more or less overlying the heart. No stomach bubble is seen on the chest film obtained in the conventional site, and the left hemidiaphragm is poorly demarcated.

(B and C Courtesy of Dr. M. Taylor.)

Figure 7-76 Systemic sclerosis with esophageal involvement. HRCT scan shows a coarse bibasal reticular infiltrate with marked traction bronchiectasis. In addition, the esophagus is moderately dilated and contains an air-fluid level.

Dilatation of Central Veins

The superior vena cava and the azygos vein may dilate because of increased pressure, increased flow, obstruction, or congenital abnormality. Increased flow in the superior vena cava is seen with supracardiac, total, anomalous pulmonary venous drainage (Figure 7-77), and in the azygos vein, with congenital absence of the inferior vena cava. Rarely, aneurysmal dilatation of the superior mediastinal veins produces an abnormal mediastinal silhouette. Likewise, obstruction of the superior vena cava may cause dilatation of the great veins in the superior mediastinum, which results in widening of the mediastinal contour. However, the clinical features are likely to be obvious by the time radiographic abnormalities become significant.

Figure 7-77 Total anomalous pulmonary venous drainage. Widening of the superior mediastinum on the chest radiograph is caused by dilatation of the superior vena cava.

Other Mediastinal Abnormalities

Pneumomediastinum or mediastinal emphysema is the presence of air between the tissue planes of the mediastinum. This condition may be secondary to interstitial pulmonary emphysema (most often caused by mechanical ventilation); to perforation of the esophagus, trachea, or a bronchus; or to a penetrating chest injury. Chest radiography may show vertical, translucent streaks in the mediastinum, which represent the soft tissue planes separated by air (Figure 7-78). The air may extend up into the neck and over the chest wall (causing subcutaneous emphysema) and also over the diaphragm. The mediastinal pleura may be displaced laterally and then become visible as a thin stripe alongside the mediastinum.

Figure 7-78 Pneumomediastinum. Air separates the tissue planes within the mediastinum and extends into the soft tissues of the neck and chest. A left-sided intercostal drain is in situ.

(Courtesy Dr. M. Taylor.)

Acute mediastinitis typically is caused by perforation of the esophagus, pharynx, or trachea, and a chest radiograph usually shows widening of the mediastinum. A pneumomediastinum often is apparent, and air-fluid levels may be visible in the mediastinum. Chronic or fibrosing mediastinitis usually manifests as SVCO. Mediastinal hemorrhage may occur from venous or arterial bleeding. The mediastinum appears widened, and blood may be seen to track over the lung apices. It is obviously imperative to identify a life-threatening cause such as aortic rupture.

Pleural Fluid

The most dependent recess of the pleural space is the posterior costophrenic angle, which is where a small effusion tends to collect. As little as 100 to 200 mL of fluid accumulated in this recess can be seen above the dome of the diaphragm on the frontal view. Even smaller effusions may be seen on a lateral radiograph, and it is possible to identify effusions of only a few milliliters by use of decubitus radiographic views made with a horizontal beam, ultrasound imaging, or CT. Eventually, the costophrenic angle on the frontal view fills in, and with increasing fluid a homogeneous opacity spreads upward, obscuring the lung base (Figure 7-81). The fluid usually demonstrates a concave upper edge, higher laterally than medially, and obscures the diaphragm. Fluid may track into the fissures. A massive effusion may cause complete opacification of a hemithorax with passive atelectasis. The space-occupying effect of the effusion may push the mediastinum toward the opposite side, especially when the lung does not collapse significantly (Figure 7-82).

Figure 7-81 Small, right pleural effusion. A, The lentiform opacity in the right middle zone is caused by a loculated interlobar effusion. B, Computed tomography scan on mediastinal settings demonstrating the position of the loculated fluid within the oblique fissure.

Figure 7-82 Large left pleural effusion. The patient presented with an acute empyema resulting from a lung abscess (note the air-fluid level). The mediastinal shift to the right is due to the space-occupying effects of the fluid.

Lamellar effusions are shallow collections between the lung surface and the visceral pleura, sometimes sparing the costophrenic angle. Subpulmonary effusions accumulate between the diaphragm and undersurface of a lung, mimicking elevation of the hemidiaphragm. Usually, the contour to the top of such an effusion differs from the normal diaphragmatic contour, the apparent apex being more lateral than usual. Also, some blunting of the costophrenic angle or tracking of fluid into fissures may be visible. On the left side, increased distance between the gastric air bubble and lung base may be apparent. A subpulmonary effusion may be confirmed by ultrasound imaging. However, because the fluid is free to shift within the pleural cavity with changes in patient position, a decubitus film may be needed for confirmation.

Encapsulated or encysted fluid may be difficult to differentiate from an extrapleural opacity, parenchymal lung disease, or mediastinal mass. Of note, however, an encysted effusion often is associated with free pleural fluid or other pleural shadowing and may extend into a fissure (see Figure 7-81). Loculated effusions tend to have comparatively little depth but considerable width, rather like a biconvex lens. Their appearance, therefore, depends on whether they are viewed end on, in profile, or obliquely. Extrapleural opacities tend to have a much sharper outline, with tapered, sometimes concave edges where they meet the chest wall. Peripheral, pleurally based lung lesions may show an air bronchogram, which differentiates them from true pleural disease. The differentiation between pleural thickening or mass and loculated pleural fluid may be difficult on plain films; CT and ultrasound imaging are particularly useful in this context.

Fluid may become loculated in the interlobar fissures and most frequently is seen in heart failure. Fluid that collects in the horizontal fissure produces a lenticular, oval, or round shadow, with well-demarcated edges. Loculated fluid in an oblique fissure may be poorly defined on a frontal radiograph, but a lateral film usually is diagnostic, because the fissure is seen tangentially and the typical lenticular configuration of the effusion is demonstrated. Loculated interlobar effusions can appear rounded on two views and may disappear rapidly. Hence, they are sometimes known as pulmonary pseudotumors (Figure 7-83). With subsequent episodes of heart failure, they may return at the same site.

