Fundamentals of Diagnostic Radiology
3rd Edition

Chapter 12
Methods of Examination, Normal Anatomy, and Radiographic Findings of Chest Disease
Santiago Miró
Jeffrey S. Klein
There are many imaging techniques available to the radiologist for the evaluation of thoracic disease (1). The decision about which imaging procedures to perform depends upon many factors, the most important of which are the availability of various modalities and the type of information sought. Although conventional radiographs of the chest still constitute 25% to 35% of the volume of any general radiology department, there has been a steady decline in favor of CT, despite the considerable increase in radiation to the patient. The recent years have seen near disappearance of diagnostic thoracic vascular interventions, thanks to CT and MR. The recent advent of multichannel, parallel MR imaging might allow for gradual replacement of CT for thoracic vascular diagnostics. Although the imaging algorithm for specific problems may seem relatively straightforward, medical judgment should be preferred. For example, a thin-section CT showing a suspicious solitary pulmonary nodule might be followed directly by a thoracotomy, or rather, in selected patients, by transthoracic needle biopsy. This type of flexible approach will often streamline the diagnostic workup and ultimately lead to better patient care.
Imaging Modalities
Conventional Chest Radiography
Posteroanterior (PA) and lateral chest radiographs are the mainstays of thoracic imaging. Conventional radiographs should be performed as the initial imaging study in all patients with thoracic disease. These films are obtained in most radiology departments on a dedicated chest unit capable of obtaining radiographs with a focus-to-film distance of 6 feet, a high kilovoltage-potential (140-kVp) technique, a grid to reduce scatter, and a phototimer to control the length of exposure (2).
The recognition of proper radiographic technique on frontal radiographs involves assessment of four basic features: penetration, rotation, inspiration, and motion. Proper penetration is present when there is faint visualization of the intervertebral disk spaces of the thoracic spine and
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discrete branching vessels can be identified through the cardiac shadow and the diaphragms. Rotation is assessed by noting the relationship between a vertical line drawn midway between the medial cortical margins of the clavicular heads and one drawn vertically through the spinous processes of the thoracic vertebrae. Superimposition of these lines (the former in the midline anteriorly and the latter in the midline posteriorly) indicates a properly positioned, nonrotated patient. An appropriate deep inspiration in a normal individual is present when the apex of the right hemidiaphragm is visible below the tenth posterior rib. Finally, the cardiac margin, diaphragm, and pulmonary vessels should be sharply marginated in a completely still patient who has suspended respiration during the radiographic exposure (Fig. 12.1).
FIGURE 12.1. Normal PA (A) and Lateral (B) Radiographs of the Chest.
Portable Radiography
Portable anteroposterior (AP) radiographs are obtained when patients cannot be safely mobilized (3). Portable radiographs help monitor a patient’s cardiopulmonary status; assess the position of various monitoring and life support tubes, lines, and catheters; and detect complications related to the use of these devices.
There are technical and patient-related compromises as well as inherent physiologic changes with portable bedside radiography. The limited maximal kilovoltage potential of portable units requires longer exposures to penetrate cardiomediastinal structures, which results in greater motion artifact. Because critically ill patients are difficult to position for portable radiographs, the patient is often rotated. Inaccuracies in directing the x-ray beam perpendicular to the patient lead to kyphotic or lordotic radiographs. The short focus-to-film distance (typically 40 inches) and AP technique result in magnification of intrathoracic structures. For instance, the apparent cardiac diameter increases by 15% to 20%, bringing the upper limit of normal for the cardiothoracic ratio from 50% on a PA radiograph to 57% on an AP. Physiologically, the supine position of critically ill patients elevates the diaphragm, thus compressing lower lobes and decreasing lung volumes. The normal gravitational effect evens out the blood flow between upper and lower zones in supine patients, which makes assessment of pulmonary venous hypertension difficult. The increase in systemic venous return to the heart produces a widening of the upper mediastinum or “vascular pedicle.” The gravitational layering of free-flowing fluid may hide small effusions. Similarly, a pneumothorax may be difficult to detect because free intrapleural air rises to a nondependent position, producing a subtle anteromedial or inferior radiolucency. A device called the inclinometer has been developed that accurately records the position of the bedridden patient from supine to completely upright. This device, which clips onto the portable film cassette, gives an accurate estimate of the patient’s position at the time of the radiograph, which helps assess the distribution of pulmonary blood flow, pleural effusions, and pneumothorax.
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Digital or Analog?
The main advantages of digital chest radiography are superior contrast resolution and the availability of the image on any computer monitor through a PACS (Picture Archiving and Communication System). Contrast levels and windows can be adjusted to enhance visualization of various regions in the chest or compensate partly for faulty exposure. Although digital images have poorer spatial resolution than their analog counterparts, these benefits render the system appealing.
Special Techniques
A lateral decubitus radiograph is obtained with a horizontal x-ray beam while the patient lies in the decubitus position. It is used to detect small effusions, to characterize free-flowing effusions on the decubitus side, or to detect a small pneumothorax on the contralateral side. As little as 5 mL of fluid (Fig. 12.2) or 15 mL of air can be demonstrated by this view. Normally, the downside diaphragm assumes a higher position than the upside one. Air trapping can be demonstrated in the dependent lung in patients with a check valve bronchial obstruction who are unable to cooperate for inspiratory/expiratory radiographs or chest fluoroscopy.
An expiratory radiographobtained at residual volume (end of maximal forced expiration) can detect focal or diffuse air trapping and eases detection of a small pneumothorax. In the absence of a direct communication between the pleura and the bronchi, the volume of air in the pleural space remains stable, whereas the volume of air in the lung parenchyma decreases. Because the lung is also displaced away from the chest wall, the visceral pleural line becomes more visible.
FIGURE 12.2. Lateral Decubitus Film for the Detection of Pleural Effusion. An upright radiograph (A) in a patient recovering from pulmonary edema shows blunting of both lateral costophrenic sulci. A left lateral decubitus film (B) demonstrates free-flowing effusion laterally on the down side (solid arrows) and within the lateral aspect of an incomplete oblique fissure (open arrows). Note the clearing of fluid from the right lateral costophrenic sulcus with the patient in the opposite decubitus position, with fluid layering medially along the mediastinal pleural surface.
An apical lordotic view improves visualization of the lung apices, which are obscured on routine PA radiographs by the clavicles and first costochondral junctions. Caudocephalad angulation of the tube projects these anterior bony structures superiorly, providing an unimpeded view of the apices. This view enhances the visualization of middle lobe atelectasis by placing the inferiorly displaced minor fissure in tangent with the x-ray beam and by increasing the AP thickness of the atelectatic middle lobe.
Chest fluoroscopy is used mainly to assess chest dynamics on patients with suspected diaphragmatic paralysis. Although it has been widely abandoned to the benefit of CT, fluoroscopy can still often bring the same answers as CT at a fraction of the radiation exposure: evaluation of a nodular opacity seen on only one view, evaluation of apparent pseudotumor images caused by vertebral lamina, osteophytes, vertebral transverse processes, healed rib fractures, skin lesions, nipples, or other external objects.
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CT and HRCT
Thoracic chest CTs can be acquired either in an incremental “stop, acquire, and go” mode, such as for HRCTs, or in a helical mode, whereby acquisition occurs while the patient translates through the gantry on the CT scan table. The latter allows single breath-hold scans with optimal contrast enhancement, without the respiratory misregistration inherent in incremental scanning. Multidetector scanners now allow for full chest coverage with collimation as narrow as 1.0 mm in approximately 20 seconds. Cardiac gating on such scanners can eliminate pulsation artifacts, for example, in the ascending aorta, and also allows for diagnostic evaluation of the heart, at a threefold or fourfold increase in radiation dose (4). Scans without contrast are usually performed for evaluation or follow-up of parenchymal disease. Iodinated contrast material is administered for mediastinal mass or cancer staging evaluation, systemic or pulmonary arterial evaluation, or for cardiac studies.
The field of view for image reconstruction is determined by measuring the widest transverse diameter, as seen on the CT scout view. An edge-enhancing computer reconstruction algorithm (“bone” or “sharp” algorithm) improves the spatial resolution of parenchymal structures and is used for all types of thoracic CT scans. Most frequently, the image is reconstructed in a 512 × 512 matrix size. Matrix sizes up to 1,024 × 1,024 are now available, but studies would be needed to assess whether there is any diagnostic benefit to this fourfold increase in image size. Although images can still be filmed using a laser camera, PACS workstation viewing offers the possibility to modify window width (WW) and window level (WL) as needed. Routine settings for CT display of mediastinal structures are WW = 400 and WL = 40 and for the lungs are WW = 1,500 and WL = –700.
HRCT technique involves incremental thinly collimated scans (1.0 to 1.5 mm) obtained at evenly spaced intervals through the thorax for the evaluation of diffuse bronchial or parenchymal lung disease. Image acquisition time is limited to minimize the effects of respiratory and cardiac motion. Expiratory HRCT scans are useful for the detection of air trapping in patients with small airways disease. Normal and abnormal HRCT findings are reviewed in Chapter 17.
The volume of data of a helical CT is acquired with a thickness (collimation) of 0.5 to 10 mm, and the user can then determine the reconstruction interval, which is chosen according to the amount of desired overlap. For example, a helical scan covering 25 cm with a 2.0-mm collimation can be reconstructed with a 2.0-mm interval, yielding 125 contiguous images with no overlap, but could also be reconstructed at a 1.25-mm interval, yielding 200 images, each of which overlaps the following image by 0.75 mm (4).
The major advantages of CT are its superior contrast resolution and cross-sectional display format. Superior contrast resolution allows for the differentiation of calcium, soft tissue, and fat within lung nodules or mediastinal structures. Intravenous enhancement improves contrast within structures or masses, as well as within blood vessels (e.g., pulmonary emboli, aortic dissection). The cross-sectional display eliminates the superimposition of structures and allows visualization of parenchymal nodules as small as 2 mm.
TABLE 12.1 Indications for Thoracic CT
Indication Example
Evaluation of an abnormality identified on conventional radiographs Densitometry of a solitary pulmonary nodule
Localization and characterization of a hilar or mediastinal mass
Staging of lung cancer Assessment of extent of the primary tumor and the relationship of the tumor to the pleura, chest wall, airways, and mediastinum
Detection of hilar and mediastinal lymph node enlargement
Detection of occult pulmonary metastases Extrathoracic malignancies with a propensity to metastasize to the lung (osteogenic sarcoma, breast and renal cell carcinoma).
Detection of mediastinal nodes Lymphoma, metastases
Infections
Distinction of empyema from lung abscess Contrast-enhanced CT can usually distinguish a peripheral lung abscess from loculated empyema
Detection of central pulmonary embolism Angio-CT with high injection rate, thin collimation, and precise contrast bolus timing
Detection and evaluation of aortic disease: aneurysm, dissection, intramural hematoma, aortitis, trauma Detection and localization of extent, including aortic branch involvement
The clinical indications for thoracic CT will vary among institutions. The indications for thoracic CT and HRCT are shown in Tables 12.1 and 12.2.
MR
As MR usage expands, studies must be tailored to the individual patient. Morphologic studies usually require only spin-echo T1W and T2W sequences in the axial plane. Coronal and sagittal planes are used in selected cases. Mass evaluation might benefit from fat-suppressed sequences such as STIR, or from gadolinium-enhanced sequences. Angiographic acquisitions are most often performed with GRE volumetric acquisitions. Cardiac sequences benefit from cardiac-gated balanced steady-state free precession
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(SSFP) techniques. Respiratory motion is minimized by performing rapid single breath-hold acquisitions or by using respiratory compensation techniques. The latest generation of multichannel scanners with parallel imaging and faster gradients show promise in evaluation of embolic disease, without the radiation cost of multidetector CTs (5).
TABLE 12.2 Indications for Thoracic HRCT
Indication Example
Solitary pulmonary nodule Breath-hold volumetric exam with thin collimation for accurate density determination without respiratory misregistration
Detection of lung disease in a patient with pulmonary symptoms or abnormal pulmonary function studies and a normal or equivocal chest film Emphysema
Extrinsic allergic alveolitis
Small airways disease
Immunocompromised patient
Evaluation of diffusely abnormal chest film  
A baseline for evaluation of patients with chronic diffuse infiltrative lung disease for follow-up changes with therapy Cystic fibrosis
Sarcoidosis
Interstitial lung disease
Histiocytosis X
Adult respiratory distress syndrome
To determine approach (type and location) of biopsy Bronchoscopy versus VATS or needle biopsy
VATS = video assisted thoracic surgery
The major advantages of MR are the superior contrast resolution between tumor and fat, the ability to characterize tissues based on T1 and T2 relaxation times, the ability to scan in direct sagittal and coronal planes, and the lack of need for intravenous iodinated contrast (6). In addition, the ability to obtain images along the long axis of the aorta and the advent of cine-MR techniques have made MR the primary modality for the imaging of most congenital and acquired thoracic vascular disorders. Direct coronal scans are of benefit in imaging regions that lie within the axial plane and are therefore difficult to depict on CT. For this reason, superior sulcus tumors, subcarinal and aortopulmonary window lesions, and certain hilar masses are better depicted by MR than CT. MR is superior to CT in the diagnosis of chest wall or mediastinal invasion because of the high contrast between tumor and chest wall fat and musculature and tumor and mediastinal fat, respectively. The characterization of tissues by their T1 and T2 relaxation times allows for the diagnosis of fluid-filled cysts, hemorrhage, and hematoma formation. The ability to distinguish tumor from fibrosis, based on their T1 and T2 relaxation times, has proven particularly useful in the follow-up of patients irradiated for Hodgkin disease. MR is currently unable to distinguish benign masses from malignant masses or lymph nodes.
TABLE 12.3 Indications for MR of the Thorax
Evaluation of aortic disease in stable patients: Dissection, aneurysm, intramural hematoma, aortitis
Assessment of superior sulcus tumors
Evaluation of mediastinal, vascular, and chest wall invasion of lung cancer
Staging of lung cancer patients unable to receive intravenous iodinated contrast
Evaluation of posterior mediastinal masses
The major disadvantages of thoracic MR scanning are the limited spatial resolution, the inability to detect calcium, and the difficulties in imaging the pulmonary parenchyma. MR is also more time-consuming and expensive than CT. These factors, along with the ability of CT to provide superior or equivalent information in most situations, have limited the use of thoracic MR for most noncardiovascular thoracic disorders. The primary indications for thoracic MR are listed in Table 12.3.
PET
PET utilizing fluorodeoxyglucose (FDG) is an imaging modality based on the metabolic activity of neoplastic and inflammatory tissues and therefore can be considered complementary to the anatomic information provided by chest radiography and CT (1). The role of PET in oncologic diagnosis and staging has developed gradually over the past decade. There is a growing published experience of whole-body PET in the evaluation of patients with malignancy, particularly bronchogenic carcinoma, and of thoracic PET for the evaluation of the solitary pulmonary nodule.
US
Transthoracic US is now commonly used for the detection, characterization, and sampling of pleural, peripheral parenchymal, and mediastinal lesions (see Chapter 39). The aspiration of small pleural effusions visualized on real-time US is preferable to blind thoracentesis. Similarly, sampling of visible pleural masses in patients with malignant effusions can diminish the number of negative pleural biopsies. The aspiration of pleural-based masses and abscesses can be safely performed by US-guided needle placement into the lesion through the point of contact between the mass and pleura. Large anterior mediastinal masses that have a broad area of contact with the parasternal chest wall may be biopsied without transgressing the lung.
Real-time US can also confirm phrenic nerve paralysis without the use of ionizing radiation. It also easily detects
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subpulmonic and subphrenic fluid collections, which may cause diaphragmatic elevation.
Ventilation/Perfusion Lung Scanning
The nuclear medicine examinations utilized in the evaluation of noncardiac thoracic disease are ventilation/perfusion (V/Q) lung scintigraphy (see Chapter 56) and gallium scintigraphy. V/Q scanning is used almost exclusively for the diagnosis of pulmonary embolism, although quantitative VQ imaging may be useful in the planning of bullectomy, lung volume reduction surgery for emphysema, and lung transplantation. Gallium-67 scanning of the chest is used in the detection of pulmonary infection (e.g., Pneumocystis carinii pneumonia in a patient with a normal radiograph) or inflammation (e.g., disease activity in idiopathic pulmonary fibrosis) and in the evaluation of suspected sarcoidosis.
Diagnostic arteriography has mainly been replaced by angio-CT. Pulmonary angiograms are only performed in cases where angio-CT is suboptimal or equivocal.
Thanks to the newer scanners and to the improvement of three-dimensional (3D) rendering tools, thoracic aortography has also been largely replaced by CT, MR, or US. On occasion, an equivocal diagnosis of an aortic laceration following blunt chest trauma can be resolved with this technique. Inflammatory changes of infectious aortitis are also better imaged with MR or CT.