Figure 7-83 Small, left basal pleural effusion. The opacity in the left middle zone is caused by fluid loculated in the oblique fissure.

Diagnosis of an empyema usually requires thoracentesis. Nevertheless, the diagnosis may be suspected radiographically by the spontaneous appearance on a plain film of an air-fluid level in a pleural effusion, because this feature usually equates with loculation and communication with the tracheobronchial tree or the presence of a gas-forming organism. Loculation is best demonstrated with ultrasound imaging.

Pneumothorax

A small pneumothorax is easily overlooked, and in an erect patient, the air usually collects at the apex. The lung retracts toward the hilum, and on a frontal chest film, the sharp white line of the visceral pleura is visible, separated from the chest wall by the radiolucent pleural space, which is devoid of lung markings. This appearance should not be confused with that of a skin fold (Figure 7-84). The lung usually remains aerated, although perfusion is reduced in proportion to ventilation, so the radiodensity of the partially collapsed lung remains relatively normal. A closed pneumothorax is easier to see on an expiratory film, although expiratory radiographs are not routinely required to detect clinically significant pneumothoraces. A lateral decubitus film made with the affected side uppermost occasionally is helpful, because the pleural air can be seen along the lateral chest wall. This view is particularly useful in infants, because small pneumothoraces are difficult to see on supine anteroposterior films, because the air tends to collect anteriorly and medially.

Figure 7-84 Shallow right pneumothorax. A, A discrete pleural white line is seen. Peripheral to this line, lung markings are absent. B, In this skin fold, although a change in density parallels the chest wall, no discrete pleural line is present, and lung markings are seen to extend beyond the apparent lung edge. This appearance is caused by a superficial fold of skin produced by the x-ray cassette.

A large pneumothorax may lead to complete relaxation and retraction of the lung, with some mediastinal shift toward the normal side (Figure 7-85). Because it constitutes a medical emergency, tension pneumothorax often is treated before a chest radiograph is obtained. However, if a radiograph is taken in this situation, it shows marked displacement of the mediastinum (Figure 7-86). Radiographically, the lung may be squashed against the mediastinum or herniate across the midline, and the ipsilateral hemidiaphragm may be depressed.

Figure 7-85 Left-sided pneumothorax. A, Complete collapse of the left lung, which is retracted to the left hilum. B, Magnified view of the left lower zone demonstrates the “short” air-fluid level commonly seen in a costophrenic angle when a pneumothorax is present (arrowheads).

Figure 7-86 Tension pneumothorax that developed after insertion of a Swan-Ganz catheter. Note the shift of the mediastinum toward the left and reversal of the normal contour of the right hemidiaphragm.

Complications of Pneumothorax

Pleural adhesions may limit the distribution of a pneumothorax and result in a loculated or encysted pneumothorax. The usual appearance is an ovoid air collection adjacent to the chest wall, which may be radiographically indistinguishable from a thin-walled, subpleural pulmonary cyst or bulla. Pleural adhesions occasionally are seen as line shadows that stretch between the two pleural layers; they prevent relaxation of the underlying lung. Rupture of an adhesion may produce a hemopneumothorax. Collapse or consolidation of a lobe or lung in association with a pneumothorax is important because it may delay reexpansion of the lung.

Because the normal pleural space contains a small volume of fluid, blunting of the costophrenic angle by a “short” fluid level commonly is seen on radiographs of a pneumothorax (see Figure 7-85). In a small pneumothorax, this fluid level may be the most obvious radiologic sign. A higher fluid level usually signifies a complication and represents exudate, pus, or blood, depending on the etiology of the pneumothorax (Figure 7-87).

Figure 7-87 Hydropneumothorax in a patient with a mesothelioma. A, Chest radiograph shows normal thickness of the visceral pleura, but with lobulated soft tissue shadowing caused by tumor within the parietal pleura. B, Computed tomography scan demonstrates the lobulated pleural tumor.

The usual radiographic appearance of a hydropneumothorax is that of a pneumothorax containing a horizontal fluid level that separates opaque fluid below from lucent air above. A hydrothorax or pyopneumothorax may arise as a result of a bronchopleural fistula (an abnormal communication between the bronchial tree and the pleural space). This may be a complication of surgery but also may occur as a complication of a subpleural lung tumor (Figure 7-88).

Figure 7-88 Pneumonectomy: appearances and complications. A, Chest radiograph showing the normal appearances after a right pneumonectomy. B, Spontaneous development of an air-fluid level, caused by a bronchopleural fistula from local recurrence.

Pleural Thickening

Blunting of a costophrenic angle is a common observation and usually is caused by localized pleural thickening secondary to previous pleuritis. In the asymptomatic patient and in the absence of other radiologic abnormalities, it is of no significance other than that it may simulate a pleural effusion. When relevant, the possibility of pleural fluid may have to be excluded by other techniques. Localized pleural thickening that extends into the inferior end of an oblique fissure may produce so-called tenting of the diaphragm and is of similar significance, although a similar appearance may result from scarring caused by previous pulmonary infection or infarction.

Bilateral apical pleural thickening is common, usually symmetric in distribution, and more frequent in elderly patients and does not necessarily indicate previous tuberculosis. The etiology is uncertain, but in some affected persons, the “caps” represent extrapleural fat that has descended because of scarring and consequent retraction of the upper lobes. By contrast, asymmetric or unilateral apical pleural thickening may be highly significant, especially if associated with pain. Asymmetric apical pleural shadowing may represent a Pancoast tumor, and bone destruction should be specifically sought (Figure 7-89).

Figure 7-89 Apical abnormalities. A, Benign apical pleural thickening is visible (right); a Pancoast tumor also is present (left). B, Coronal reformatted image from a computed tomography scan from another patient who also had an apical tumor.

More extensive unilateral pleural thickening usually is the result of a previous thoracotomy or an exudative pleural effusion. A simple transudate typically resolves completely, but empyema and hemothorax are more likely to resolve with residual pleural fibrosis. The thickened pleura may calcify (Figure 7-90), and the entire lung may become surrounded by fibrotic pleura, which may be as much as a few centimeters thick (Figure 7-91). Bilateral (parietal) pleural plaques are a common manifestation of asbestos exposure, and occasionally more diffuse, visceral pleural thickening is seen.

Figure 7-90 Previous thoracotomy (note sternotomy sutures) for mitral valve replacement. Pleural calcification is seen on the right side (arrows).

Figure 7-91 Previous tuberculosis. Extensive right-sided pleural thickening and calcification, with reduction in volume of the right hemithorax, are evident.

Pleural Calcification

In general, pleural calcification has the same causes as for pleural thickening. Unilateral pleural calcification is therefore likely to be the result of previous empyema or hemothorax, and bilateral calcification occurs after asbestos exposure (Figure 7-92). Pleural calcification may be discovered in a patient who was not aware of previous chest disease.

Figure 7-92 Calcified pleural thickening secondary to asbestos exposure. The subtle plaques seen on the chest radiograph (A) are better demonstrated on the computed tomography scan (B).

The calcification associated with previous pleurisy, empyema, or hemothorax occurs in the visceral pleura (Figure 7-93); associated pleural thickening is almost always present and separates the calcium from the ribs. The calcium may be in a continuous sheet or in discrete plaques, which usually produce dense, coarse, irregular shadows, often sharply demarcated laterally. When a plaque is viewed end on, it may be less well defined, mimicking a pulmonary infiltrate.

Figure 7-93 Previous sternotomy resulting in pleural thickening and calcification. A small pneumothorax is visible. Of note, the pleural thickening is associated with the visceral pleura.

Pleural Masses

Primary tumors of the pleura are rare. Benign tumors of the pleura include pleural fibroma and lipoma (Figure 7-94). The most common malignant disease of the pleura is metastatic, usually adenocarcinoma from the bronchus or breast (Figure 7-95). Malignant mesothelioma typically is associated with previous asbestos exposure.

Figure 7-94 The appearances of a pleural lipoma. A, Localized view of the right lung from a posteroanterior chest radiograph. A pleurally based opacity is present in the right middle zone, well defined medially but fading out laterally. B, Computed tomography scan of the same lesion. The opacity was due to a pleural lipoma. Note the identical signal attenuation with this mass and the subcutaneous fat.

Figure 7-95 Malignant pleural involvement from metastatic adenocarcinoma. A, Appearance on chest radiograph. B, Computed tomography after contrast enhancement shows a lobulated rind of pleural thickening extending from the right apex down to the right diaphragm, which appears elevated. The overall volume of the right hemithorax is reduced.

Anatomy of the Mediastinum

The soft tissue contrast provided by CT, as well as its cross-sectional nature, makes the diagnostic information available from CT far superior to that provided by two-dimensional radiography. Modern CT scanners can acquire a volume of imaging information that includes the whole of the mediastinum within the time of a single breath-hold. This three-dimensional dataset can then be displayed as continuous or overlapping axial slices, free from breathing movement artifact. Usually, a collimation and slice width of between 5 and 10 mm is used, and it is usual, but not always essential, to give intravenous contrast. The normal mediastinal anatomy is demonstrated in Figures 7-96 to 7-101.

Figure 7-96 Mediastinal anatomy at the level of the great vessels: computed tomography scan (A) with labeled diagram (B).

Figure 7-97 Mediastinal anatomy at the level of the aortic arch: computed tomography scan (A) with labeled diagram (B).

Figure 7-98 Mediastinal anatomy at the level of the subaortic fossa: computed tomography scan (A) with labeled diagram (B).

Figure 7-99 Mediastinal anatomy through the division of the main pulmonary artery: computed tomography scan (A) with labeled diagram (B).

Figure 7-100 Mediastinal anatomy through the aortic root: computed tomography scan (A) with labeled diagram (B).

Figure 7-101 Contrast-enhanced computed tomography scan showing left hilar lymph node enlargement with extension of abnormal tissue anterior to the descending aorta.

Lymph Nodes

Numerous lymph nodes occur within the mediastinum, usually less than 1 cm in long axis and discrete; they may not be visible on CT scanning. Previous granulomatous disease may result in extensive mediastinal lymph node calcification, which reveals the true extent of normal mediastinal lymph node distribution (Figure 7-102). An extensive chain of lymph nodes also accompanies the internal mammary vessels bilaterally. Additional nodes are present in the intercostal chain adjacent to the heads of the ribs in a posterior, paraspinal position and alongside the esophagus and descending thoracic aorta. These merge with the retrocrural lymph node chain and the paraaortic nodes in the abdomen.

Figure 7-102 Unenhanced computed tomography scan through the thorax showing faint eggshell calcification in mediastinal lymph nodes secondary to previous granulomatous disease.

Computed Tomographic Evaluation of Mediastinal Masses

Most patients who have a mediastinal mass present with symptoms from the local compressive or invasive effects of the mediastinal mass, but in a surprising number, the mass is discovered on a chest radiograph taken for an unrelated cause. Generally, the PA and lateral chest radiographs enable localization of the mass to one of the compartments of the mediastinum, which refines the differential diagnosis. However, current practice is for patients who present with a mediastinal mass to undergo a contrast-enhanced CT scan or sometimes MRI.

The differential diagnosis of a mediastinal mass is wide in scope. Masses can arise from any of the normal structures in the mediastinum, as well as from metastatic disease from a distant primary tumor. In addition, mediastinal abscesses also may manifest as a mass. The diagnosis is considerably narrowed by CT, which enables the organ of origin of the mass to be assessed, defines the attenuation and enhancement characteristics, and detects evidence of invasion of adjacent structures. It is usual to classify mediastinal masses according to the anatomic portion of the mediastinum from which they appear to arise (Figure 7-103).