Active bleeding through a bronchial artery is still best addressed by bronchial arteriography, as an active bleeding site is often difficult to pinpoint. When massive or recurrent hemoptysis occur, most commonly from bronchiectasis, neoplasm, or mycetoma, arteriography and embolization can be performed in the same setting.
Transthoracic needle biopsy guided by CT, fluoroscopy, or US is a diagnostic technique utilized in selected patients with pulmonary, pleural, or mediastinal lesions (7).
Percutaneous catheter drainage of intrathoracic air or fluid collections, performed by imaging-guided placement of small-bore multihole catheters, is used for the treatment of empyema, pneumothorax, malignant pleural effusion, and other intrathoracic fluid collections (3).
NORMAL LUNG ANATOMY
Tracheobronchial Tree (Fig. 12.3)
The trachea is a hollow cylinder composed of a series of C-shaped cartilaginous rings. The rings are completed posteriorly by a flat band of muscle and connective tissue called the posterior tracheal membrane. The tracheal mucosa consists of pseudostratified, ciliated columnar epithelium, which contains scattered neuroendocrine (APUD) cells. The submucosa contains cartilage, smooth muscle, and seromucous glands. The left lateral wall of the distal trachea is indented by the transverse portion of the aortic arch.
The trachea is approximately 12 cm long in adults, with an upper limit of normal coronal tracheal diameter of 25 mm in men and 21 mm in women. In cross section, the trachea is oval or horseshoe-shaped, with a coronal-to-sagittal diameter ratio of 0.6:1.0. A narrowing of the coronal diameter producing a coronal/sagittal ratio of <0.6 is termed a saber sheath trachea and is seen in patients with chronic obstructive pulmonary disease.
On chest radiographs, the trachea is seen as a vertically oriented cylindric lucency extending from the cricoid cartilage superiorly to the main bronchi inferiorly. A slight tracheal deviation to the right after entering the thorax can be a normal radiographic finding. The interface of the right upper lobe (RUL) with the right lateral tracheal wall is called the right paratracheal stripe (Fig. 12.4A). This stripe should be uniformly smooth and should not exceed 4 mm in width; thickening or nodularity reflects disease in any of the component tissues, including medial tracking pleural effusion. The left lateral wall is surrounded by mediastinal vessels and fat and is not normally visible radiographically. The posterior trachea can be visualized on the lateral chest (Fig. 12.4B). The presence of air in the esophagus produces the tracheoesophageal stripe, which represents the combined thickness of the tracheal and esophageal walls and intervening fat. This stripe should measure less than 5 mm; thickening is most commonly seen with esophageal carcinoma.
The bronchial system exhibits a branching pattern of asymmetric dichotomy, with the daughter bronchi of a parent bronchus varying in diameter, length, and the number of divisions. The bronchial generation “n” indicates the number of divisions since the trachea, which bears generation number 1 (8). The main bronchi arise from the trachea at the carina, with the right bronchus forming a more obtuse angle with the long axis of the trachea. The right main bronchus is considerably shorter than the left main bronchus (mean lengths of 2.2 cm and 5 cm, respectively). The tracheal and main, lobar, and segmental bronchial anatomy are easily seen on CT (Fig. 12.5). Bronchi on end can be seen as a ring shadow on chest radiographs. Bronchi gradually lose their cartilaginous support between generations 1 and 12 to 15. Once this happens, these 1- to 3-mm airways are called bronchioles (9). Bronchioles bearing alveoli on their walls are termed respiratory bronchioles. The latter divide into alveolar ducts and alveolar sacs. The airway just before the first respiratory bronchiole is the terminal bronchiole. It is the smallest bronchiole without respiratory exchange structures. In average, a total of 21 to 25 generations are found between the trachea and the alveoli.
Lobar and Segmental Anatomy (Fig. 12.6). The lungs are divided by the interlobar fissures, which are invaginations of the visceral pleura. On the right, the minor fissure
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separates the middle from the upper lobe. The major fissure separates the lower lobe from the upper lobe superiorly and from the middle lobe inferiorly. The upper lobe bronchus and its artery, arising from the truncus anterior, branch into three segmental branches: anterior, apical, and posterior. The middle lobe bronchus arises from the intermediate bronchus and divides into medial and lateral segmental branches, with its blood supplied by a branch of the right interlobar pulmonary artery. The right lower lobe (RLL) is supplied by the RLL bronchus and pulmonary artery. It is subdivided into a superior segment and four basal segments: anterior, lateral, posterior, and medial.
FIGURE 12.3. Prevailing Pattern of Segmental Bronchi. Virtual bronchography three-dimensional rendered images of the usual bronchial anatomy. A. Left and right bronchial tree. B. Oblique view of the left bronchial tree. C. Oblique view of the right bronchial tree. Tr, trachea; RUL, right upper lobe; LUL, left upper lobe; RM, right main bronchus; LM, left main bronchus; BT, left lower lobe basal trunk; RML, right middle lobe; B1, apical (upper lobe); B2, posterior (upper lobe); B3, anterior (upper lobe); B4, lateral (middle lobe) and superior (lingula); B5, medial (middle lobe) and inferior (lingula); B6, superior (lower lobe); B7, medial basilar (lower lobe); B8, anterior (lower lobe); B9, lateral basilar (lower lobe); B10, posterior (lower lobe).
FIGURE 12.4. Trachea. A. The right paratracheal stripe (open arrows) is composed of the right lateral tracheal wall, a small amount of mediastinal fat, paratracheal lymph nodes, and the visceral and parietal pleural layers of the right upper lobe. B. Left lateral chest film shows the anterior (open arrow) and posterior (short solid arrow) walls of the trachea. The posterior wall of the bronchus intermedius (long solid arrow) is readily visible on lateral radiographs as it crosses the end-on view of the left upper lobe bronchus. Because these structures are central, their relationship tends to remain even on rotated films. This is easily seen on CT (see Fig. 12.5B, image 3).
The left lung is divided into upper and lower lobes by the left major fissure. The left upper lobe (LUL) is analogous to the combined right upper and middle lobes. The LUL is subdivided into four segments: anterior, apicoposterior, and the superior and inferior lingular segments. Arterial supply to the anterior and apicoposterior segments parallels the bronchi and is via branches of the upper division of the left main pulmonary artery. The superior and inferior lingular arteries are proximal branches of the left interlobar pulmonary artery, analogous to the middle lobe’s blood supply. The left lower lobe (LLL) has a superior segment and three basal segments: anteromedial, lateral, and posterior.
Respiratory Portion of Lung
The respiratory bronchioles contain a few alveoli along their walls and give rise to the gas-exchanging units of the lung: the alveolar ducts and the alveolar sacs. The pulmonary alveolus is lined by two types of epithelial cells (pneumocytes). Type 1 pneumocytes are flattened squamous cells covering 95% of the alveolar surface area and are invisible by light microscopy. These cells are incapable of mitosis or repair. The rarer type 2 pneumocytes are cuboidal cells, which are visible under light microscopy and are capable of mitosis. Type 2 pneumocytes are the source of new type 1 pneumocytes and provide a mechanism for repair following alveolar damage. These cells are also thought to be the source of alveolar surfactant, a phospholipid that lowers the surface tension of alveolar walls and prevents alveolar collapse at low lung volumes.
Pulmonary subsegmental anatomy is discussed in Chapter 17, along with the HRCT description of these anatomic structures.
Fissures
The interlobar pulmonary fissures represent invaginations of the visceral pleura deep into the substance of the lung (Fig. 12.6) (10). These fissures may completely or incompletely separate the lobes from one another. An incomplete fissure has important consequences regarding interlobar spread of parenchymal consolidation, collateral air drift in patients with lobar bronchial obstruction,
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and the appearance of pleural effusion in the supine patient. The fissures are well delineated on CT or HRCT (Fig. 12.7).
FIGURE 12.5. Tracheobronchial and Hilar Anatomy. A. Three-dimensional volume-rendered virtual bronchographic view of the bronchial tree. Tr, trachea; RM, right main bronchus; LM, left main bronchus; RUL, right upper lobe; RML, right middle lobe; LUL, left upper lobe; BI, bronchus intermedius; BT, basal trunk. B. Levels of the CT images depicting the bronchial and hilar anatomy. 1. Level of tracheal carina. Right apical bronchus (1); right superior posterior pulmonary vein (rv); left apicoposterior bronchus (1 and 2 on the left). 2. Level of right upper lobe bronchus. Right main bronchus (RM); right upper lobe bronchus (ru); right upper lobe anterior (3) and posterior (2) segmental bronchi; right superior pulmonary vein (rv); left main bronchus (LM); left apicoposterior segmental bronchus (1+2); left superior pulmonary vein (lv). 3. Level of left upper lobe bronchus, superior division. Bronchus intermedius (BI), with its posterior border at the level of the left main (LM); right superior pulmonary vein (rv); superior division of left upper lobe bronchus (small arrows); left upper lobe anterior (3) and apicoposterior (1+2) segmental bronchi; left descending pulmonary artery (Ld). 4. Level of left upper lobe bronchus, inferior (lingular) division. Bronchus intermedius (BI); right descending pulmonary artery (Rd); lingular bronchus (4+5); left lower lobe bronchus (LL); left lower lobe superior segmental bronchus (6); left descending pulmonary artery (Ld). 5. Level of middle lobe bronchus. Middle lobe bronchus (4+5); right lower lobe bronchus (RL); right descending pulmonary artery (Rd); lingular superior segmental bronchus (4); left lower lobe basal trunk (BT); left lower lobe segmental arteries (a). 6. Level of lower lobe basal trunks. Lateral (4) and medial (5) segmental bronchi of the middle lobe; right lower lobe basal trunk (BT); right lower lobe basal segmental arteries (a, on right); lingular segmental bronchus (5); left lower lobe anteromedial segmental bronchus (7+8); left lower lobe lateral and posterior basal segmental bronchi (9+10); left lower lobe basal segmental arteries (a, on left).7. Level of basal segmental bronchi. Right lower lobe medial (7, on right), anterior (8, on right), lateral (9, on right), and posterior (10, on right) basal segmental bronchi; right inferior pulmonary vein (v, on right); left lower lobe medial (7, on left), anterior (8, on left), lateral (9, on left), and posterior (10, on left) basal segmental bronchi; left inferior pulmonary vein (v, on left).
FIGURE 12.6. Normal Lobar and Fissural Anatomy. A. Frontal view. B. Lateral view. RUL, right upper lobe; LUL, left upper lobe; RML, right middle lobe; RLL, right lower lobe; LLL, left lower lobe; ULs, upper lobes; LLs, lower lobes.
In most individuals, there are two interlobar fissures on the right and one on the left. The fissures are complete laterally and incomplete medially, fusing with the adjacent lobe. The minor fissure is complete in about 25% of individuals but fuses with the RUL in about 50%. The inferior fissure of the right middle lobe (RML) is well developed and there is very little fusion between the RML and the RLL. This oblique fissure is complete in less than 35% of individuals, with fusion between the lobes most common along the posteromedial portion of the fissure. The left major fissure is similar to the right major fissure, with fusion along the posterior aspect in approximately 35% of individuals.
The major and minor fissures are best visualized on lateral radiographs. Variable portions of the major fissures
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are seen as obliquely oriented, thin white lines coursing anteroinferiorly from posterior to anterior. The left major fissure usually begins more superiorly and has a slightly more vertical course than the right major fissure. At their points of contact with the diaphragm or chest wall, the fissures often have a triangular configuration, with the apex of the triangle pointing toward the fissure. This appearance is the result of the presence of a small amount of fat within the distal aspect of the fissure. Although the major fissures are not usually visualized on frontal radiographs because of their oblique course relative to the x-ray beam, occasional extrapleural fat infiltration along their superolateral aspect can give rise to a curvilinear edge in the upper thorax. The minor fissure projects at the level of the right fourth rib and is seen as a thin undulating line on frontal radiographs in approximately 50% of individuals. On a lateral radiograph, the minor fissure is often seen as a thin curvilinear line with a convex superior margin. Not uncommonly, the posterior aspect of the minor fissure extends posterior to the margin of the right major fissure. This is because the minor fissure abuts the entire convexity of the anterior lower lobe, but the major fissure interface is caused by the crest of the convexity.
FIGURE 12.7. Fissural Anatomy on HRCT. The oblique fissures appear as thin curvilinear lines (solid arrows) concave anteriorly in the upper thorax (A), flat lines in the midthorax (B), and convex anterior lines in the lower chest (C). The apex of the domed minor fissure is seen as an avascular zone in the midthorax (open arrow in B).
The inferior accessory fissure is the most common accessory fissure and is found in approximately 10% to 20% of individuals. This fissure, which separates the medial basal from the remaining basal segments of the lower lobe, is often incomplete (Fig. 12.6). It may be seen on frontal radiographs as a thin curvilinear line extending superiorly from the medial third of the hemidiaphragm toward the lower hilum. The inferior accessory fissure has been misidentified as the inferior pulmonary ligament (invisible on normal chest radiographs) and is responsible for the juxtaphrenic peak described in upper lobe volume loss. A small triangle of extrapleural fat, seen at its point of insertion on the diaphragm, helps identify the inferior accessory fissure. An inferior accessory fissure can be seen on CT scans through the lower thorax, where it is identified
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as a curvilinear line extending anterolaterally from just in front of the inferior pulmonary ligament toward the major fissure.
FIGURE 12.8. Inferior Pulmonary and Pericardiophrenic Ligaments. A CT scan just above the diaphragm demonstrates a thin line (small solid arrow) extending posterolaterally at the level of the esophagus that represents the sublobar septum extending to the inferior pulmonary ligament. On the right, a curvilinear line (large solid arrow) extending from just lateral to the inferior vena cava represents the right pericardiophrenic ligament containing branches of the phrenic nerve and pericardiophrenic vessels. More anteriorly, a thin line (open arrow) is seen just above the apex of the right hemidiaphragm (H), which represents fat within the inferior aspect of the major fissure.
The azygos fissure is seen in 0.5% of individuals (Fig. 12.6). It is composed of four layers of pleura (two visceral, two parietal) and represents an invagination of the right apical pleura by the azygos vein, which has incompletely migrated to its normal position at the right tracheobronchial angle. The azygos fissure appears as a vertical curvilinear line, convex laterally, which extends inferiorly from the lung apex and ends in a teardrop, which is the azygos vein. The significance of this fissure lies in its ability to limit the spread of apical segmental consolidation to the azygos lobe (that portion of the apical segment delineated by the azygos fissure) and in excluding pneumothorax from the apical portion of the pleural space.
The superior accessory fissure separates the superior segment from the basal segments of the lower lobe. On the right side it may be distinguished from the minor fissure on lateral radiographs, because it extends posteriorly from the major fissure to the chest wall.
The left minor fissure is a rarely seen normal variant that separates the lingula from the remaining portions of the upper lobe.
Ligaments
The inferior pulmonary ligament is a sheet of connective tissue that extends from the hilum superiorly to a level at or just above the hemidiaphragm. Thus, it comprises fused visceral and parietal pleura and binds the lower lobe to the mediastinum and runs alongside the esophagus. The ligament contains the inferior pulmonary vein superiorly and a variable number of lymph nodes. The inferior pulmonary ligament is sometimes seen on CT scans through the lower thorax as a small laterally directed beak of mediastinal pleura adjacent to the esophagus (Fig. 12.8). The tethering effect of this ligament on the lower lobe accounts for the medial location and triangular appearance of lower lobe collapse. The ligament may also act as a barrier to the spread of pleural and mediastinal fluid and may marginate medial pleural or mediastinal air collections to produce a characteristic appearance on radiographs.
The sublobar septum (Fig. 12.8) has been mistaken for the inferior pulmonary ligament. It is a linear structure seen on CT near the inferior pulmonary ligament extending into the lung from the mediastinal pleura.
The pericardiophrenic ligament is a triangular density extending toward the lung that is seen along the posterior aspect of the right heart border on lung windows on chest CT (Fig. 12.8). It represents a reflection of pleura over the inferior portion of the phrenic nerve and pericardiophrenic vessels. It is distinguished from the sublobar septum by its more anterior location and by its characteristic ramifications as branches of the nerve and vessel reflect over the hemidiaphragm.
Pulmonary Arteries (Fig. 12.9A-C) (11)
The pulmonary artery is an elastic artery that arises from the right ventricle approximately the 1:00 position relative to the ascending aorta. These two structures then rotate from right to left until the pulmonary artery lies at the 5:00 position. The left pulmonary artery is a direct continuation of the main pulmonary artery. The right artery branches just below the carina, with an angle close to 90°. Within the left hilum, the artery envelopes the upper margin of the left main bronchus, at which point it divides into the upper and lower lobe arteries. The arch formed by the left lower lobe artery over the left hilar bronchi (i.e., the bronchus is hypoarterial) is easily seen on the lateral view. On the other hand, the right pulmonary artery courses laterally and anterior to the main bronchus. The right artery divides within the pericardium into the truncus anterior and interlobar arteries. In contradistinction to the left side, the right interlobar artery courses anterolateral to the bronchus (i.e., the bronchus is epi arterial). The different spatial relationships are essential when determining bronchial and pulmonary situs. At the same level that the bronchi lose their cartilage and become bronchioles, the elastic arteries lose their elastic lamina and become muscular arteries. Thickening of the alveolocapillary membrane from edema fluid or
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fibrosis impedes gas exchange and results in dyspnea and hypoxemia.