Figure 7-103 Distribution and classification of mediastinal masses depending on density derived from computed tomography scan.

Superior Mediastinal Masses

Thyroid

An enlarged thyroid may extend inferiorly into the superior mediastinum and may be large enough to reach into the middle mediastinum. However, this picture rarely presents a diagnostic problem, because the mass is obviously continuous with the cervical thyroid tissue and enhances avidly after intravenous contrast. Frequently, the enlarged gland contains low-density cysts and areas of calcification, particularly within cyst walls. Large thyroid masses may cause tracheal deviation or narrowing and may enlarge acutely with hemorrhage into the gland (Figure 7-104). Although the thyroid originates anterior to the trachea, extension to the right and even posterior to the trachea within the upper mediastinum may be observed.

Figure 7-104 Retrosternal thyroid mass. A, Posteroanterior chest radiograph shows a large superior mediastinal mass mainly to the right of the trachea. B, The lateral view demonstrates an extension behind the trachea, which is narrowed in its anteroposterior dimension (arrowheads). C, The thyroid frequently extends into a retrotracheal position in the upper mediastinum, as demonstrated on this computed tomography scan from a different patient.

Lymphatic Malformations

Lymphatic malformations are rare and may arise in the superior mediastinum. The most common of these is the cystic hygroma, which usually manifests in infants as a cervical mass with an extensive intrathoracic component. Although these lesions are considered benign, complete resection is difficult to accomplish because of their tendency to spread around normal structures.

Anterior Mediastinal Masses

Most anterior mediastinal masses arise from the thymus, thyroid (see earlier), germ cell tumors, and enlarged lymph nodes.

Thymus

The normal thymus involutes after puberty but may show reactive enlargement in certain disease states or after chemotherapy. Intrinsic neoplasia of the thymus, however, is a relatively common cause of an anterior mediastinal mass in adult life. Causes of thymic neoplasia include thymoma, thymic carcinoma, thymic cysts (Figure 7-105), thymic lipoma, thymic carcinoid, and thymic lymphoma. With CT, fat or fluid elements may be identified within a thymic mass, and invasion of adjacent structures can be shown. With the exception of thymolipoma and thymic cysts, histopathologic examination usually is required for definitive diagnosis.

Figure 7-105 Thymic cyst. A, Anteroposterior chest radiograph shows mediastinal widening. B, Contrast-enhanced computed tomography scan confirms an anterior mediastinal abnormality of fluid density.

Teratomas and Germ Cell Tumors

Teratomas and germ cell tumors originate from primitive stem cell rests. It is useful to separate these neoplasms into benign and malignant forms—the former is the benign cystic teratoma (synonymous with dermoid cyst). Benign cystic teratomas (Figure 7-106) may contain differentiated elements and consequently may display a variety of densities on CT, ranging from fat to calcified tissue, and even that of teeth. The malignant teratomas comprise a variety of tumors that usually arise in the testes—namely, seminomas, teratocarcinoma, embryonal carcinoma, yolk sac tumors, and choriocarcinoma. Some mediastinal germ cell tumors may be secondary to a primary tumor arising within the gonads. Malignant germ cell tumors usually are found in young men, secrete tumor markers, and are chemosensitive.

Figure 7-106 Cystic teratoma. A, Posteroanterior, erect chest radiograph demonstrates a mass arising from the mediastinum. Note that the posterior aortic arch and descending aorta are still visualized, which indicates an anterior position. B, Computed tomography scan shows fluid and fat elements within an anterior mediastinal mass.

Lymph Node Enlargement

Lymph node enlargement is a common cause of an anterior mediastinal mass, although many processes that involve lymph nodes cause generalized mediastinal nodal enlargement. These processes may be infective (such as tuberculosis or histoplasmosis), neoplastic, reactive, or of unknown etiology (such as sarcoidosis).

Lymphoma

Hodgkin disease and, to a lesser extent, non-Hodgkin lymphoma and lymphatic leukemia frequently involve the mediastinum, especially the paratracheal, tracheobronchial, and anterior mediastinal nodes. The lymph node enlargement typically is asymmetric.

Posterior Mediastinal Masses

The posterior mediastinum contains neural elements, which give rise to a range of benign and malignant neural tumors. These may attain considerable size by the time of clinical presentation, and modeling abnormalities may occur in the adjacent ribs and spine, which provide a clue to their chronicity. On CT scanning, they typically are paraspinal in location and of soft tissue density, with patchy calcification. Also, CT may show the typical dumbbell extension of a neurofibroma, from an extraspinal position through an intervertebral foramen. In the assessment of neurogenic tumors, MRI has a distinct advantage over CT in that it can definitively confirm or exclude tumor extension into the spinal canal (Figure 7-107).

Figure 7-107 Paraganglionoma in an adult: appearance on magnetic resonance imaging. A right paraspinal T2-weighted high-signal-intensity lobulated mass is present. There is no extension into the soft tissues of the chest wall or through the neural foramina into the spinal canal.

The esophagus lies in the posterior mediastinum. Esophageal carcinoma usually manifests with dysphagia or weight loss, without presence of a mass on the chest radiograph. CT usually is reserved for the staging of esophageal malignancy, in addition to the assessment of local tumor bulk. Benign esophageal lesions may reach a considerable size before the onset of symptoms, so at initial detection on the plain radiograph, the mass may be quite large. Such tumors include fibroma, leiomyoma, and lipomas.

Neuroenteric cysts are rare congenital masses that occur in the posterior mediastinum, usually inseparable from the esophagus, and sometimes within the esophageal wall. If a vertebral or neural canal abnormality is present, these are known as neuroenteric cysts, but if not, they are termed esophageal duplication cysts. Posterior mediastinal masses may arise directly from the spinal column and may represent primary or secondary tumors, infective processes, or sequelae of trauma or degeneration.