FIGURE 12.9. Prevailing Pattern of Segmental Arteries and Venous Returns. Three-dimensional volume-rendered images of the pulmonary arterial system in different views depict the most usual arterial anatomy. The branches of the right and left pulmonary arteries accompany and divide in parallel with the corresponding bronchi. A. Left and right pulmonary arteries, (1) anterior view; (2) posterior view. B. Right pulmonary artery, (1) anterior view; (2) posterior view. C. Left pulmonary artery, (1) anterior view; (2) posterior view. TrSup, truncus superior; A1, apical (upper lobe); A2, posterior (upper lobe); A3, anterior (upper lobe); A4, lateral (middle lobe) and superior (lingula); A5, medial (middle lobe) and inferior (lingula); A6, superior (lower lobe); A7, medial basal (lower lobe); A8, anterior basal (lower lobe); A9, lateral basal (lower lobe); A10, posterior basal (lower lobe). Note that the right upper lobe receives an accessory branch from the proximal right interlobar pulmonary artery (Aas). D. Left atrium and venous returns, (1) anterior view; (2) posterior view. Three-dimensional volume-rendered images of the left atrium and venous returns depict the most usual venous return anatomy. Significantly more variation exists than in the bronchial/arterial systems. Although only the main returns are depicted here, the reader will find an extensive discussion in Yamashita (11). RSup, Right superior venous return; LSup, left superior venous return; RInf, right inferior venous return; LInf, left inferior venous return. Several branches can join the left atrium separate from their lobar venous return. The most common ones are RSup (RML), right middle lobe branch of the RSup; LInf(SupSeg) and RInf(SupSeg), branches from the superior segments of the lower lobes. Lapp, Left atrial appendage; MV, mitral valve plane.
Bronchial arteries are the primary nutrient vessels of the lung. They supply blood to the bronchial walls to the level of the terminal bronchioles. In addition, several mediastinal structures receive a variable amount of blood supply from the bronchial circulation. These include the tracheal wall, middle third of the esophagus, visceral pleura, mediastinal lymph nodes, vagus nerve, pericardium, and thymus.
The bronchial arteries usually arise from the proximal descending thoracic aorta at the level of the carina but may show significant variability. Most commonly there are one right-sided and two left-sided arteries. The right bronchial artery usually arises from the posterolateral wall of the aorta in common with an intercostal artery as an intercostobronchial trunk. The left bronchial arteries arise individually from the anterolateral aorta or, rarely, from an intercostal artery. Approximately two thirds of the blood from the bronchial arterial system returns to the pulmonary venous system via the bronchial veins (a small right-to-left shunt). The remaining blood, which includes veins draining the large bronchi, tracheal bifurcation, and mediastinum, drains into the azygos or hemiazygos systems.
Pulmonary veins (Fig. 12.9D) arise within the interlobular septa from the alveolar and visceral pleural capillaries. The veins travel in connective tissue envelopes that are separate from the bronchoarterial trunks. The pulmonary veins, which may number from three to eight, drain into the left atrium.
Pulmonary lymphatics help clear fluid and particulate matter from the pulmonary interstitium. There are two major lymphatic pathways in the lung and pleura. The visceral pleural lymphatics, which reside in the vascular
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(innermost) layer of the visceral pleura, form a network over the surface of the lung that roughly parallels the margins of the secondary pulmonary lobules. These peripheral lymphatics penetrate the lung to course centrally within interlobular septa, along with the pulmonary veins, toward the hilum. The parenchymal lymphatics originate in proximity to the alveolar septa (“juxta-alveolar lymphatics”) and course centrally with the bronchoarterial bundle. The perivenous and bronchoarterial lymphatics communicate via obliquely oriented lymphatics located within the central regions of the lung. These perivenous lymphatics and their surrounding connective tissue, when distended by fluid, account for the radiographic appearance of Kerley A lines.
FIGURE 12.10. Diagram of the Pulmonary Interstitium.
Pulmonary interstitium is the scaffolding of the lung and as such provides support for the airways and pulmonary vessels (Fig. 12.10) (10). It begins within the hilum and extends peripherally to the visceral pleura. The interstitial compartment that extends from the mediastinum and envelopes the bronchovascular bundles is termed the axial interstitium. The axial fiber system continues distally as the centrilobular interstitium along with the arterioles, capillaries, and bronchioles to provide support for the air-exchanging portions of the lung. The subpleural interstitium and interlobular septa are parts of the peripheral interstitium, which divides secondary pulmonary lobules. The pulmonary veins and lymphatics lie within the peripheral interstitium. The intralobular interstitium is a thin network of fibers that bridges the gap between the centrilobular and peripheral compartments.
Edema involving the axial interstitium is recognized radiographically as peribronchial cuffing. Pathologic involvement of the intralobular interstitium is difficult to discern radiographically, but may account for some cases of so-called “ground-glass” opacity on chest radiographs and HRCT scans. Thickening of portions of this interstitium are occasionally seen as intralobular lines on HRCT. Radiographically, edema of the peripheral and subpleural interstitium accounts for Kerley B lines (or interlobular lines on HRCT) and “thickened” fissures on chest radiographs.
Posteroanterior Chest Radiograph
A firm knowledge of the normal anatomy displayed on the frontal (usually PA) chest radiograph is key to detecting and localizing pathologic conditions and to avoid mistaking normal structures for pathologic findings.
Soft tissues of the chest wall consist of the skin, subcutaneous fat, and muscles. The lateral edges of the sternocleidomastoid muscles are readily visible in most patients. The visualization of normal fat in the supraclavicular fossae and the companion shadows of skin and subcutaneous fat paralleling the clavicles helps exclude mass, adenopathy, or edema in this region. The inferolateral edge of the pectoralis major muscle is normally seen curving toward the axilla. Both breast shadows should be evaluated routinely to detect evidence of prior mastectomy or distorting mass. The soft tissues lateral to the bony thorax should be smooth, symmetric, homogeneous densities.
FIGURE 12.11. Radiolucent Spaces on Lateral Chest Radiographs. The retrosternal space is demarcated anteriorly by the posterior margin of the sternum (small arrows) and the heart and ascending aorta posteriorly and accounts for the anterior junction line seen on frontal radiographs. The retrotracheal triangle is marginated by the posterior wall of the trachea anteriorly (open triangle), the spine posteriorly (broken triangle), and the aortic arch inferiorly (solid triangle). The retrocardiac space is demarcated anteriorly by the posterior cardiac margin (upper open arrow) and the inferior vena cava (I, lower open arrow).
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Bones
The thoracic spine, ribs and costal cartilages, clavicles, and scapulae are routinely visible on frontal chest radiographs. The bodies of the thoracic vertebrae should be vertically aligned, with endplates, pedicles, and spinous processes visualized. Twelve pairs of symmetric ribs should be seen; the upper ribs have smooth superior and inferior cortical margins, while the middle and lower ribs have flanged inferior cortices where the intercostal neurovascular bundles run. Cervical ribs are identified in approximately 2% of individuals and may be associated with symptoms of thoracic outlet syndrome. Companion shadows paralleling the inferior margins of the first and second ribs represent extrapleural fat, which may be abundant in obese individuals. Costal cartilage calcification is seen in a majority of adults, increases in prevalence with advancing age, and can add multiple shadows to the PA view. Men typically show calcification at the upper and lower margins, while the majority of women develop central cartilaginous calcification.
Lung–Lung Interfaces
A familiarity with the normal mediastinal interfaces is key to the interpretation of frontal chest radiographs (2). The lung–mediastinal interfaces are seen as sharp edges where the lung and adjacent pleura reflect off of various mediastinal structures. The lung–lung interfaces as seen on frontal radiographs relate directly to the space available in three regions viewed on the lateral film: the retrosternal space, the retrotracheal triangle, and the retrocardiac space (Fig. 12.11).
FIGURE 12.12. Anterior and Posterior Junction Lines. A. A posteroanterior chest film shows both anterior (solid arrows) and posterior (open arrows) junction lines. B. CT through the upper thorax in another patient shows the anterior junction line in the retrosternal space, while the posterior junction line lies in the retrotracheal space.
The retrosternal airspace reflects contact of the anterosuperior aspect of the upper lobes (Fig. 12.11). On frontal radiographs the anterior junction line is seen as a thin vertical line that overlies the thoracic spine (Fig. 12.12). The anterior junction anatomy is an inferior extension of the upper lobe reflections off the innominate veins, with the latter producing an inverted V-shaped retromanubrial opacity. The anterior junction line often disappears after sternotomy, or when abundant anterior mediastinal fat precludes retrosternal contact of the upper lobes.
A second potential lung–lung interface is seen on the lateral chest radiograph as the retrotracheal triangle, a radiolucent region representing contact of the posterosuperior portions of the upper lobes (Fig. 12.11). If the retrotracheal space available is small, only a right paraesophageal interface is visualized on the PA view (Fig. 12.13). If the space is large, a posterior junction line is seen (Figs. 12.12, 12.13) (Table 12.4).
The third potential lung–lung interface occurs in the retrocardiac space (Fig. 12.11). If that space is large, the azygoesophageal recess of the RLL can abut the preaortic recess of the left lower lobe to produce an inferior posterior junction line (Fig. 12.13).
Lung–Mediastinal Interfaces (Table 12.5)
The right lateral margin of the superior vena cava is commonly seen as a straight or slightly concave interface with the RUL extending from the level of the clavicle to the superior margin of the right atrium. Prominence or convexity of the
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caval interface may represent caval dilatation or lateral displacement by a dilated or tortuous aortic arch or other mediastinal mass.
FIGURE 12.13. Lung–Lung Interfaces on a Frontal Radiograph. Coned down view of a PA film shows the right paraesophageal interface (solid arrows). The azygos arch (open arrows) separates the supra-azygos lung from the infra-azygos lung, which creates the azygoesophageal recess interface (solid triangles). The retrocardiac left lung creates the preaortic recess interface (open triangles).
Along the right upper mediastinum, the RUL contacts the right lateral tracheal wall in a majority of individuals. This produces the right paratracheal stripe (Fig. 12.4A). The thickness of this line, measured above the level of the azygos vein, should not exceed 4 mm. Thickening or nodularity of the paratracheal stripe is seen in abnormalities of the tissues comprising the strip, including tracheal tumors, paratracheal lymph node enlargement, and right pleural effusion (Fig. 12.2).
TABLE 12.4 Anterior and Posterior Junction Lines
Line Features
Anterior junction line Obliquely oriented from right superior to left inferior
Extends from upper sternum to base of heart
Posterior junction line Vertically oriented in the midline
Extends from upper thoracic spine to level of azygos and aortic arches
TABLE 12.5 Normal Lung–Mediastinal Interfaces
Right-sided Right paraesophageal interface
Superior vena cava/right paratracheal stripe
Anterior arch of the azygos vein
Right paraspinal interface
Azygoesophageal recess
Lateral margin of right atrium
Confluence of right pulmonary veins (right border of left atrium)
Lateral margin of inferior vena cava
Left-sided Lateral margin of left subclavian artery
Transverse aortic arch
Left superior intercostal vein (“aortic nipple”)
Aortopulmonary window interface
Aortopulmonary interface
Lateral margin of main pulmonary artery
Preaortic recess
Left paraspinal interface
Left atrial appendage
Left ventricle
Epipericardial fat pad
The arch of the azygos vein separates the right paraesophageal from the upper azygos esophageal space (Fig. 12.13). The measurement should be made through the midpoint of the azygos arch perpendicular to the right main bronchus. Supine positioning or performance of the Müller maneuver (forced inspiration against a closed glottis) will increase azygos venous diameter. In general, a diameter of >10 mm on a PA radiograph should raise the possibility of mass, adenopathy, or dilatation of the azygos vein; the latter may be seen with right heart failure, obstruction of venous return to the heart, or a congenital venous anomaly such as azygos continuation of the inferior vena cava. An increase in diameter of the azygos vein from prior comparable radiographs is more important than the actual measurement.
The azygoesophageal recess interface is a vertically oriented interface overlying the thoracic spine. (Fig. 12.13). While normally straight or concave in contour, the middle third of the interface may have a slight rightward convexity at the level of the right inferior pulmonary veins. Convexity of the superior third of the interface should suggest subcarinal lymph node enlargement or a mass. Convexity of the middle third of this recess is usually a result of the confluence of right pulmonary veins or the right border of the left atrium. Left atrial dilatation will enlarge and laterally displace this interface, producing a double-density interface composed of the right lateral borders of both the right and the left atria. Convexity of the inferior third is most commonly due to a sliding hiatal hernia.
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Occasionally a tortuous descending aorta or enlarged paraesophageal lymph nodes can cause this recess to be convex to the right in its lower third. When air is present in the distal portion of the esophagus and the azygoesophageal recess interfaces with the right lateral wall of the esophagus, a line (the right inferior esophagopleural stripe) rather than an edge is seen.
The paraspinal interface is a straight, vertical interface extending the length of the right hemithorax and represents contact of the right lung with a small amount of tissue lateral to the thoracic spine. It is inconsistently visualized on the right side. A focal convexity of this interface suggests spinal or paraspinal disease.
The right heart projects just to the right of the lateral margin of the thoracic spine on a normal PA radiograph (Fig. 12.11). This portion of the heart is the lateral margin of the right atrium, which creates a smooth convex interface with the medial segment of the middle lobe. Individuals with pectus excavatum have leftward cardiac displacement and may not demonstrate this interface. In patients with right atrial dilatation, this interface may extend well into the right lung.
The right lateral border of the inferior vena cava may be seen at the level of the right hemidiaphragm as a concave lateral interface. The inferior vena caval interface is best visualized on lateral radiographs (Fig. 12.11). This interface may be absent in patients with azygos continuation of the inferior vena cava.
In the uppermost portion of the left mediastinum, one or more interfaces may be recognized cephalad to the aortic arch. The interface most often visualized is the subclavian artery (Fig. 12.14). It is unusual for the LUL to interface with the left lateral wall of the trachea to form the left paratracheal stripe, because the subclavian artery and adjacent fat usually intervene.
The transverse portion of the aortic arch (“aortic knob”) creates a small convex indentation on the left lung in normal individuals (Fig. 12.14). As the aorta elongates and dilates with age, this interface projects more laterally, and lung may be seen to encircle a greater circumference of the knob.
In approximately 5% of individuals, the left superior intercostal vein may be seen on frontal radiographs as a rounded or triangular opacity that focally indents the lung immediately superolateral to the aortic arch. This density, termed the “aortic nipple” (Fig. 12.15), represents the superior intercostal vein as it arches anteriorly from its paraspinal position around the aortic arch to drain into the posterior aspect of the left innominate vein. This structure, which normally measures <5 mm, may enlarge with elevation of right atrial pressure or with congenital or acquired obstruction of venous return to the right heart.
Immediately inferior to the aortic arch, the LUL contacts the mediastinum to produce the aortopulmonary
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window interface (Fig. 12.14). This interface is usually straight or concave toward the lung; the latter appearance is seen with a tortuous aorta, emphysema, or congenital absence of the left pericardium. A convex lateral interface should suggest mass or lymph node enlargement in the aortopulmonary window.
FIGURE 12.14. Lung–Mediastinal Interfaces, Left Side. Posteroanterior chest radiograph shows the normal contours along the left mediastinum (from superior to inferior): left subclavian artery (long straight white arrow), aortic knob (curved white arrow), aortopulmonary window (straight black arrow), main pulmonary artery (curved open white arrow), left atrial appendage (open black arrow), and left ventricle (solid white arrow).
FIGURE 12.15. Aortic Nipple. The contour of the “aortic nipple” is formed by the left superior intercostal vein (white arrowheads). The small black arrows denote the contour of the aortic knob.
Immediately inferior to the aortopulmonary window is the left lateral border of the main pulmonary artery (Fig. 12.14). The interface of this structure may be convex, straight, or concave toward the lung. Enlargement of the main pulmonary artery is seen as an idiopathic condition in young women, as a result of poststenotic dilatation in valvular pulmonic stenosis, or in conditions where there is increased flow or pressure in the pulmonary arterial system, such as left-to-right intracardiac shunts.
The preaortic recess interface is seen in a small percentage of normal individuals as a reflection of the LLL with the esophagus anterior to the descending aorta, extending vertically from the undersurface of the aortic knob a variable distance toward the diaphragm. It is usually etched in black (negative Mach effect).