Appearance of Normal Lung Anatomy

Accurate interpretation of HRCT scans of the lung requires an understanding of the normal appearance of the bronchi, blood vessels, and the secondary pulmonary lobule. The close correspondence between gross pathologic specimen appearance and HRCT features enables the use of anatomic terms to describe the patterns of lung disease depicted by HRCT.

Throughout the lung, the bronchi and pulmonary arteries run together and taper slightly as they travel radially; this anatomic feature is easiest to appreciate in the bronchovascular bundles that run within and parallel to the plane of HRCT section. At any given point, the diameter of the bronchus is the same as its accompanying pulmonary artery. The bronchovascular bundle is surrounded by connective tissue from the hilum to the bronchioles in the lung periphery. The concept of connected components making up the lung interstitium is useful for the understanding of HRCT findings in interstitial lung disease—the peripheral interstitium around the surface of the lung beneath the visceral pleura extends into the lung to surround the secondary pulmonary lobules. Within the lobules, a finer network of septal, connective tissue fibers supports the alveoli. The “axial” fibers form a sheath around the bronchovascular bundles. Thus, the connective tissue stroma of these three separate components is in continuity, forming a fibrous skeleton for the lungs.

In normal persons, HRCT shows a clear and definite interface between the bronchovascular bundle and surrounding lung. Any thickening of the connective tissue interstitium results in apparent bronchial wall thickening and blurring of this interface. The size of the smallest subsegmental bronchi visible on HRCT scans is determined by the thickness of the bronchial wall, rather than by the bronchial diameter. In general, bronchi with a diameter less than 3 mm and walls less than 300 mm thick are not consistently identifiable on HRCT scans. Airways reach this critical size at approximately 2 to 3 cm from the pleural surface. The secondary pulmonary lobule is the smallest anatomic unit of the lung that is surrounded by a connective tissue septum (Figure 7-108). Within the septa lie lymphatic vessels and venules. The lobule contains between 5 and 12 acini, which each measure approximately 6 to 10 mm in diameter. Each lobule is approximately 2 cm in diameter and polyhedral in shape and often resembles a truncated cone. In the lung periphery, the bases of the cone-shaped lobules lie on a visceral pleural surface. In the central parts of the lung, the interlobular septa and thus the lobules are less well developed. The centrilobular bronchiole and accompanying pulmonary artery enter through the apex of the lobule.

Figure 7-108 Anatomy of the secondary pulmonary lobule.

The interlobular septa measure approximately 100 µm in thickness. The lower limit of resolution with HRCT is approximately 200 µm, so normal septa are infrequently identified on HRCT scans. The few interlobular septa that are visible in normal persons are seen as straight lines 1 to 2 cm in length that terminate at a visceral pleural surface. Sometimes several septa that join end to end are seen as a nonbranching, linear structure, which can measure up to 4 cm in length; these are most frequent at the lung bases, just above the diaphragmatic surface.

The secondary pulmonary lobule is supplied by a centrilobular artery and bronchiole that are approximately 1 mm in diameter as they enter the lobule. In the normal state, the core structures, effectively the 500-µm-diameter centrilobular artery, are visible as dots 1 cm deep to the pleural surface. On standard window settings, the lung parenchyma is of almost homogeneous low density, marginally greater than that of air.

Patterns of Parenchymal Disease

Vague terms traditionally used in the lexicon of plain chest radiography can be replaced by precise descriptions derived from an understanding of HRCT anatomy. Abnormal patterns on HRCT scans that represent pulmonary disease usually can be categorized into one of four patterns: reticular and linear opacities, nodular opacities, increased lung density, and cystic air spaces with areas of decreased lung density.

Although each of these patterns generally has a corresponding pattern on chest radiography, they are seen with much greater clarity on cross-sectional HRCT images, and the precise distribution of disease can be more readily appreciated. Increasing conformity is emerging in the terminology used to describe the HRCT abnormalities of diffuse infiltrative lung diseases.

Reticular Pattern

A reticular pattern on HRCT scans always indicates significant pathology. A reticular pattern caused by thickening of interlobular septa is a cardinal sign of many interstitial lung diseases. Numerous interlobular septa that join up to form an obvious network indicate an extensive interstitial abnormality caused by infiltration with fibrosis, abnormal cells, or fluid (e.g., fibrosing alveolitis, lymphangitis carcinomatosa, or pulmonary edema, respectively). Interlobular septal thickening that results from fibrosing alveolitis often is associated with intralobular, interstitial thickening (beyond the resolution of HRCT) and a coarse reticular pattern that contains cystic air spaces and produces the honeycomb pattern of destroyed lung. Thickening of the interlobular septa may be smooth or irregular, but this distinction is not always obvious. Irregular septal thickening is a feature of lymphangitic spread of tumor, whereas pulmonary edema and alveolar proteinosis cause smooth thickening. Sarcoidosis is typified by some nodular septal thickening, although widespread septal thickening is not characteristic of this condition.

Because the various parts of the lung interstitium are in continuity, widespread interstitial disease that causes interlobular septal thickening also results in bronchovascular interstitial thickening (e.g., by lymphangitis carcinomatosa). The bronchovascular thickening seen on HRCT is equivalent to the peribronchial “cuffing” seen around bronchi in end-on views on chest radiography. The HRCT finding of peribronchovascular thickening in isolation must be interpreted with caution, because it may be seen in reversible pure airway disease, for example, asthma. With thickening of the subsegmental and segmental bronchovascular bundles caused by lymphangitis carcinomatosa, for example, the interface between the thickened bronchial wall and surrounding lung sometimes has a “feathery” appearance (Figure 7-109).

Figure 7-109 High-resolution computed tomography scan showing generalized, irregular thickening of the interlobular septa in the right lung. The patient had lymphangitis carcinomatosa.

The coarseness of the network that makes up the reticular pattern on HRCT is determined by the level at which the interstitial thickening is most severe. Thickening of the intralobular septa results in a very fine reticular pattern on HRCT, visible only on an optimal HRCT scan. Some of the very delicate linear structures that make up such a fine reticular pattern are so small as to be below the resolution limits of HRCT, even with the narrowest collimation. The result is an amorphous increase in lung density (“ground glass” opacification) (see further on) caused by volume averaging within the section.

Extensive pulmonary fibrosis causes complete destruction of the architecture of the secondary pulmonary lobules, which results in a coarse reticular pattern made up of irregular, linear opacities. The reticular pattern of end-stage fibrotic or honeycomb lung mirrors the appearance on chest radiographs and is characterized by cystic spaces that measure a few millimeters to several centimeters across and are surrounded by discernible walls (Figure 7-110). Paradoxically, thickened interlobular septa are not an obvious feature of advanced fibrosing alveolitis, probably because of the severe disturbance of the normal lung architecture. The distortion that accompanies interstitial fibrosis may result in irregular dilatation of the segmental and subsegmental bronchi without honeycomb change, a phenomenon termed traction bronchiectasis (see Figure 7-110).

Figure 7-110 High-resolution computed tomography in fibrosing alveolitis. A, In the first patient, coarse cystic spaces are visible throughout the lung bases. B, In a second patient, finer fibrotic changes are seen. Traction bronchiectasis is evident in both cases, which is a typical feature of the usual interstitial pneumonitis (UIP) pattern. C, In a third patient, the much more marked ground glass changes are characteristic of nonspecific interstitial pneumonia (NSIP) pattern.

Nodular Pattern

A nodular pattern on HRCT consists of innumerable, small, discrete opacities that range in diameter from 1 to 10 mm and is a feature of both interstitial and air space diseases. The location of nodules in relation to the lobules and bronchovascular bundles, as well as their density, clarity of outline, and uniformity of size, may indicate whether the nodules lie predominantly within the interstitium or air spaces. Because most diffuse lung pathoses have both interstitial and air space components, this distinction does not always aid in the diagnosis. Whether pulmonary nodules can be detected on CT depends on their size, profusion, and density and on the scanning technique. Narrow-collimation HRCT clearly is superior to conventional CT for the detection of micronodular disease because it is associated with less partial volume effect, which can average out the attenuation of tiny nodules. A further refinement is the use of maximum-intensity projection images obtained with spiral CT to detect extremely subtle micronodular disease. Nodules within the lung interstitium are seen in the interlobular septa, subpleural regions (particularly in relation to the fissures), and in a peribronchovascular distribution. Nodular thickening of the bronchovascular interstitium results in an irregular interface between the margins of the bronchovascular bundles and the surrounding lung parenchyma. These features are most pronounced in cases of sarcoidosis, in which coalescent, perilymphatic granulomas cause a beaded appearance of the thickened bronchovascular bundles. The bronchovascular distribution of nodules, in conjunction with a perihilar concentration of disease, is virtually pathognomonic for sarcoidosis (Figure 7-111).

Figure 7-111 High-resolution computed tomography imaging of the lungs in a patient with sarcoidosis. A, Parenchymal nodularity together with thickening and beading of the bronchovascular bundles is typical of sarcoidosis. B, Coronal reformatted image through the lungs of the same patient demonstrates the middle and upper zone predominance of disease.

The nodular pattern seen in coal worker’s pneumoconiosis and silicosis generally is more uniform in distribution. Centrilobular nodules may be more numerous in the upper zone and in subpleural regions, but overall they tend to be more evenly spread throughout the lung parenchyma than those seen in sarcoidosis.

When the air spaces are filled, or partially filled, with exudate, individual acini may become visible as poorly defined nodules approximately 8 mm in diameter. Acinar nodules may merge with areas of ground glass opacification and sometimes are seen around the periphery of areas of dense parenchymal consolidation (Figure 7-112). Such nodules usually are centrilobular, although this localization may be difficult to appreciate if the nodules are very profuse. Conditions in which this nonspecific pattern is seen include organizing pneumonia, hypersensitivity pneumonitis (Figure 7-113), endobronchial spread of tuberculosis, idiopathic pulmonary hemorrhage, and some cases of bronchoalveolar cell carcinoma.

Figure 7-112 Poorly defined acinar nodules. Generalized ground glass density and interlobular septal thickening also are evident. The patient had cardiogenic pulmonary edema.

Figure 7-113 High-resolution computed tomography scan showing poorly defined nodular opacities merging with ground glass opacification. The patient had subacute hypersensitivity pneumonitis.

Increased Lung Density

An amorphous increase in lung density on HRCT often is described as a ground glass opacification appearance (Figure 7-114). Unlike the equivalent abnormality on chest radiography, in which the pulmonary vessels often are indistinct, a ground glass pattern on HRCT does not obscure the pulmonary vasculature. In cases in which the presence of a ground glass pattern is equivocal, HRCT often is useful to compare the density of the lung parenchyma with air in the bronchi—in the normal state, the difference in density is marginal. Although this HRCT abnormality usually is easily recognizable, particularly when it is interspersed with areas of normal lung parenchyma, subtle degrees of increased parenchymal opacification may not be obvious. It is important to recognize that a normal increase in parenchymal density, indistinguishable from a generalized opacification caused by infiltrative lung disease, results in a ground glass pattern in patients who breath-hold at end expiration.

Figure 7-114 Ground glass appearance on high-resolution computed tomography. Extensive ground glass opacification in a patient with desquamative interstitial pneumonitis. Note that the vessels are visible within the areas of ground glass opacification.

On a pathologic level, the changes responsible for ground glass opacification are complex and include partial filling of the air spaces and thickening of the interstitium, or a combination of the two (Figure 7-115). Conditions that are characterized by these pathologic changes and result in the nonspecific pattern of ground glass opacification include fibrosing alveolitis in the active cellular phase, Pneumocystis pneumonia, subacute hypersensitivity pneumonitis, sarcoidosis, drug-induced lung damage, diffuse pulmonary hemorrhage, and acute lung injury. The amorphous ground glass density seen on HRCT in these conditions usually represents a potentially reversible process. However, mild thickening of the intralobular interstitium by irreversible fibrosis may rarely produce a ground glass appearance in fibrosing alveolitis. Furthermore, ground glass opacification may be seen in areas of bronchoalveolar cell carcinoma, usually in conjunction with patches of denser, consolidated lung (Figure 7-116).