The left paraspinal interface represents the reflection of the left lung off the paraspinal soft tissues, which largely consist of fat but also contain the sympathetic chain, proximal intercostal vessels, intercostal lymph nodes, and hemiazygos and accessory hemiazygos veins. The left paraspinal interface, which is etched in white (positive Mach effect), is seen in a majority of individuals, in contrast to the right paraspinal interface. Neurogenic tumors, hematoma, paraspinal abscess, lipomatosis, and medial pleural effusion can cause lateral displacement of this interface.
The left atrial appendage forms a concave interface immediately below the main pulmonary artery (Fig. 12.14). Straightening or convexity of this interface used to be seen commonly in rheumatic mitral valve disease but may be seen in patients with left atrial enlargement of any cause.
The left ventricle comprises most of the left heart border. A gentle convex margin with the lingula is normal (Fig. 12.14). Abnormalities of the left ventricular contour will be discussed in detail in the section on cardiovascular disease.
Fat adjacent to the cardiac apex may create a focal bulge in the left cardiac contour that obscures the heart border at the left cardiophrenic angle. This epipericardial fat pad is usually unilateral or more prominent on the left and is most often seen in obese patients and those on corticosteroids. A typical appearance on the lateral radiograph is usually diagnostic; CT is helpful in equivocal cases.
The Lungs (Fig. 12.14)
The opacity of the lungs as visualized radiographically is attributable solely to the presence of the pulmonary vasculature and enveloping interstitial structures. The arteries are solid cylinders branching along the airways. Both gradually diminish in caliber as they divide. Bronchi smaller than subsegmental are not visible radiographically. The pulmonary veins can often be traced horizontally to the left atrium, whereas the arteries can be followed to their hilar origin, which lies more cephalad than the left atrium. The effects of gravity explain the predominance of vasculature in an upright patient, as well as isodistribution of vessels in the supine patient. The normal dark gray opacity of the upper lungs increases inferiorly in women as a result of summation of overlying breast tissue, or in men with prominent pectoralis muscles. The opacity of the lung may be increased by processes that render the interstitium or airspaces opaque or decreased by any process associated with diminished blood flow to the lung or destruction of parenchymal structures.
Diaphragm
The diaphragm is the major inspiratory muscle comprised of muscular origins along the costal margins and insertions into the membranous dome. The right hemidiaphragm overlies the liver, and the left hemidiaphragm overlies the stomach and spleen. On frontal radiographs exposed in deep inspiration, the apex of the right hemidiaphragm typically lies at the level of the sixth anterior rib, approximately one half interspace above the apex of the left hemidiaphragm (Fig. 12.14). A scalloped appearance to the hemidiaphragm is not uncommon. Focal bulges in the diaphragmatic contour are usually a result of acquired diaphragmatic eventration (thinning).
Upper Abdomen
Portions of the liver, spleen, and gastric fundus are routinely visualized on most frontal chest radiographs. Abnormalities of abdominal situs may be identified by noting the location and appearance of the liver, stomach, and spleen. Enlargement of the liver may cause right diaphragmatic elevation and right lateral compression of the stomach. Intrahepatic air may be seen within the biliary tree, portal vein, or a hepatic abscess. Calcified hepatic lesions or calcified gallstones overlying the lower portion of the liver may be visible. A mass arising within the gastric fundus can occasionally be seen as a soft tissue opacity protruding into a gas-filled gastric lumen. Splenomegaly may be identified by noting a soft tissue mass in the left upper quadrant that displaces the stomach bubble anteromedially and the splenic flexure of the colon inferiorly.
Lateral Chest Radiograph
The normal lateral chest film is a challenge because of summation of the right hemithorax over the left (Fig. 12.1). However, knowledge of normal lateral radiographic anatomy can greatly aid in detection and localization of parenchymal and cardiomediastinal processes (12,13).
Soft Tissues
Air outlining the anterior axillary folds may render the anterior edges of these skin folds visible overlying the superior aspect of the thorax. The edges are
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seen as bilateral opacities that are concave anteriorly and can be followed through the level of the thoracic inlet to merge with the soft tissues of the arms.
Bones
The anterior margins of the scapulae project as oblique straight edges overlying the superior and posterior aspects of the thorax, often over the retrotracheal triangle. The anterior and posterior cortical margins of the thoracic vertebral bodies should be aligned, forming a gradual kyphosis.
Lung Interfaces
The retrotracheal (or Raider) triangle is bordered by the posterior border of the trachea/esophagus, the anterior border of the spine, and the top of the aortic arch (Fig. 12.11). Masses and air-space disease near the apices, retrotracheal masses (e.g., aberrant subclavian artery or posterior thyroid goiter), or esophageal masses may produce an abnormal opacity in this region.
If the descending aorta is tortuous, its posterior margin and occasionally its anterior margin may be followed for varying distances, depending upon where the aorta returns to a prespinal position to traverse the aortic hiatus and enter the abdomen. Rarely, the superior margin of the arch of the azygos vein is visible projecting over the lower aspect of the aortic arch. In certain individuals, the posterior edges of the innominate or left subclavian arteries may be visible in relation to the tracheal air column.
The appearance of the retrosternal space depends upon the shape of the sternum and the amount of anterior mediastinal fat. On well-penetrated lateral radiographs, the body of the sternum is readily visible (Fig. 12.11). A thin retrosternal stripe from a small amount of fat immediately behind the body of the sternum is usually seen. Sternal fracture, infection, tumor, or prior sternotomy can distort or thicken this stripe. Enlargement of internal mammary arteries (e.g., coarctation of the aorta) or lymph nodes (typically with lymphoma or metastatic breast carcinoma) produces masses seen projecting through the concavities between the costal cartilages. Inferiorly, the left lung may be excluded from contacting the anteromedial chest wall by a round or triangular opacity, which represents the cardiac apex and adjacent extrapleural fat. This impression on the anterior surface of the lingula has been termed the cardiac incisura and should not be mistaken for a mass. CT will prove helpful in equivocal cases. A mass arising within the anterior mediastinum may not be visible on a PA view but will usually encroach on this retrosternal clear space.
The anterior pericardium can be identified separately from the myocardium in 20% of subjects. This thin line represents the pericardial layers between the epicardial and pericardial fat. Nodularity or thickness >2.0 mm suggests disease or effusion.
The posterior aspect of the inferior vena cava is visible in a majority of individuals as a concave posterior or straight edge that is visible at the posteroinferior cardiac margin, just above the diaphragm (Fig. 12.11). In the pediatric population, its absence often concurs with cardiac abnormalities.
The hemidiaphragms appear as parallel domed structures on lateral radiographs (Fig. 12.1). The posterior portion lies at a more inferior level than the anterior portion, creating a deep posterior costophrenic sulcus and a shallow anterior sulcus. There are several methods of distinguishing the right from the left hemidiaphragm on the lateral view. The anterior left hemidiaphragm is obliterated (silhouetted) by the cardiac contact, whereas the right hemidiaphragm is seen in its entire anteroposterior course. On a well-positioned left lateral chest radiograph, with the right side of the thorax farther from the x-ray cassette than the left, the right anterior and posterior costophrenic sulci should project beyond the corresponding left-sided sulci as a result of x-ray beam divergence. Identification of the right and left costophrenic sulci allows identification of the corresponding hemidiaphragms. The presence of air in the stomach or splenic flexure projecting above one hemidiaphragm and below another identifies the more cephalad structure as the left hemidiaphragm. Occasionally, when the right and left major fissures are distinguishable (the left is more vertically oriented than the right), following a major fissure to its point of contact with the diaphragm will allow identification of that hemidiaphragm.
Anatomy of the Normal Mediastinum and Thoracic Inlet
The mediastinum is a narrow, vertically oriented structure that resides between the medial parietal pleural layers of the lungs. It contains central cardiovascular, tracheobronchial structures and the esophagus enveloped in fat with intermixed lymph nodes (Fig. 12.16) (Table 12.6) (14). The thoracic inlet structures are best depicted by CT and MR (Fig. 12.17A). Several schemes have been described to divide the mediastinum into separate compartments. We will use an anatomic method, in which a line drawn through the sternal angle anteriorly and fourth thoracic intervertebral space posteriorly divides the mediastinum into superior and inferior compartments. The inferior mediastinum is further subdivided into anterior, middle, and posterior compartments. This division of the mediastinum is purely arbitrary, as there are no true anatomic boundaries between the three compartments. However, by using the most easily recognizable mediastinal structure—the heart—as the focal point, the relationship of mediastinal masses to the heart allows for simple and consistent compartmentalization. Furthermore, this division of the mediastinum corresponds to easily recognizable regions seen on the lateral chest radiograph. A minor variation of the anatomic method, in which there is no superior and inferior division and the anterior, middle, and posterior compartments extend vertically from the thoracic inlet
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superiorly to the diaphragm inferiorly, is most practical to radiologists and is used here (Fig. 12.16). Within each compartment are readily identifiable structures and a number of spaces, in free communication with one another, which contain fat and lymph nodes. The structures and spaces native to each compartment and their normal appearance are reviewed here.
FIGURE 12.16. Mediastinal Compartments as Defined on Lateral View. A, Anterior mediastinum; M, middle mediastinum; P, posterior mediastinum.
TABLE 12.6 Contents of the Thoracic Inlet and Mediastinum
Compartment Contents
Thoracic inlet Thymus
Confluence of right and left internal jugular and subclavian veins
Right and left carotid arteries
Right and left subclavian arteries
Trachea
Esophagus
Prevertebral fascia
Phrenic, vagus, recurrent laryngeal nerves
Muscles
Anterior mediastinum Internal mammary vessels
Internal mammary and prevascular lymph nodes
Thymus
Middle mediastinum Heart and pericardium
Ascending and transverse aorta
Main and proximal right and left pulmonary arteries
Confluence of pulmonary veins
Superior and inferior vena cava
Trachea and main bronchi
Lymph nodes and fat within mediastinal spaces
Posterior mediastinum Descending aorta
Esophagus
Azygos and hemiazygos veins
Thoracic duct
Sympathetic ganglia and intercostal nerves
Lymph nodes
Anterior Mediastinum
The anterior (prevascular) mediastinal compartment includes all structures behind the sternum and anterior to the heart and great vessels, plus the internal mammary vessels and lymph nodes, thymus, and the brachiocephalic veins (Table 12.6). The internal mammary vessels reside within the parasternal fat and lie on either side of the sternum. Normal lymph nodes accompany the vessels but are not routinely visualized on CT. The interface of the retrosternal space with the anterior portion of the right and left lungs may be visualized on lateral chest radiographs (see the section “Lateral Chest Radiograph”). The thymus is a triangular or bilobed structure that is maximal in size at puberty and then undergoes gradual fatty involution. In most individuals over the age of 35, the thymus is predominantly fatty, with little or no intermixed glandular (soft tissue) component (Fig. 12.17A). The margins of the gland in an adult should be flat or concave toward the lung. The left lobe is commonly larger than the right. Anatomically, the thymus lies in the prevascular space, which is continuous with the retrosternal space anteriorly. It lies immediately anterior to the superior vena cava, aortic arch and great vessels, the main pulmonary artery, and, more inferiorly, the heart. The prevascular space generally retains the triangular configuration of the involuted thymus. Normal lymph nodes may be visible on CT within the fat of the prevascular space. Beginning at the level of the aortic arch in most individuals, the anterior portion of the prevascular space tapers to form a thin, vertically oriented linear density that represents the anterior junction line. The right and left brachiocephalic veins occupy the posterior aspect of the prevascular space at the level of the root of the great vessels. The right brachiocephalic vein is seen on CT as a round density owing to its vertical orientation, while the crossing left brachiocephalic vein appears oval or tubular in configuration.
Middle Mediastinum
The middle (vascular) mediastinal compartment comprises the pericardium and its contents, the aortic arch and proximal great arteries, the central pulmonary arteries and veins, the trachea and main bronchi, and lymph nodes (Table 12.6). The hila may be considered as extensions of the middle mediastinal compartment. The phrenic and vagus nerves are not visible on CT scans, but run together in the space between the subclavian arteries and brachiocephalic veins. The recurrent laryngeal nerves lie on each side within the tracheoesophageal groove. Four middle mediastinal spaces surrounding the trachea and carina can be distinguished
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(Fig. 12.17C). The right paratracheal space, containing lymph nodes and a small amount of fat, appears as the right paratracheal stripe on PA views. This space extends from the thoracic inlet superiorly to the azygos vein inferiorly. The pretracheal space is seen between the trachea posteriorly and the posterior margin of the ascending aorta anteriorly and is contiguous with the precarinal space inferiorly. It contains fat, lymph nodes, and the retroaortic portion of the superior pericardial recess and is the anatomic route used during routine transcervical mediastinoscopy. The retrotracheal space varies in AP dimension, depending upon the degree of invagination of the RUL behind the upper trachea. To the left of the trachea lies the aortopulmonary window. The borders of the aortopulmonary window are: the aortic arch superiorly; the left pulmonary artery inferiorly; the distal trachea, left main bronchus, and esophagus medially; the mediastinal pleural surface of the left upper lobe laterally; the posterior surface of the ascending aorta anteriorly; and the anterior surface of the proximal descending aorta posteriorly.
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This space contains fat, lymph nodes, the ligamentum arteriosum, and the left recurrent laryngeal nerve.
FIGURE 12.17. Normal Mediastinal Anatomy on CT. A. Thoracic inlet. Tr, trachea; t, thyroid; e, esophagus; j, internal jugular vein; c, common carotid artery; a, anterior scalene muscle; m, middle scalene muscle. B. Supra-aortic level. CT scan demonstrates the triangular appearance of the fatty thymus (arrows) occupying the anterior mediastinum. lb, Left brachiocephalic vein; rb, right brachiocephalic vein; B, brachiocephalic artery; C, common carotid artery; Sa, left subclavian artery. C. Aortic arch level. Four main structures are identified at this level: A, aortic arch; S, superior vena cava; Tr, trachea; E, esophagus. Normal-sized lymph nodes are seen in the retrocaval, pretracheal space (open arrow). D. Aortopulmonary window level. The aortopulmonary window contains fat and small lymph nodes (large open arrow). The retro-aortic portion of the superior pericardial recess is seen as a crescent-shaped fluid-filled structure (small open arrow). As, ascending aorta; De, descending aorta; S, superior vena cava; Ca, tracheal carina; a, azygos vein; E, esophagus. E. Main and left pulmonary artery level. As, ascending aorta; S, superior vena cava; De, descending aorta, M, main pulmonary artery; L, left pulmonary artery; TA, truncus anterior branch of right pulmonary artery. F. Right pulmonary artery and azygoesophageal recess level. M, main pulmonary artery; R, right pulmonary artery; As, ascending aorta; De, descending aorta; S, superior vena cava; rv, right superior pulmonary veins; lv, left superior pulmonary veins; Ld, left descending pulmonary artery; AER, azygoesophageal recess. G. Right ventricular outflow tract/atrial appendages. RVOT, Right ventricular outflow tract; RA, right atrium; LA, left atrium; rv, right superior pulmonary vein; As, ascending aorta; De, descending aorta. H. Ventricles and intraventricular septum. RA, right atrium; RV, right ventricle; LV, left ventricle.
Continuing inferiorly, the main and left pulmonary arteries occupy the left anterolateral portion of the middle mediastinum (Fig. 12.17D). The tracheal carina forms the posterior margin of the middle mediastinum. The RUL bronchus is seen just below the tracheal carina. More inferiorly, the right pulmonary artery is seen coursing toward the right and slightly posteriorly, just behind the ascending aorta and anterior to the bronchus intermedius (Fig. 12.17E). The subcarinal space is outlined posteriorly by air in the azygoesophageal recess and anteriorly by the posterior aspect of the transverse right pulmonary artery. The left superior pulmonary vein lies immediately anterior to the left main and upper lobe bronchi.
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The main pulmonary artery can be followed inferiorly to the level of the outflow tract of the right ventricle. At this level, the right and left atrial appendages and the top of the left atrium proper may be seen (Fig. 12.17F). Also at this level, the right superior pulmonary vein lies anterior to the middle lobe bronchus, which in turn lies immediately anterior to the RLL bronchus. Inferiorly, the right atrium proper, right ventricle, and left ventricle are identified (Fig. 12.17G).
ATS Nodal Stations
To provide greater uniformity in the nodal staging of bronchogenic carcinoma and thereby help guide diagnostic and therapeutic efforts in this disease, the American Thoracic Society (ATS) has devised a standard classification scheme for mediastinal lymph nodes (see Fig. 13.8).
Posterior Mediastinum
The posterior (postvascular) mediastinal compartment lies behind the pericardium and includes the esophagus, the descending aorta, the azygos and hemiazygos veins, the thoracic duct, and the intercostal and autonomic nerves (Table 12.5). The esophagus lies posterior or posterolateral to the trachea, from the level of the thoracic inlet superiorly to the tracheal carina inferiorly. From the thoracic inlet to the level of the aortic arch, the right and left upper lobes of the lungs meet behind the esophagus and anterior to the spine to form the narrow posterior junction line seen on CT scans through the upper thorax and appearing as a vertical line through the tracheal air column on frontal radiographs. The esophagus then maintains a constant relationship with the descending thoracic aorta, usually lying anteromedial to the aorta (Figs. 12.17, 12.18) down to the level of the aortic hiatus, where the aorta is in a direct prevertebral position while the esophagus crosses the aorta anteriorly to exit the thorax via the esophageal hiatus. There are lymph nodes about the descending aorta that are not normally visible. The descending aorta lies anterolateral to the thoracic spine at the level of the aortopulmonary window. In young adults, the aorta maintains this position to the level of the aortic hiatus of the diaphragm, where it lies directly in the midline. In older patients and those with a tortuous or dilated aorta, the vessel lies more laterally and protrudes into the LLL as it descends, carrying the esophagus with it before returning to a midline position at the level of the aortic hiatus. The azygos and hemiazygos veins lie on the right and left sides, respectively, posterolateral to the descending aorta within a fat-containing space that contains the thoracic duct and the sympathetic chains (normally not visible) and small lymph nodes (Fig. 12.18). Inferiorly, this space is continuous with the retrocrural space and laterally with the paraspinal space, which contains the intercostal arteries, veins, and lymph nodes.
FIGURE 12.18. Posterior Mediastinal Anatomy. A CT scan shows a contrast-filled esophagus (curved arrow) anteromedial to the proximal descending aorta (De). Also visible within the posterior mediastinum are the azygos vein (a), hemiazygos vein (long arrow), and thoracic duct (short arrow).
Normal Hilar Anatomy
Frontal View
The hilum represents the junction of the lung with the mediastinum and is composed of upper lobe pulmonary veins and branches of the pulmonary artery and corresponding bronchi (Fig. 12.19). These are all enveloped by small amounts of fat, with intermixed lymph nodes.
The shape of the right hilum on frontal radiographs has been likened to a sideways V, with the opening pointing rightward (Fig. 12.19A, B). The upper portion of the V is composed primarily of the truncus anterior and the posterior division of the right superior pulmonary vein. The right interlobar artery forms the lower half of the V, as it descends lateral to the bronchus intermedius. The right inferior pulmonary vein crosses the lower right hilar shadow but does not contribute to its opacity (Fig. 12.19A).
On CT, the upper portion of the right hilum is composed of the right superior pulmonary vein, truncus anterior division of the right pulmonary artery, and the RUL bronchus. The RUL pulmonary vein courses vertically, anterolateral to the truncus anterior (Figs. 12.5B, 12.17D–F). Here again, the epi-arterial position of the bronchus can be recognized. The lower portion of the right hilum is composed of the right descending (or interlobar) pulmonary artery laterally and the bronchus intermedius and proximal RLL bronchus medially (Fig. 12.17E, F).
The upper left hilar shadow is composed centrally of the distal left main pulmonary artery and, more peripherally, of one or more branches of its LUL division and the posterior division of the left superior pulmonary vein (Fig. 12.19). The left pulmonary artery and left descending artery arch over the left mainstem bronchus and are thus named hypo-arterial. The descending artery then forms the
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lower portion of the left hilar shadow as it descends behind the left heart.
FIGURE 12.19. Normal Frontal and Lateral Hilar Anatomy. A. Cone-down frontal view. Right hilum: Short white arrows, border of the interlobar artery; small black arrowheads, right superior pulmonary vein; small white arrowheads, truncus anterior. The lucency between these (long black arrow) is from the apical segmental bronchus. Left hilum: Large white arrowhead, left pulmonary artery; short black arrows, border of the left descending pulmonary artery; black dots, left superior pulmonary vein; white dots, left upper lobe artery; long white arrow, apicoposterior segmental bronchus. The asterisk is in the AP window. B. Using two-dimensional imaging techniques, one can gain adequate insight of the complex lateral hilar anatomy. This view shows a 50-mm average sagittal projection over the hila of a contrast CT with 3-mm collimation reconstructed at 2-mm. (1) The left hilum. Small white arrows outline the left upper lobe bronchus; small black arrowheads border the left lower lobe bronchus; long black arrows delineate the left descending artery; AP window (asterisk) lies between the inferior border of the aorta (lined with small black dots) and the left pulmonary artery (white arrowheads). (2) The right hilum. Note the relationship between the right upper lobe bronchus (small white arrows) and the right pulmonary artery (black dots). Black arrowheads indicate the posterior border of the bronchus intermedius; small white arrowheads line the middle lobe bronchus; large white arrowheads outline the right lower lobe bronchus; white dots line the right lower venous return; black arrows delineate the superior vena cava (SVC). The differential density is the result of the heavier contrast layering along the posterior aspect of the vessel in a supine acquisition. (3) Two-dimensional average merge of (1) and (2). Using the data from (1) and (2), note the relationship between the different structures described above.
On CT of the upper left hilum, the left superior pulmonary vein courses anterior to the left pulmonary artery and, more inferiorly, anterior to the LUL bronchus to empty into the superolateral aspect of the left atrium (Fig. 12.17D–F). The left pulmonary artery arches posteriorly, superiorly, and to the left, over the left main and upper lobe bronchi (thus being hypo-arterial), to bifurcate into upper and lower lobe arteries (Fig. 12.17D, E). The lower portion of the left hilum is composed of the left descending artery, which lies posterolateral to the LLL bronchus (Fig. 12.17E). The left inferior pulmonary vein courses horizontally at a level slightly behind that of the right inferior vein to empty into the left atrium, just medial to the left basal trunk bronchus.
As seen on frontal radiographs, the right and left pulmonary arteries comprise the predominant portion of the hilar opacity, with the superior pulmonary veins, lobar bronchi, bronchopulmonary lymph nodes, and a small amount of fat contributing little to the overall hilar density (Fig. 12.19A). In over 90% of normal individuals, the left hilar shadow is higher than the right. This is because the left pulmonary artery, which comprises the predominant portion of the left hilar shadow, ascends over the left main and upper lobe bronchus, whereas the right pulmonary artery lies inferior to the RUL bronchus. In the remainder of individuals, the right and left hila lie at the same level; a right hilum that lies above the left suggests volume loss in the right upper or left lower lobe.
Left Lateral View
On a true lateral radiograph, the right and left hilar shadows are not completely superimposed and comprise a combination of the right and left pulmonary arteries and the superior pulmonary veins (Fig. 12.19C, D). The anterior aspect of the hilar shadow is composed of the transverse portion of the right pulmonary artery, which produces a vertically oriented oval opacity projecting immediately anterior to the bronchus intermedius. The confluence of right superior pulmonary veins overlaps the lower portion of the right pulmonary artery and contributes to its opacity. Superiorly and posteriorly, the comma-shaped left pulmonary artery passes above and behind the round or oval lucency representing the horizontally oriented LUL bronchus summating on a portion of the left mainstem bronchus, and then descends behind the LLL bronchus. The confluence of left superior pulmonary veins, which lies behind the level of the right superior pulmonary vein, creates an opacity that occupies the posteroinferior aspect of the composite hilar shadow. The avascular aspect of the composite hilar shadow, inferior to the shadow of the right pulmonary artery and veins and anterior to the descending left pulmonary artery and left superior vein, is called the inferior hilar window. This region is roughly triangular in shape, with its apex at the junction of the LUL and LLL bronchi and its base directed anteriorly and inferiorly. The RML and lingular veins cross the inferior hilar window, but because of their small size, they do not contribute significant opacity to this area.
The vascular structures of the composite hilar shadow are suspended around the central bronchi (Fig. 12.19). Beginning superiorly, the RUL bronchus is seen in approximately 50% of individuals as an end-on, round lucency at the upper margin of the composite hilar shadow. Recognition of this bronchus, when not visible on prior radiographs, should suggest a mass or lymph node enlargement about the bronchus. The posterior wall of the bronchus intermedius is a thin vertical line, 2 mm or thinner, extending inferiorly from the posterior aspect of the RUL bronchus. The line is seen in 95% of patients and extends inferiorly to bisect the end-on lucency of the LUL bronchus on a lateral film. This structure is rendered visible because air within the intermediate bronchus anteriorly and lung within the azygoesophageal recess posteriorly outlines its posterior wall. Thickening or nodularity of this line is seen in bronchogenic carcinoma, pulmonary edema, or enlargement of azygoesophageal recess lymph nodes. The LUL bronchus, which is seen in 75% of individuals, lies no more than 4 cm directly inferior to the RUL bronchus. This bronchus is visualized with greater frequency than the RUL bronchus because it is outlined by the left pulmonary artery and by other mediastinal structures, while the RUL bronchus is contacted only by the right main pulmonary artery anteroinferiorly and the azygos arch superiorly. The projection of the posterior wall of the bronchus intermedius over the LUL bronchus also helps identify the LUL bronchus. Below the oval lucency of the latter, the basal trunk of the LLL bronchus can sometimes be identified, with its anterior wall visible as a white line, outlined by air in the bronchial lumen and air in the lung. The LLL bronchus is seen immediately below and continuous with the horizontal LUL bronchus.
The appearance of the hila changes with a slight degree of rotation. If on a left lateral radiograph, the patient is rotated slightly right side back and left side forward, the more posteriorly positioned left pulmonary artery will be summated on the more anterior right main pulmonary artery, and the hila are termed “closed.” If on the other hand, the rotation is slightly left side back and right side forward, the left pulmonary artery is further separated from the right and the hila are termed “open.” If the patient is in a true lateral position, the beam divergence will magnify the right-sided structures and simulate minimal “closing” of the hila. The relationship of the right-sided bronchus intermedius to the round hole of the end-on LUL bronchus can be helpful in evaluating differences in rotation between serial lateral views on the same patient. Analyzing this normal hilar relationship is helpful in determining the side of the posterior costophrenic sulcus if the ribs are not completely superimposed.
FIGURE 12.20. HRCT of the Pleura. HRCT scan through the lung bases demonstrates normal intercostal stripes (solid arrows) that are separated from the intercostal muscles by a layer of fat. An intercostal vein (small open arrow) is seen in the paravertebral region. Anteriorly, the transverse thoracic muscles (large open arrows) line the parasternal pleural surface.
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Pleural Anatomy
The pleura is a serosal membrane that envelops the lung and lines the costal surface, diaphragm, and mediastinum (15). It is composed of two layers, the visceral and the parietal pleura, that join at the hilum. Blood supply to the parietal pleura is via the systemic circulation, while the visceral pleura is supplied by the pulmonary circulation. The parietal pleura is contiguous with the chest wall and diaphragm and therefore extends deep posteriorly into the costophrenic sulci, while the visceral pleura is adherent to the surface of the lung. The pleural space is a potential space between the two pleural layers and normally contains a small amount of fluid (<5 mL) that reduces friction during breathing.
FIGURE 12.21. Normal Pleural and Chest Wall Anatomy. The visceral pleura is 0.1 to 0.2 mm thick and is composed of a single layer of mesothelial cells and its associated fibroelastic fascia, called the subpleural interstitium, that is part of the peripheral interstitial network. The parietal pleura is 0.1 mm thick and is composed of a single layer of mesothelial cells lining a loose connective tissue layer containing systemic capillaries, lymphatic vessels, and sensory nerves. Outside the parietal pleura is the fibroelastic endothoracic fascia, which is separated from the pleura by a thin layer of extrapleural fat. The endothoracic fascia lines the ribs and intercostal muscles.
The normal costal, diaphragmatic, and mediastinal pleura is not visible on plain radiographs or CT. On HRCT, a 1- to 2-mm stripe may be seen lining the intercostal spaces between adjacent ribs (Fig. 12.20). This “intercostal stripe” represents the combination of the two pleural layers, the endothoracic fascia, and the innermost intercostal muscle (Fig. 12.21). Internal to the ribs, the normal pleura is not seen and the inner cortex of rib appears to contact the lung. The presence of soft tissue density between the inner rib and the lung, best appreciated on HRCT studies, indicates pleural thickening. The innermost intercostal muscle is anatomically absent in the paravertebral area, and if a thin line is visible between the lung and paravertebral fat or rib, it represents a combination of the two pleural surfaces and the endothoracic fascia.
Chest Wall Anatomy
The radiographic anatomy of the soft tissues and bony structures of the chest wall were discussed in the section on the normal frontal radiograph. CT provides detailed anatomic information about the normal chest wall and axillae. A detailed knowledge of normal cross-sectional chest wall and axillary anatomy is key to accurate localization and characterization of disease processes. Chest wall anatomy as seen on CT at six representative levels is shown in Fig. 12.22.
FIGURE 12.22. Normal Chest Wall Anatomy on CT. A. Level of the thoracic inlet. PM, pectoralis major muscle; Tr, trapezius muscle; L, levator scapulae muscle; Sc, scalene muscle; Scm, sternocleidomastoid muscle; H, humeral head; G, glenoid; C, distal clavicle; T1, first thoracic vertebral body. B. Level of the axillary vessels. Pm, pectoralis minor muscle; Sa, serratus anterior muscle; Su, supraspinatus muscle; In, infraspinatus muscle; Ss, subscapularis muscle; P, paraspinal muscles; M, manubrium of the sternum; S, body of the scapula; A, axilla with normal lymph nodes. C. Level of the sternomanubrial joint. Ld, latissimus dorsi muscle; Tma, teres major muscle; Tri, long head of the triceps muscle; Tmi, teres minor muscle; D, deltoid muscle. D. Level of the body of the sternum. P, pectoralis muscles; Ss, subscapularis muscle; In, intraspinatus muscle; Tr, trapezius muscle; St, body of the sternum. E. Level of tip of scapula. Ld, Latissimus dorsi muscle; Sa, serratus anterior muscle. F. Level of the xiphoid process. Ld, latissimus dorsi muscle; Sa, serratus anterior muscle; X, xiphoid process of the sternum.
FIGURE 12.23. Normal Anatomy of the Diaphragm on CT. A. A scan through the upper abdomen demonstrates the crura of the diaphragm posteriorly (small open arrows), the costal origins of the diaphragm laterally (large open arrows), and the costal cartilaginous origins anterolaterally (solid arrows). B. More inferiorly, the esophageal hiatus is seen between the crura (open arrows).
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Anatomy of the Diaphragm
The diaphragm is composed of striated muscle and a large central tendon separating the thoracic and abdominal cavities. The diaphragmatic muscle arises anteriorly from the posterior aspect of the xiphoid process and anterolaterally, laterally, and posterolaterally from the sixth to the twelfth costal cartilages and ribs. The diaphragmatic crura originate from the upper lumbar vertebrae and course to the posterior aspect of the central tendon. They have no direct action on the rib cage (Fig. 12.23). The diaphragm has three normal openings and two potential gaps. The aortic hiatus lies in the midline, immediately behind the diaphragmatic crura and anterior to the twelfth thoracic vertebral body. The aorta, thoracic duct, and azygos and hemiazygos veins traverse this opening. The esophageal hiatus usually lies slightly to the left of midline, cephalad to the aortic hiatus, and transmits the esophagus and vagus nerves. The inferior vena cava pierces the central tendon of the diaphragm at the level of the eighth thoracic intervertebral disk space. The foramina of Morgagni are triangular gaps in the muscles of the anteromedial diaphragm. This cleft is normally occupied by fat and the internal mammary vessels; it is a site of potential intrathoracic herniation of abdominal contents. The foramina of Bochdalek are defects in the closure of the posterolateral diaphragm at the junction of the pleuroperitoneal membrane with the transverse septum. Hernias through the foramina of Morgagni and Bochdalek are discussed in Chapter 19.
On CT scans, the domes of the diaphragms appear as rounded opacities on either side of the chest at the level of the base of the heart. In some patients scanned on deep inspiration, the diaphragm has an undulating or nodular appearance from contraction of slips of diaphragmatic muscle. This appearance is seen with increasing frequency in older patients, and is more common on the left than the right. Posteriorly, the superior aspects of the diaphragmatic crura are seen. The crura are curvilinear opacities that arise from the upper two to three lumbar vertebrae. Their associated esophageal and aortic openings within the bundles of the crura are well visualized on CT (Fig. 12.23). Continuing inferiorly into the upper abdomen, the inferior aspects of the diaphragmatic crura may have a rounded appearance in cross section and should not be mistaken for enlarged retrocrural lymph nodes. Review of contiguous CT images will allow for proper identification of these structures.
RADIOGRAPHIC FINDINGS IN CHEST DISEASE
Parenchymal lung disease can be divided into those processes that produce an abnormal increase in the density of all or a portion of the lung on chest radiographs (pulmonary opacity) and those that produce an abnormal decrease in lung density (pulmonary lucency). The normal density of the lungs is a result of the relative proportion of air to soft tissue (blood or parenchyma) in a ratio of 11 to 1. Therefore, it stands to reason that processes that increase the relative amount of soft tissue will create a significant decrease in this ratio and be more easily discernible
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than diffuse processes, which destroy blood vessels and parenchyma and cause little change in this ratio, thereby producing only small decreases in overall lung density. CT, by virtue of its superior contrast resolution, is more sensitive than plain radiography to subtle decreases in overall radiographic density.