Figure 7-115 Normal and diseased lung voxels. A, In the normal state, most of the volume of these voxels is made up of air. B, Gross thickening of the interstitium and some cells within the air spaces causes displacement of air and a corresponding increase in density within the voxels—this produces ground glass opacification on a high-resolution computed tomography image. C, In established pulmonary fibrosis, the strands of fibrotic lung occupy much of the volume of individual voxels, which is reflected in their density; pulmonary fibrosis thus has a reticular pattern on high-resolution computed tomography.

Figure 7-116 Patchy areas of ground glass opacification in a patient with biopsy-proven bronchoalveolar cell carcinoma.

A pitfall in identifying a ground glass pattern on HRCT occurs when regional differences in pulmonary perfusion are present—regional alterations in pulmonary blood flow, caused by thromboembolism, for example, may result in striking differences in lung density (Figure 7-117). The density difference between the underperfused lung and normal lung may give the appearance of a ground glass density in normal (but relatively overperfused) lung parenchyma. These areas of different density have often been termed mosaic oligemia. A similar appearance is seen in patients who have patchy air trapping caused by small airway disease, such as in an obliterative bronchiolitis: The relatively transradiant areas of underventilated and thus underperfused lung make the normal lung parenchyma appear more than usually dense and thus simulate a ground glass infiltrate. This potential pitfall often can be recognized for what it is by the relative paucity of vessels in the underventilated parts of the lungs caused by hypoxic vasoconstriction. The vessels in the relatively normal lung of higher density are engorged because of shunting of blood to these regions (see Figure 7-117).

Figure 7-117 Coronal reformatted images from MDCT dataset. Uneven density of the lung parenchyma caused by perfusion inhomogeneity. The patient had chronic thromboembolism. A, Coronal reformatted image using lung window settings demonstrates the mosaic attenuation pattern. B, On mediastinal window settings, the large central pulmonary arteries are evident.

Cystic Air Spaces

The term cystic air space describes a clearly defined, air-containing space that has a definable wall 1 to 3 mm thick. Many conditions are characterized by a profusion of cystic air spaces, which may not be recognizable as such on chest radiography (Figure 7-118), whereas the size and distribution of these cysts on HRCT may suggest the diagnosis.

Figure 7-118 Cystic air spaces. A, Nonspecific shadowing on a chest radiograph, with the suggestion of a cavitating nodule in the right upper zone. B, High-resolution computed tomography scan through the upper lobes reveals multiple curious-shaped, cavitating lesions, typical of Langerhans cell histiocytosis.

The destruction of alveolar walls that characterizes emphysema produces areas of low attenuation on HRCT, which often merge imperceptibly with normal lung (Figure 7-119). In patients who have predominantly centrilobular emphysema, circular areas of lung destruction may resemble cysts; however, the centrilobular core usually is visible as a dotlike structure in the center of the apparent cyst. Although bullae of varying sizes are clearly seen on HRCT in patients who have emphysema, usually a background permeative, destructive parenchyma prevents confusion with other conditions in which cystic air spaces are a prominent feature.

Figure 7-119 High-resolution computed tomography in centrilobular versus other forms of emphysema. A, Centrilobular emphysema. Note the permeative destruction of the lung parenchyma with scattered centrilobular lucent areas. B, Paraseptal emphysema. The disease is concentrated in the subpleural lung. C, Panacinar emphysema. Large swathes of completely destroyed lung are evident, with almost no vascular or soft tissue structures demonstrated within.

Cystic air spaces as the dominant abnormality are seen in only a few conditions, which include lymphangioleiomyomatosis, Langerhans cell histiocytosis, end-stage fibrosing alveolitis, and postinfective pneumatoceles. In lymphangioleiomyomatosis, the cysts usually are uniformly scattered throughout the lungs, with normal lung parenchyma intervening; the individual cysts rarely are larger than 4 cm in diameter (Figure 7-120). As the disease progresses, the larger cystic air spaces coalesce; the circumferential, well-defined walls of the cysts become disrupted; and the HRCT pattern in advanced lymphangioleiomyomatosis, and indeed in Langerhans cell histiocytosis, may be practically indistinguishable from that in severe centrilobular emphysema. Distinction of the delicate, “lacelike” reticular pattern of lymphangioleiomyomatosis on HRCT from that of end-stage fibrosing alveolitis usually is possible, because the cystic air spaces in a fibrotic honeycomb lung are smaller and have thicker walls. Furthermore, the tendency for fibrosing alveolitis to have a peripheral distribution, even in its end stage, usually is still obvious in the upper zones.

Figure 7-120 High-resolution computed tomography in advanced lymphangioleiomyomatosis. Note the coalescence of cystic air spaces, which resembles that in severe centrilobular emphysema.

Similar, confluent cystic air spaces that give a delicate pattern on HRCT are seen in images obtained in patients who have advanced Langerhans cell histiocytosis. Earlier in the disease, however, a nodular component is present, and some of the nodules cavitate. The combination of cavitating nodules, some of which have curious shapes (e.g., cloverleaf shape), and cystic air spaces with a predominantly upper zone distribution is virtually pathognomonic for this diagnosis (see Figure 7-118). Serial HRCT scans show the natural history of nodules, which cavitate, become cystic air spaces, and, in end-stage disease, coalesce. In a few cases, these pathologic changes may resolve, with the lung parenchyma reverting to a normal appearance. Some of the cavitating nodules in Langerhans cell histiocytosis superficially resemble bronchiectatic airways, but a lack of continuity between these lesions will be observed on adjacent sections, and the segmental bronchi, when they can be identified, do not have any of the HRCT features of bronchiectasis.