TABLE 12.7 Patterns of Parenchymal Opacity
Type Example
Airspace (alveolar) filling Pneumococcal pneumonia
Interstitial opacities
   Reticular/linear Idiopathic pulmonary fibrosis
   Reticulonodular Sarcoidosis
   Branching Allergic bronchopulmonary aspergillosis
Nodular
   Miliary (<2 mm) Miliary tuberculosis
   Micronodule (2–7 mm) Acute hypersensitivity pneumonitis
   Nodule (7–30 mm) Metastatic disease, granuloma
   Mass (>30 mm) Bronchogenic carcinoma
Atelectasis Endobronchial neoplasm
Abnormal pulmonary opacities may be classified into airspace-filling opacities, opacity resulting from atelectasis, interstitial opacities, nodular or masslike opacities, and branching opacities (Table 12.7). These patterns have been shown to accurately represent pulmonary pathologic processes in correlative radiographic–pathologic studies, and are a practical means of generating a differential diagnosis based on the known patterns of parenchymal involvement in a wide variety of pulmonary diseases.
Pulmonary Opacity
Airspace Disease
Radiographic findings of airspace disease are listed in Table 12.8. Airspace patterns of opacity develop when the air normally present within the terminal airspaces of the lung is replaced by material of soft tissue density, such as blood, transudate, exudate, or neoplastic cells. A segmental distribution of disease may be seen in a process such as pneumococcal pneumonia, which begins in the terminal airspaces and spreads from involved to uninvolved airspaces via interalveolar channels (pores of Kohn) and channels bridging preterminal bronchioles with alveoli (canals of Lambert). Initially, the opacity is poorly marginated, because the airspace-filling process extends in an irregular fashion to involve adjacent airspaces, creating an irregular interface with the x-ray beam. Not uncommonly, airspace nodules, which are poorly marginated, rounded opacities 6 to 8 mm in diameter, may be seen at the leading edge of an airspace-filling process. These nodules represent filling of acini or other sublobular structures and are most often seen in diffuse alveolar pulmonary edema and transbronchial spread of cavitary tuberculosis.
TABLE 12.8 Radiographic Characteristics of Airspace Disease
Lobar or segmental distribution
Poorly marginated
Airspace nodules
Tendency to coalesce
Air bronchograms
Bat’s wing (butterfly) distribution
Rapidly changing over time
A characteristic of airspace-filling processes is the tendency of airspace shadows to coalesce as they extend through the lung (16). When the airspaces are rendered opaque by the presence of intra-alveolar cellular material and fluid, the normally aerated bronchi become visible as tubular lucencies called air bronchograms (Fig. 12.24). Occasionally, small intraacinous bronchi or groups of uninvolved alveoli may be visible within an airspace nodule as air bronchiolograms or air alveolograms, respectively. Rarely, severe interstitial disease encroaching upon the airspaces may produce an air bronchogram; this is most typically seen in “alveolar” sarcoid. When the airspace-filling process extends to the interlobar fissure, it is seen as a sharply marginated lobar opacity.
FIGURE 12.24. Air Bronchograms in Airspace Disease. Cone-down view of the right upper lobe in a patient with pneumococcal pneumonia shows homogeneous lobar airspace disease delineated inferiorly by the minor fissure. Note the presence of air bronchograms (arrows) within the opacified lobe.
TABLE 12.9 Diffuse Confluent Airspace Opacities: Differential Diagnosis
Type Example
Pulmonary edema Cardiogenic
Fluid overload/renal failure
Noncardiogenic (ARDS) (see Table 14.2)
Pneumonia Pneumocystis carinii
Gram-negative bacteria
Influenza
Fungi
   Histoplasmosis
   Aspergillosis
Hemorrhage See Table 14.3
Neoplasm Bronchoalveolar cell carcinoma
Lymphoma
Alveolar proteinosis Acute silica inhalation
Lymphoma
Leukemia
AIDS
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A pattern of parenchymal opacity that reliably represents an airspace-filling process is the “bat’s wing” or “butterfly” pattern of disease. In this pattern, dense opacities occupy the central regions of lung and extend laterally to abruptly marginate before reaching the peripheral portions of the lung; hence the term “bat’s wing” (see Fig. 14.2). To date, there is no explanation for this distribution of disease, which appears almost exclusively in patients with pulmonary edema or hemorrhage. Another feature of airspace-filling processes is the tendency to rapidly change in appearance over short intervals of time. The development or resolution of parenchymal opacities within hours usually indicates an airspace-filling process; prominent exceptions include atelectasis and interstitial pulmonary edema. The differential diagnosis of diffuse confluent airspace opacities is reviewed in Table 12.9.
The CT and HRCT findings of airspace disease are similar to those described on plain chest radiographs. These are: (1) lobar, segmental, and/or lobular distribution of disease; (2) poorly marginated opacities that tend to coalesce; (3) airspace nodules; and (4) air bronchograms. A lobar or segmental distribution of disease is easily appreciated on cross-sectional imaging. CT and HRCT are further capable of showing individually opacified lobules, termed a “patchwork quilt” appearance, which is seen in many airspace processes, most classically bronchopneumonia (see Fig. 17.3). Coalescence of opacities, commonly seen in pulmonary edema and pneumonia, is best assessed on serial CT studies. With isolated airspace disease, the interlobular septa are normal or obscured. As with plain films, the presence of airspace nodules provides further evidence of an airspace process. On HRCT studies, these nodules are usually seen within the peribronchiolar (centrilobular) region of the pulmonary lobule. Air bronchograms or bronchiolograms are usually better appreciated on CT and HRCT than on plain radiographs owing to superior contrast resolution and the cross-sectional nature of CT. This is particularly true in those regions of the lung where bronchi course in the transverse plane (anterior segments of upper lobes, middle lobe and lingula, and superior segments of the lower lobes).
Atelectasis literally means “incomplete expansion.” It is used to describe any condition in which there is loss of lung volume, and it is usually but not invariably associated with an increase in radiographic density. There are four basic mechanisms of atelectasis (Table 12.10) (17).
The most common form of atelectasis is obstructive or resorptive atelectasis and is secondary to complete endobronchial obstruction of a lobar bronchus with resorption of gas distally. Incomplete bronchial obstruction more often produces air trapping from a check-valve effect rather than atelectasis, because air enters but cannot exit the lung. Complete obstruction of a central bronchus may not produce atelectasis if collateral airflow to the obstructed lung (via pores of Kohn, canals of Lambert, or incomplete interlobar fissures) allows the lung to remain inflated. An obstructed lobe or lung containing 100% oxygen, as may be seen in some mechanically ventilated patients, will collapse more rapidly (sometimes within minutes) than lung containing ambient air. This is the result of the rapid absorption of oxygen from the alveolar spaces into the alveolar capillaries. Bronchogenic carcinoma, foreign bodies, mucous plugs, and malpositioned endotracheal tubes are the most common causes of endobronchial obstruction and secondary resorptive atelectasis.
Passive or relaxation atelectasis results from the mass effect of an air or fluid collection within the pleural space on the subjacent lung. Since the natural tendency of the lung is to collapse when dissociated from the chest wall, pleural collections will produce atelectasis. The degree of atelectasis depends upon the size of the pleural collection and upon the compliance of the lung and visceral pleura. A large pleural or chest wall mass or an elevated diaphragm can also produce passive atelectasis. Compressive atelectasis
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is a form of passive atelectasis in which an intrapulmonary mass compresses adjacent lung parenchyma; common causes include bullae, abscesses, and tumors.
TABLE 12.10 Types of Pulmonary Atelectasis
Type Example
Obstructive (resorptive) Bronchogenic carcinoma (endobronchial)
Passive (relaxation) Pleural effusion
Pneumothorax
Compressive Bulla
Cicatricial Post–primary tuberculosis
Radiation fibrosis
Adhesive Respiratory distress syndrome of the newborn
Processes resulting in parenchymal fibrosis reduce alveolar volume and produce cicatricial atelectasis. Localized cicatricial atelectasis is most often seen in association with chronic upper lobe fibronodular tuberculosis. The radiographic appearance is that of severe lobar volume loss with scarring, bronchiectasis, and compensatory hyperinflation of the adjacent lung. Diffuse cicatricial atelectasis is seen in interstitial fibrosis of any etiology. An overall increase in lung density, with reticular opacities and diminished lung volumes, is characteristic of this condition.
Adhesive atelectasis occurs in association with surfactant deficiency. Type 2 pneumocytes, the cells responsible for surfactant production, may be injured as a result of general anesthesia, ischemia, or radiation. Surfactant deficiency causes increased alveolar surface tension and results in diffuse alveolar collapse and volume loss. Radiographs show a diminution in lung volume, which may be associated with an increase in density.
Lobar Atelectasis
The only direct radiographic finding of lobar atelectasis is the displacement of an interlobar fissure (Table 12.11) (18). There are several indirect findings of atelectasis, most of which reflect attempts to compensate for the volume loss (Fig. 12.25). Diminished aeration results in increased density in the affected portion of lung, plus bronchovascular crowding. Ipsilateral shift of the trachea, heart, or mediastinum and hilar structures is a common finding in lobar atelectasis. Shift of the entire mediastinum is typical of collapse of an entire lung. Compensatory hyperinflation represents an attempt by the remaining normal lung to partially fill the space lost by the affected lung. This mechanism usually develops with chronic volume loss and is not seen in acute collapse. It is seen as increased lucency with attenuation of pulmonary vascular markings. In complete lung or upper lobe atelectasis, the contralateral upper lobe may herniate across the midline, bowing the anterior junction line toward the affected side. A characteristic but seldom seen plain radiographic finding of compensatory hyperinflation is the “shifting granuloma,” in which a preexisting granuloma in an adjacent aerated lung changes position as it moves toward the collapsed lobe. In chronic atelectasis of a lung, a decrease in size of the hemithorax with approximation of the ribs may be seen. The absence of an air bronchogram helps distinguish resorptive lobar atelectasis from lobar pneumonia, particularly if the atelectatic lobe is only slightly diminished in volume. A triangular configuration with the apex at the pulmonary hilum is common to all types of lobar atelectasis. The fissure bordering the collapse typically assumes a concave configuration. Complete lobar atelectasis can easily be missed on PA and lateral radiographs but is easily appreciated on CT.
FIGURE 12.25. Lobar Atelectasis. Upright frontal chest radiograph in a postoperative patient with right lower lobe atelectasis shows a homogeneous triangular opacity in the right lower lung that partially obscures the right hemidiaphragm. The upper margin of the collapsed lobe is marginated by the inferiorly displaced major fissure (arrows). Bronchoscopy retrieved a mucous plug from the right lower lobe bronchus, and the lobe subsequently re-expanded.
TABLE 12.11 Radiographic Signs in Lobar Atelectasis
Direct Signs Indirect Signs
Displacement of interlobar fissure Increased density of atelectatic lung
Bronchovascular crowding
Ipsilateral diaphragm elevation
Ipsilateral tracheal/cardiac/mediastinal shift
Hilar elevation (upper lobe atelectasis) or depression (lower lobe atelectasis)
Compensatory hyperinflation of other lobe(s)
Shifting granuloma
Ipsilateral small hemithorax
Ipsilateral rib space narrowing
Segmental Atelectasis
Atelectasis of one or several segments of a lobe is difficult to determine on plain radiographs. The appearance ranges from a thin linear opacity to a wedge-shaped opacity that does not abut an interlobar fissure. Segmental atelectasis is better appreciated on CT.
Subsegmental (Platelike) Atelectasis
Bandlike linear opacities representing linear atelectasis are commonly associated with hypoventilation. This is seen in patients with pleuritic chest pain, postoperative patients, or patients
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with massive hepatosplenomegaly or ascites. Subsegmental atelectasis tends to occur at the lung bases. The linear shadows are 2 to 10 cm in length and are typically oriented perpendicular to the costal pleura (Fig. 12.26). Pathologically, these areas of linear collapse are deep to invaginations of visceral pleura formed by incomplete fissures or scars.
FIGURE 12.26. Subsegmental (Platelike) Atelectasis. A. Frontal chest radiograph in a woman 1 day following a cholecystectomy shows diminished lung volumes and numerous bilateral middle and lower zone linear opacities coursing perpendicular to the costal pleura, representing areas of subsegmental atelectasis. B. The opacities resolved within several days.
Rounded Atelectasis
This is an uncommon form of atelectasis in which the collapsed lung forms a round mass in the lower lobe. This condition is most closely associated with asbestos-related pleural disease but may be seen in any condition associated with an exudative (proteinaceous) pleural effusion. The process develops when pleural adhesions form in the resolving phase of a pleural effusion and cause the adjacent lung to roll up into a ball as it re-expands. The round opacity is most often found along the inferior and posterior costal pleural surfaces adjacent to an area of pleural fibrosis or plaque formation. Plain radiographs reveal a well-defined, pleural-based mass between 2 and 7 cm adjacent to an area of pleural thickening in the lower lung. The identification of a curvilinear bronchovascular bundle or “comet tail” entering the anterior inferior margin of the mass, as seen on lateral radiographs or tomograms, is characteristic. The CT appearance of round atelectasis is characteristic (Fig. 12.27). The round or wedge-shaped mass forms an acute angle with the pleura and is seen adjacent to an area of pleural thickening, usually in the inferior and posterior thorax. The “comet tail” of vessels and bronchi is seen curving between the hilum and the apex of the mass. The atelectatic lung enhances following intravenous contrast administration. When the characteristic CT findings are seen in a patient with a known history of pleural disease, the appearance is diagnostic and no further evaluation is necessary. However, if any of the above criteria are not satisfied, the lesion should be biopsied to exclude malignancy.
Right Upper Lobe Atelectasis (Fig. 12.28A) (19)
In RUL atelectasis, the lung collapses superiorly and medially, with superomedial displacement of the minor fissure and anteromedial displacement of the upper half of the major fissure, producing a right upper paramediastinal density on frontal radiographs, which can obliterate the normal right paratracheal stripe and azygos vein. A central convex mass will prevent part of the usual fissure concavity. This appearance produces the S sign of Golden. The trachea is deviated toward the right, and the right hilum and hemidiaphragm are elevated. “Tenting” or “peaking” of the diaphragm is occasionally seen and represents fat within the inferior aspect of a stretched inferior accessory fissure. Compensatory hyperinflation of the middle and lower lobes may be seen in chronic atelectasis, and the LUL may herniate across the midline anteriorly toward the right. Scarring from tuberculosis, endobronchial tumor, and mucous plugging are common causes of RUL atelectasis.
Left upper lobe/lingular atelectasis (Fig. 12.28B) has a different appearance from RUL atelectasis because of the absence of a minor fissure. The LUL collapses anteriorly, maintaining a broad area of contact with the anterior costal pleural surface. The major fissure shifts anteriorly and is seen marginating a long, narrow band of increased opacity paralleling the anterior chest wall on lateral radiographs. Diagnosis on frontal radiographs may be difficult. There is a veil of increased opacity over the left upper thorax, which can obliterate the aortic knob, AP window, and
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left upper cardiac margin. The apex of the left hemithorax remains lucent as a result of hyperinflation of the superior segment of the LLL. Leftward tracheal displacement, hilar and diaphragmatic elevation, and leftward bulging of the anterior junction line from an overinflated RUL are additional clues to the diagnosis. An uncommon finding on the frontal radiograph in LUL atelectasis is a crescent of air (“Luftsichel”) along the left upper mediastinum, which represents a portion of the overinflated superior segment of the LLL interposed between the aortic arch medially and the collapsed upper lobe laterally (see Fig. 15.9). Postinflammatory cicatrization and endobronchial tumor are the most common causes of LUL atelectasis.
FIGURE 12.27. Round Atelectasis. Prone CT scan through the lung bases in a patient with asbestos-related pleural disease and rounded atelectasis shows a triangular opacity in the posteromedial right lower lobe associated with pleural thickening. Note the bronchus at the apex of the triangle (curved arrow). Bilateral pleural plaques are also evident (straight arrows).
FIGURE 12.28. Lobar Atelectasis, PA, Lateral, and Schematic Representations. A. Right upper lobe. Black arrowheads outline the elevated and bowed minor fissure; black arrows outline the right major fissure, as in diagram ii. Note the elevated right hilum, with the white arrows showing the interlobar artery, and the silhouetting of the normal contours of the SVC and upper hilum (white question mark). The significant density is caused by mucus retention within the atelectatic lobe (courtesy of Dr. Louise Samson). B. Left upper lobe (LUL). Large black arrowheads outline the major fissure, as in diagram iii, reaching down to the slightly elevated left hemidiaphragm (small black arrowheads). The nondisplaced right minor fissure demonstrates this is a left-sided process. On the posteroanterior view, we note the diffuse opacity of the LUL. Note that the contours of the aortic knob and anteroposterior window are silhouetted (black question mark) and that the LUL bronchus is retracted superiorly (white arrowheads). The black broken line outlines the manubrium, not to be mistaken for the aortic knob. The small black arrows outline the descending aorta, which remains visible in LUL atelectasis. The congruent white double arrows (pair “a” and pair “b”) show the narrowing of the rib cage from the volume loss. C. Right middle lobe. On the lateral view, the black arrowheads outline the upper and lower edges of the minor fissure, as in diagram iv. On the posteroanterior view, we note that the mid-cardiac of the right mediastinal contour (small black arrows) is silhouetted (black question marks). D. Right and left middle lobes. Both lower lobes collapse in a similar fashion. In this example of left lower lobe atelectasis with effusions (black arrows), note how the major fissure (large black arrowheads) outlines the atelectatic lobe (asterisk), as depicted on diagram iii. The contour of the left hemidiaphragm is lost (question mark). The inferior displacement of the hilum demonstrates volume loss: note the vertical migration of the left mainstem bronchus (small black arrows), and the contour of the left descending pulmonary artery (white arrowheads). (Diagrams from Reed (19); used with permission from RSNA.)
Middle lobe atelectasis (Fig. 12.28C) displaces the minor fissure inferiorly and the major fissure superiorly. Because of the minimal thickness of the collapsed middle lobe and the oblique orientation of the inferiorly displaced minor fissure, the detection of middle lobe atelectasis on frontal radiographs is difficult. The only finding on frontal radiographs may be a vague density over the right lower lung, with obscuration of the right heart margin. The lateral radiograph shows a typical triangular density, with its apex at the hilum. A lordotic frontal radiograph, which projects the minor fissure tangent to the frontal x-ray beam, will depict the atelectatic middle lobe as a triangular opacity, which is sharply marginated superiorly by the minor fissure, with its apex directed laterally. Middle lobe atelectasis is most often cicatricial and follows middle lobe infection with secondary fibrosis and bronchiectasis.
Right Lower Lobe Atelectasis (Fig. 12.28D)
The RLL collapses toward the lower mediastinum owing to the tethering effect of the inferior pulmonary ligament. This results in inferior displacement of the upper half of the major fissure and posterior displacement of the lower half, producing a triangular opacity in the right lower paravertebral space that obscures the medial right hemidiaphragm on frontal radiographs (Fig. 12.25). The lateral margin of this triangular opacity is formed by the displaced major fissure. The right hemidiaphragm may be elevated. The right interlobar pulmonary artery is obscured within the opaque collapsed lower lobe, a finding that helps distinguish the triangular opacity of RLL atelectasis from a medial pleural effusion, which tends to displace the interlobar artery laterally rather than obscure it. On lateral radiographs, a vague triangular opacity with its apex at the hilum and its base over the posterior portion of the right hemidiaphragm and posterior costophrenic sulcus may be seen. Mucous plugs, foreign bodies, and endobronchial tumors are the most common etiologic agents.
Left lower lobe atelectasis (Fig. 12.28D) is similar in appearance to atelectasis of the RLL. A triangular opacity in the left lower paramediastinal region, with loss of the medial retrocardiac diaphragmatic outline, is seen on frontal radiographs. In addition, the left hilum is displaced inferiorly and the interlobar artery is obscured. The diaphragm may be elevated and the heart shifted toward the left. Compensatory hyperinflation of the LUL may be seen. The LLL commonly is atelectatic in patients with large hearts and in postoperative patients, particularly those who have had coronary bypass surgery.
Combined middle and right lower lobe atelectases may be seen with obstruction of the bronchus intermedius by a mucous plug or tumor. The radiographic appearance on the frontal radiograph is characteristic, with a homogeneous triangular opacity sharply marginated superiorly by the depressed minor fissure and obscuration both of the right heart border and the right hemidiaphragm. Cardiac and mediastinal shift toward the right is common.
Collapse of an entire lung is most often seen with obstructing masses in the main bronchus. The lung is opacified, with an absence of air bronchograms. The trachea and heart are shifted toward the side of collapse, with herniation of the contralateral anteromedial lung across the midline to widen the retrosternal space on lateral radiographs and bulge the anterior junction line on frontal radiographs. The chest wall may show approximation of the ribs in chronic collapse. Compensatory diaphragmatic elevation in left lung atelectasis may be recognized by noting superior displacement of the gastric air bubble or splenic flexure of the colon.
Interstitial Disease
Interstitial opacities are produced by processes that thicken the interstitial compartments of the lung. Water, blood, tumor, cells, fibrous tissue, or any combination of these may render the interstitial space visible on radiographs. Interstitial opacities are usually divided into reticular, reticulonodular, nodular, and linear patterns on plain radiographs (Fig. 12.29) (Table 12.12) (20,21). The predominant pattern of opacity produced by an interstitial process depends upon the nature of the underlying disease and the portion of the interstitium affected.
Reticular pattern refers to a network of curvilinear opacities that usually involves the lungs diffusely. The subdivision of reticular opacities into fine, medium, and coarse opacities refers to the size of the lucent spaces created by these intersecting curvilinear opacities (Fig. 12.29). A fine reticular pattern, also known as a “ground-glass pattern,” is seen in processes that thicken or line the parenchymal interstitium of the lung to produce a fine network of lines with intervening lucent spaces on the order of 1 to 2 mm in diameter. Diseases that most commonly produce this appearance include interstitial pulmonary edema and usual interstitial pneumonitis. Medium reticulation, also termed “honeycombing,” refers to reticular interstitial opacities where the intervening spaces are 3 to 10 mm in diameter. This pattern is most commonly seen in pulmonary fibrosis involving the parenchymal and peripheral interstitial spaces. Coarse reticular opacities with spaces greater
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than 1 cm in diameter are seen most commonly in diseases that produce cystic spaces as a result of parenchymal destruction. The most common interstitial diseases associated with coarse reticulation are idiopathic pulmonary fibrosis, sarcoidosis, and Langerhans cell histiocytosis of the lung.
FIGURE 12.29. Patterns of Interstitial Opacity on Chest Radiographs.
TABLE 12.12 Patterns of Pulmonary Opacities
Predominantly linear  
   Chronic interstitial edema
   Lymphangitic carcinomatosis
   Interstitial fibrosis of any etiology
 
Predominantly reticular: acute  
   Edema Heart failure
  Fluid overload
Nephropathy
   Infection Viral
Mycoplasma
Pneumocystis carinii
Malaria
   Drug reactions  
   Predominantly reticular: chronic  
   Postinfectious scarring Tuberculosis (postprimary)
Histoplasmosis (chronic)
Coccidioidomycosis (chronic)
Pneumocystis carinii
   Chronic interstitial edema Mitral valve disease
   Collagen vascular disease Rheumatoid lung
Scleroderma
Dermatomyositis/polymyositis
Ankylosing spondylitis
Mixed connective tissue disease
Idiopathic pulmonary hemorrhage
   Granulomatous disease Sarcoidosis
Eosinophilic granuloma
   Neoplasm Lymphangitic carcinomatosis
Lymphoma and lymphocytic disorders
Lymphocytic interstitial pneumonitis
   Inhalational Asbestosis
Silicosis and coal worker’s pneumoconiosis
Hypersensitivity pneumonitis (chronic phase)
Chronic aspiration
   Drug reaction Nitrofurantoin
Chemotherapeutic agents
Amiodarone
Radiation pneumonitis (chronic)
   Idiopathic Idiopathic pulmonary fibrosis
Lymphangioleiomyomatosis
Tuberous sclerosis
Neurofibromatosis
Amyloidosis (alveolar septal form)
Predominantly nodular  
   Infection Mycobacteria
   Tuberculosis
   Nontuberculous mycobacteria
Fungi
   Histoplasmosis
   Blastomycosis
   Coccidioidomycosis
   Cryptococcosis
Virus
   Varicella (healed)
Bacterial
   Septic emboli
Parasites
Inhalation diseases Inorganic (pneumoconiosis)
   Silicosis* and coal worker’s pneumoconiosis*
   Berylliosis*
   Siderosis
   Heavy metal dust
   Talcosis
Organic
   Hypersensitivity pneumonitis
Toxic inhalants
   Isocyanates
Granulomatous disease Sarcoidosis*
Langerhans cell histiocytosis (early)
Vascular Arteriovenous malformation
Vasculitis
   Wegener
   Lymphomatoid granulomatosis
   Systemic lupus erythematosus
Neoplasm  
   Primary Synchronous bronchogenic carcinoma
   Metastatic Lymphoma*
   Hodgkin
   Non-Hodgkin
Bronchogenic carcinoma*
Thyroid carcinoma
Renal cell carcinoma*
Breast carcinoma*
Melanoma
Choriocarcinoma
Osteogenic carcinoma
Idiopathic Alveolar microlithiasis
Amyloidosis (nodular form)
*These entities can also present as reticulonodular disease.
Adapted from Reed (21); information used with permission.
Nodular opacities represent small rounded lesions within the pulmonary interstitium. In contrast to airspace nodules, interstitial nodules are homogeneous (they lack air bronchiolograms or air alveolograms) and well defined, as their margins are sharp and they are surrounded by normally aerated lung. In addition, unlike airspace nodules, which tend to be uniform in diameter (approximately 8 mm), these opacities can be divided into miliary opacities (<2 mm), micronodules (2 to 7 mm), nodules (7 to 30 mm), or masses (>30 mm). A micronodular or miliary pattern is seen predominantly in granulomatous processes (e.g., miliary tuberculosis or histoplasmosis)
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(see Fig. 16.9), hematogenous pulmonary metastases (most commonly thyroid and renal cell carcinoma), and pneumoconioses (silicosis) (see Fig. 17.10). Nodules and masses are most often seen in metastatic disease to the lung.
Reticulonodular opacities may be produced by the overlap of numerous reticular shadows or by the presence of both nodular and reticular opacities. Although this appearance appears to be frequent on radiographs, only a few diseases actually show reticulonodular involvement on pathology specimens. Silicosis, sarcoidosis, and lymphangitic carcinomatosis are diseases that may give rise to true reticulonodular opacities.
Linear patterns of interstitial opacities are seen in processes that thicken the axial (bronchovascular) or peripheral interstitium of the lung. Because the axial interstitium surrounds the bronchovascular structures, thickening of this compartment produces parallel linear opacities radiating from the hila when visualized in length or peribronchial “cuffs” when viewed end-on. A central distribution of linear interstitial disease is most often seen with interstitial pulmonary edema or “increased markings” emphysema. This pattern of interstitial disease may be impossible to distinguish from airways diseases, such as bronchiectasis and asthma, which primarily thicken the walls of airways. Thickening of the peripheral interstitium of the lung produces linear opacities that are either 2 to 6 cm long, <1-mm-thick lines that are obliquely oriented and course through the substance of the lung toward the hila (Kerley A lines) or shorter (1 to 2 cm) thin lines that are peripheral and course perpendicular to and contact the pleural surface (Kerley B lines). Kerley A lines correspond to thickening of connective tissue sheets within the lung, which contain lymphatic communications between the perivenous and bronchoarterial lymphatics, while Kerley B lines represent thickened peripheral subpleural interlobular septa (see Fig. 14.1) (22). A linear pattern of disease is seen in pulmonary edema, lymphangitic carcinomatosis, and acute viral or atypical bacterial pneumonia. The HRCT findings of interstitial lung disease are reviewed in Chapter 17.
Pulmonary nodule refers to a discrete rounded opacity within the lung measuring less than 3 cm in diameter. A round opacity greater than 3 cm in diameter is termed a pulmonary mass. A solitary pulmonary nodule presents a common diagnostic dilemma that will be discussed in a subsequent section.
Mucoid Impaction
Branching tubular opacities that are distinguished from normal vascular shadows invariably represent mucus-filled, dilated bronchi and are termed bronchoceles or mucoid impactions. Their appearance has been likened to that of a gloved finger or the shape of the letters V or Y, depending upon the length of airway and number of branches involved. When in a central perihilar location, these bronchoceles are a result of nonobstructive bronchiectasis, as in cystic fibrosis or allergic bronchopulmonary aspergillosis, or of postobstructive bronchiectasis distal to an endobronchial tumor or a congenitally atretic bronchus. In the latter condition, a typical location—immediately distal to the expected location of the apical segmental bronchus and a hyperlucent segment or lobe distal to the bronchocele owing to collateral air drift—should suggest the diagnosis. Peripheral bronchoceles are most often seen in cystic fibrosis and posttuberculous bronchiectasis.
Pulmonary Lucency
Abnormal lucency of the lung may be localized or diffuse (Table 12.13) (21). Focal radiolucent lesions of the lung include cavities, cysts, bullae, blebs, and pneumatoceles (Fig. 12.30). These lesions are usually recognized by identification of the wall that marginates the lucent lesion.
Cavities form when a pulmonary mass undergoes necrosis and communicates with an airway, leading to gas within
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its center. The wall of a cavity is usually irregular or lobulated and, by definition, is greater than 1 mm thick. Lung abscess and necrotic neoplasm are the most common cavitary pulmonary lesions. A bulla is a gas collection within the pulmonary parenchyma that is >1 cm in diameter and has a thin wall <1 mm thick. It represents a focal area of parenchymal destruction (emphysema) and may contain fibrous strands, residual blood vessels, or alveolar septa. An air cyst is any well-circumscribed intrapulmonary gas collection with a smooth thin wall >1 mm thick. While some of these lesions will have a true epithelial lining (bronchogenic cyst that communicates with a bronchus), most do not and likely represent postinflammatory or posttraumatic lesions (23). A bleb is a collection of gas <1 cm in size within the layers of the visceral pleura. It is usually found in the apical portion of the lung. These small gas collections are not seen on plain radiographs but may be visualized on chest CT, where they are indistinguishable from paraseptal emphysema. Rupture of an apical bleb can lead to spontaneous pneumothorax. Pneumatoceles are thin-walled, gas-containing structures that represent distended airspaces distal to a check-valve obstruction of a bronchus or bronchiole, most commonly secondary to staphylococcal pneumonia. A traumatic air cyst results from pulmonary laceration following blunt trauma. These lesions generally resolve within 4 to 6 months. Bronchiectatic cysts are usually multiple, rounded, thin-walled lucencies found in clusters in the lower lobes, and represent saccular dilatations of airways in varicose or cystic bronchiectasis.
TABLE 12.13 Causes of Pulmonary Lucency
Localized Cavity
Cyst
Bulla
Bleb
Pneumatocele
Diffuse Technical factors
   Unilateral    Grid cutoff
   Patient rotation
Extrapulmonary disorder
   Soft tissue abnormalities
      Absent pectoralis muscle
      Mastectomy
   Contralateral pleural effusion/thickening
   Pneumothorax
Pulmonary disease
   Diminished pulmonary blood flow
      Hypoplastic lung/pulmonary artery
      Obstruction of pulmonary artery
         Pulmonary embolism
         Mediastinal/hilar tumor
         Fibrosing mediastinitis
   Diminished pulmonary blood flow and hyperinflation
      Lobar atelectasis/resection
      Swyer-James syndrome
Endobronchial tumor/foreign body producing a check-valve effect
   Bilateral Technical factors
   Overpenetrated radiograph
Diminished pulmonary blood flow
   Congenital pulmonary outflow obstruction
   Mediastinal tumor
   Pulmonary arterial hypertension
   Chronic thromboembolic disease
   Fibrosing mediastinitis
Diminished pulmonary blood flow and hyperinflation
   Emphysema
   Asthma
Adapted from Reed (21); information used with permission.
Unilateral pulmonary hyperlucency must be distinguished from differences in lung density resulting from technical factors or overlying soft tissue abnormalities. Grid cutoff from a combination of lateral and near or far focus-grid decentering may lead to a graduated increase in density across the width of the chest film, simulating unilateral hyperlucency. Rotation of the patient will produce an increase in density over the lung rotated away from the film cassette. Congenital absence of the pectoralis muscle (Poland syndrome) or mastectomy can produce apparent hyperlucency.
True unilateral hyperlucent lung is a result of decreased blood flow to the lung. Diminished blood flow may result from a primary vascular abnormality, shunting of blood away from a lung that traps air, or a combination of the two. Hypoplasia of the right or left pulmonary artery produces a lung that is hyperlucent and diminished in size. A similar appearance may be produced by lobar resection or atelectasis, where the remaining lobe or lung hyperinflates to accommodate the hemithorax, thereby attenuating pulmonary vessels and producing hyperlucency. Pulmonary arterial obstruction may be secondary to extrinsic compression or invasion by a hilar mass or to pulmonary embolism. A check-valve effect from an endobronchial tumor or foreign body can produce air trapping, resulting in shunting of blood and unilateral hyperlucency. The Swyer-James syndrome or unilateral hyperlucent lung is a condition that follows adenoviral infection during infancy (see Fig. 18.16). An asymmetric obliterative bronchiolitis with severe air trapping on expiration and secondary unilateral pulmonary artery hypoplasia produces the hyperlucency in this condition. Finally, asymmetric involvement of lung by emphysema can produce a hyperlucent lung; this is most common with severe bullous disease.