Diseases of the Airways

Now that bronchography is rarely performed, the imaging modality of choice to diagnose bronchiectasis is HRCT. Bronchiectasis is defined as damage to the bronchial wall that results in irreversible dilatation of the bronchi, whatever the cause. Thus, the main feature of bronchiectasis on HRCT is dilatation of the bronchi with or without bronchial wall thickening. Criteria for the HRCT identification of abnormally dilated bronchi depend on the orientation of the bronchi in relation to the plane of the HRCT section (Figure 7-121).

Figure 7-121 High-resolution computed tomography features of bronchiectasis: nontapering or flaring of bronchi lying within the plane of section; “signet ring” sign of dilated bronchi running perpendicular to the plane of computed tomography section; mucous plugging of large, dilated airways; plugging and peribronchiolar thickening of small peripheral airways; crowding with associated loss of volume (see position of oblique fissure); and areas of decreased attenuation, which reflect associated small airway disease.

Vertically oriented bronchi are seen in transverse section, so reference can be made to the accompanying pulmonary artery, which in normal persons is of approximately the same caliber; any dilatation of the bronchus results in the so-called signet ring sign (Figure 7-122). Although this generally constitutes reliable evidence of abnormal bronchial dilatation, care must be taken in comparing the diameter of the bronchi and adjacent pulmonary arteries just below the division of the lower lobe bronchus. At this level, pairs of segmental and sometimes subsegmental bronchi converge, and the resulting fusion of the two bronchi may give the spurious impression of an abnormally dilated bronchus. Bronchi that have a more horizontal course on CT scans, particularly the anterior segmental bronchi of the upper lobes and the segmental bronchi of the lingula and right middle lobe, are demonstrated along their length, and abnormal dilatation is seen as nontapering parallel walls or even flaring of the bronchi as they course distally (Figure 7-123). In more severe cases of bronchiectasis, the bronchi are obviously dilated and have a varicose or cystic appearance.

Figure 7-122 Bronchiectasis in two different patients. A, Cylindrical bronchiectasis without plugging has a characteristic signet ring appearance. B, With more severe disease, some airway plugging is seen in the tip of the lingula.

Figure 7-123 High-resolution computed tomography scan obtained in a patient with cystic fibrosis. Nontapering and flaring of the bronchiectatic airways are evident in the apical segment of the right lower lobe. In addition, mosaic perfusion is present, reflecting associated small airway disease.

Bronchial wall thickening is a frequent but not invariable feature of bronchiectasis. The definition of what constitutes abnormal bronchial wall thickening remains contentious, particularly because mild degrees of wall thickening are seen in normal subjects, asymptomatic smokers, asthmatic individuals, and patients affected by an acute, lower respiratory tract, viral infection. In brief, no robust and reproducible criterion for the identification of abnormal bronchial wall thickening has been identified, so bronchial wall thickening remains a subjective sign with an attendant high variation in observer interpretation. However, it is the presence of peribronchial thickening that renders the smaller peripheral airways visible on HRCT. Although there is no exact level beyond which visualization of the bronchi can be regarded as abnormal on HRCT, normal bronchi should not be visible within 2 to 3 cm of the pleural surface. Large elliptical and circular opacities, which represent secretion-filled, dilated bronchi, constitute a sign of gross bronchiectasis and are almost invariably seen in the presence of other obviously dilated bronchi, some of which may contain air-fluid levels (Figure 7-124). When mucous plugging of the smaller airways occurs, minute branching structures or dots in the lung periphery may be identifiable. In some cases, plugging of the numerous centrilobular bronchioles gives a curious nodular appearance to the lungs (Figure 7-125).

Figure 7-124 Severe bronchiectasis in the left upper lobe. Some bronchi are filled with secretions, which results in multiple tubular and elliptical opacities. The patient had allergic bronchopulmonary aspergillosis.

Figure 7-125 Numerous small irregular opacities in the left lower lobe representing plugged bronchioles. The patient had panbronchiolitis.

Supplementary HRCT evidence of bronchiectasis includes crowding of the affected bronchi, with obvious volume loss of the lobe as shown by the position of the major fissures. In many lobes affected by bronchiectasis, areas of decreased attenuation of the lung parenchyma adjacent to the abnormal airways can be identified; this pattern of mosaic attenuation is thought to reflect accompanying small airway disease, and the extent of the pattern correlates well with functional evidence of airflow obstruction, particularly indices of small airway dysfunction.

A positive diagnosis of bronchiectasis on HRCT is straightforward in patients who have moderate and severe disease. In some situations, however, subtle signs of bronchiectasis may be obscured by technical artifacts. Conversely, the HRCT appearance of bronchiectasis may be mimicked by other lung pathoses. Some of the causes of false-negative and false-positive diagnoses of bronchiectasis are listed in Table 7-2.

Table 7-2 Causes of False-Positive and False-Negative Diagnosis of Bronchiectasis on High-Resolution Computed Tomography

Interest in the ability of HRCT to detect small airway disease is increasing. In the exudative form of bronchiolar disease (typified by Japanese panbronchiolitis), HRCT directly shows the plugged small airways as small, irregularly branching opacities. The HRCT signs of constrictive obliterative bronchiolitis (e.g., in patients with rheumatoid arthritis or postviral obliterative bronchiolitis) are indirect—areas of decreased attenuation occur within which the vessels are of reduced caliber (but not distorted, in contrast with emphysema). The areas of decreased attenuation may merge with those of more normal lung or may have sharply demarcated, “geographic” boundaries (mosaic attenuation pattern). The density differences that characterize constrictive obliterative bronchiolitis may be extremely subtle, but because they represent areas of reduced ventilation with consequent air trapping, they may be dramatically emphasized on scans performed at end expiration. Most patients affected by small airway disease ill exhibit some bronchiectatic changes on HRCT, which tend to be more severe in those who have immunologically mediated obliterative bronchiolitis.