Bilateral hyperlucent lungs may be simulated by an overpenetrated film or by a thin patient. As with unilateral hyperlucency, true bilateral hyperlucent lungs are the result of diminished pulmonary blood flow. This may be the result of congenital pulmonary stenosis, most commonly
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associated with the tetralogy of Fallot, or secondary to an acquired obstruction of the pulmonary circulation, as in pulmonary arterial hypertension or chronic thromboembolic disease. Pulmonary emphysema results in hyperinflation with air trapping on expiration, destruction of the pulmonary microvasculature, and attenuation of lobar and segmental vessels, thereby producing bilateral hyperlucency (24). Asthma produces transient air trapping and diffuse bilateral vascular attenuation, resulting in both hyperinflation and hyperlucency.
FIGURE 12.30. Focal Lucent Pulmonary Lesions.
Mediastinal Masses
Mediastinal masses are recognized on frontal radiographs by the presence of a soft tissue density that causes obliteration or displacement of the mediastinal contours or interfaces. The lung–mass interface typically is well defined laterally, where it is convex with the adjacent lung, and it creates obtuse angles with the lung at its superior and inferior margins. This latter characteristic is diagnostic of an extrapulmonary lesion, whether intramediastinal or pleural. Lateral displacement of the trachea or heart may be seen with large mediastinal masses, sometimes first recognized by displacement of an indwelling endotracheal tube, nasogastric tube, or intravascular catheter. The presence of calcification, fat, or, rarely, a fat–fluid level (as in a cystic teratoma) can limit the differential diagnosis of a mediastinal mass.
Virtually every patient with a mediastinal mass will have thoracic CT or MR performed, with US usually limited to evaluation of vascular masses and for real-time imaging guidance during transthoracic needle biopsy.
The vascular origin of a mediastinal mass is readily apparent on contrast-enhanced CT, MR, and, occasionally, transthoracic or transesophageal US. The recognition of fat within a mediastinal mass on CT or MR limits the differential diagnosis to a small number of entities, including diaphragmatic hernia, lipoma, teratoma, epicardial fat pad, and thymolipoma. A fat–fluid level is virtually diagnostic of a mature teratoma. Although calcification is occasionally detected radiographically within mediastinal masses, CT is considerably more sensitive and provides more specific characterization of the calcification. The presence of coarse calcification within an anterior mediastinal mass should suggest the diagnosis of a teratoma (especially if a tooth is seen) or thymoma (coarse calcification). Curvilinear rimlike calcification should suggest a cyst or aneurysm. Conversely, the presence of calcification within an untreated mediastinal mass virtually excludes the diagnosis of lymphoma.
Frontal and lateral chest radiographs usually localize a mediastinal mass to a structure within the anterior, middle, or posterior mediastinal compartments (see Chapter 13). For instance, if the contours of a
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lesion are outlined by air and seen above the clavicles, then the lesion must be in the posterior mediastinum. Conversely, if the contours of a lesion are lost at the thoracic inlet level, it must be anterior. Obviously, CT and MR provide more precise information regarding structures involved by the mass. This not only helps narrow the differential diagnosis but is key in guiding further diagnostic procedures (Fig. 12.31). For example, a posterior mediastinal mass intimately related to the esophagus may best be evaluated by esophagoscopy and transesophageal biopsy, while a subcarinal mass is best approached by bronchoscopy and transcarinal needle aspiration biopsy.
FIGURE 12.31. Anterior Mediastinal Mass Resulting From Seminoma. Frontal (A) and lateral (B) chest radiographs in a 35-year-old man with a history of cough and fatigue demonstrate a lobulated mass (arrows) in the right anterior mediastinum. A CT-guided biopsy showed seminoma.
Mediastinal Widening
Mediastinal widening is described as a smooth, uniform increase in the transverse diameter of the mediastinum on frontal chest radiographs. True mediastinal disease is often difficult to distinguish from technical factors, including AP technique, supine positioning, and rotation. Clues to the presence of disease include change in mediastinal width from prior frontal radiographs, mass effect on adjacent mediastinal structures (tracheal deviation or displacement of an indwelling nasogastric tube or central venous catheter), increased density of the mediastinum, and obscuration of the normal mediastinal contours, most specifically the aortic knob and paratracheal stripe. While normal measurements have been developed for mediastinal width, there is such great individual variability that absolute measurements are somewhat useless.
Pneumomediastinum and Pneumopericardium
The diagnosis of pneumomediastinum is usually made by findings on conventional radiographs. Small amounts of extraluminal air appear as linear or curvilinear lucencies lining anatomic structures within the mediastinal contours (see Fig. 13.20). Larger collections may be seen outlining the cardiac silhouette, mediastinal vessels, tracheobronchial tree, or esophagus. The most common finding is air outlining the left heart border, where a curvilinear lucency representing pneumomediastinum is paralleled by a thin curvilinear opacity representing the combined thickness of the visceral and parietal pleura of the lingula. Another sign of pneumomediastinum is the “continuous diaphragm” sign, in which air dissects between the pericardium above and central diaphragm below to allow visualization of the central portion of the diaphragm in contiguity with the right and left hemidiaphragms, each of which is outlined by air in the lower lobes, respectively. While this sign is fairly specific for pneumomediastinum, pneumopericardium may produce a similar finding. Small amounts of mediastinal air are often more easily appreciated on the lateral film, with air outlining the aortic root or main or central pulmonary arteries.
Pneumomediastinum should be distinguished from three entities that may mimic some of the radiographic findings and have significantly different etiologies and
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therapeutic implications: pneumopericardium, medial pneumothorax, and Mach bands. Air in the pericardial sac is limited by the normal pericardial reflections and extends superiorly to the proximal ascending aorta and main pulmonary artery. Additionally, pneumopericardium is often secondary to an infectious process with associated pericardial fluid and thickening, which will produce an air–fluid level on horizontal beam radiographs. Air within the pericardial sac will rise to a nondependent position on decubitus positioning, unlike mediastinal air, which is not mobile. The differentiation of pneumomediastinum from a medial pneumothorax is also aided by decubitus views, because pleural air will rise nondependently along the lateral pleural space. In contrast to pneumothorax, pneumomediastinum may be seen to outline intramediastinal structures (pulmonary artery, trachea) and is often bilateral. However, the distinction between pneumomediastinum and pneumothorax may be impossible, and the two conditions often coexist, particularly in the neonatal period. Paramediastinal lucent bands created by Mach effect are easily distinguished from pneumomediastinum. The lateral margin of lucent Mach bands consists of lung parenchyma, as opposed to the thin pleural line seen with mediastinal air. These bands represent an optical illusion (caused by a retinal reinforcement response [25]) that disappears when the interface between mediastinal soft tissues and lung is covered.
FIGURE 12.32. Hilar Lymph Node Enlargement. A. A posteroanterior radiograph in a 49-year-old woman with metastatic renal cell carcinoma demonstrates a lobulated enlargement and increased density of the right hilum (solid arrows) with concomitant paratracheal lymph node enlargement (open arrow). B. A CT scan through the hila shows the lobulated soft tissue mass (short arrows) within the right hilum surrounding the bronchus intermedius (curved arrow).
Hilar Disease
Signs of enlarged bronchopulmonary lymph nodes or hilar mass on frontal chest radiographs include hilar enlargement, increased hilar density, lobulation of the hilar contour, and distortion of central bronchi (26). An abnormal hilum is most easily appreciated by comparison with the contralateral hilum and by review of prior chest radiographs (Fig. 12.32). CT will often show a left hilar mass that is not evident on routine radiographs. On the right, the normally sharp right hilar angle, formed by the intersection of the lower lateral aspect of the right superior pulmonary vein with the upper lateral aspect of the right interlobar pulmonary artery, is often distorted or obscured by a right hilar mass. An increase in density of the hilar shadow is seen with a hilar mass that lies primarily anterior or posterior to the normal hilar vascular shadows. In such patients, the enlarged hilar nodes will produce an increase in density on frontal views and a lobulated appearance when viewed in profile on a lateral radiograph.
When an abnormally dense hilum is noted, the relationship between the vessels and the density must be assessed. A density through which the normal hilar vessels (interlobar artery, upper lobe arteries, left descending artery) can be seen constitutes a “hilum overlay” sign, which indicates a mass superimposed on the hilum. Conversely, vascular structures that converge only as far as the lateral margin of
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the increased hilar density indicate enlargement of intrahilar vascular structures (the “hilum convergence” sign). The lateral radiograph or a CT will clarify the abnormality. In patients with small lung volumes or exaggerated kyphosis, a mass in the lower right hilum on frontal radiographs may be simulated by the end-on projection of a horizontally oriented right interlobar artery. Comparison with prior radiographs will usually resolve the matter, with CT reserved for equivocal cases.
Tumors involving the lobar bronchi or bronchus intermedius may produce luminal narrowing of the bronchi with enlargement of the hilar shadow. Occasionally, an endobronchial mass produces an abrupt cutoff of the bronchial air column, which is associated with lobar atelectasis or obstructive pneumonitis. In a small percentage of normal individuals, the right or left anterior segment, upper lobe bronchi are visualized as end-on ring shadows at the superolateral margin of the hila. The presence of a soft tissue density greater than 5 mm in thickness lateral to an anterior segmental bronchus is suspicious for mass or adenopathy in this region; the posterior division of the superior vein that lies immediately lateral to the anterior segmental bronchus should not exceed this thickness. Abnormal thickening of the walls of the main or lobar bronchi is a prominent feature of hilar abnormality on lateral chest films.
Enlargement of the right or left hilar shadow from pulmonary artery dilatation is produced by increased flow or increased pressure in the pulmonary arterial circulation. Pulmonary artery dilatation is usually assessed by measurement of the right interlobar pulmonary artery on PA radiographs. The margins of this vessel are readily visible, with the lateral margin outlined by air in the lower lobe and the medial margin outlined by air in the bronchus intermedius. The upper limit of normal for the transverse diameter of the proximal right interlobar artery, as measured on a PA radiograph at a level immediately lateral to the proximal portion of the bronchus intermedius, is 17 mm in men and 15 mm in women (see Fig. 14.14).
The lateral radiograph can confirm the impression of hilar abnormality seen on frontal radiographs and may demonstrate a mass when the frontal radiograph is normal. Hilar masses that lie predominantly anterior or posterior to the hilar vessels are best visualized on the lateral view. Because the lateral radiograph is a composite of both hilar shadows, the cumulative density of bilateral hilar masses may produce a significant increase in the normal density of the composite shadow, which is more easily appreciated on a lateral than on a frontal view.
The radiographic findings of a hilar mass on lateral radiographs are an abnormal size of or a lobulated contour to the normal vascular shadows, the presence of soft tissue in a region that is normally radiolucent, an increase in density of the composite hilar shadow, and abnormalities of the central bronchi. An increase in the size and density of the composite hilar shadow is best appreciated by comparison with prior radiographs, as is usually seen with bilateral hilar lymph node enlargement from sarcoidosis. Hilar lymph node enlargement produces lobulation of the normally smooth outlines of the right and left main pulmonary arteries. There are additional findings unique to the lateral radiograph that suggest the presence of a hilar mass and may allow lateralization of the hilar abnormality. Because the RUL bronchus is visualized on the lateral radiograph in only a minority of individuals, visualization of the RUL bronchial lumen, particularly if it was invisible on a prior lateral radiograph, is strong evidence of mass or adenopathy in the upper right hilum. A lobulated posterior wall of the bronchus intermedius, or a thickness >3 mm, indicates an abnormality of the bronchus (bronchitis or bronchogenic carcinoma), edema of the axial interstitium (pulmonary edema or, lymphangitic carcinomatosis), or enlargement of lymph nodes in the posterior aspect of the lower right hilum.
The normal anatomy of the inferior hilar window was reviewed earlier in this chapter. The identification of a soft tissue mass >1 cm in diameter within this radiolucent region is an accurate indicator of unilateral or bilateral hilar mass. Occasionally, the silhouetting of the anterior wall of the LLL bronchus, recognized as a concave anterior curvilinear structure contiguous with the anterior aspect of the LUL bronchus, allows lateralization of a mass to the left lower hilum (Fig. 12.33). The added opacity of a mass within the normally radiolucent inferior hilar window produces an oval opacity to the composite hilar shadow on lateral radiographs.
On a lateral radiograph, enlargement of pulmonary arteries is assessed by measuring the left descending pulmonary artery as it arches over the left mainstem/LUL bronchus at a 2:00 position (Fig. 12.19B).
Helical CT is the most sensitive method of detecting and localizing enlarged hilar (bronchopulmonary) lymph nodes and masses. Although contrast enhancement is almost never necessary to assess mediastinal nodes, it simplifies identification of enlarged vascular structures or nonenhancing hilar nodes (defined as nodes that exceed 10 mm in short-axis diameter) or masses. Hilar masses are seen on axial or coronal spin-echo MR as round masses of low or intermediate signal intensity, in distinction to the signal void of flowing blood within the hilar vessels or of air in the bronchi. Coronal MR may be superior to CT in the detection of enlarged hilar lymph nodes because it displays the hilar vessels, which are oriented in the cephalocaudad direction, in length rather than in cross section. Displacement or distortion of the hilar vessels provides indirect evidence of hilar disease. Tumor invasion of a branch of the pulmonary artery or vein within the hilum produces a filling defect within the vessel on contrast-enhanced CT or intraluminal signal on MR. The density characteristics of hilar masses on CT can help provide important information
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for differential diagnosis; for example, a round, cystic hilar mass with imperceptible walls in an asymptomatic young person is typical of a bronchogenic cyst.
FIGURE 12.33. Hilar Mass Within the Inferior Hilar Window. A. A cone-down view of a lateral radiograph in a patient subsequently found to have a plasmacytoma of the left hilum shows a mass (large arrows) within the inferior hilar window obliterating the anterior wall of the left lower lobe bronchus (small arrows). B. A CT scan through the lower hila confirms the presence of a left hilar mass (asterisk).
Enlarged hilar lymph nodes can be detected by CT without the use of intravenous contrast. A detailed knowledge of the normal hilar vascular and bronchial anatomy, as seen on CT, is necessary for the identification of subtle hilar contour abnormalities. In those portions of the hilum where lung directly contacts a wall of a bronchus, thickening or lobulation of the normal thin linear shadow of the bronchial wall indicates hilar abnormality. This is particularly well seen where the RLL and LLL contact the posterior walls of the bronchus intermedius and the LUL bronchus, respectively (Fig. 12.34). Lymph node enlargement in these regions is obscured on frontal radiographs by the overlying cardiac and hilar vascular shadows. CT is more sensitive than plain radiographs or MR for the detection of soft tissue masses within lobar or proximal segmental bronchi. In most patients with an endobronchial mass, a large extraluminal component produces a radiographically visible hilar soft tissue mass and obstructive atelectasis.
FIGURE 12.34. Enlarged Hilar Nodes on CT. Enhanced CT in a patient with biopsy-proven sarcoidosis demonstrates bilateral hilar lymph node enlargement (arrows).
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Enlarged hilar lymph nodes may have different appearances on CT. Enlargement of discrete lymph nodes, most commonly seen in sarcoidosis, appears as multiple distinct round masses (Fig. 12.34). When tumor or an inflammatory process extends through the nodal capsule to involve contiguous nodes, a single large mass of confluent lymph nodes is produced that may be difficult to distinguish from a primary hilar bronchogenic carcinoma. This latter appearance is most often seen in hilar nodal metastases from small cell carcinoma of the lung or lymphoma (see Fig. 15.10). As in enlargement of mediastinal lymph nodes, the CT density of enlarged hilar nodes can provide clues to the diagnosis (see Table 13.5).
An abnormally small hilum indicates a diminution in the size of the right or left pulmonary artery.
Pleural Effusion
The radiographic appearance of pleural effusions depends upon the amount of fluid present, the patient’s position during the radiographic examination, and the presence or absence of adhesions between the visceral and parietal pleura. Small amounts of pleural fluid initially collect between the lower lobe and diaphragm in a subpulmonic location. As more fluid accumulates, it spills into the posterior and lateral costophrenic sulci. A moderate amount of pleural fluid (>175 mL) in the erect patient will have a characteristic appearance on the frontal radiograph, with a homogeneous lower zone opacity seen in the lateral costophrenic sulcus with a concave interface toward the lung. This concave margin, known as a pleural meniscus, appears higher laterally than medially on frontal radiographs because the lateral aspect of the effusion, which surrounds the costal surface of the lung, is tangent to the frontal x-ray beam. Similarly, the meniscus of pleural fluid as seen on lateral radiographs peaks anteriorly and posteriorly (Fig. 12.35) (27).
FIGURE 12.35. Pleural Effusion on Chest Radiographs. Posteroanterior (A) and lateral (B) chest radiographs demonstrate the typical meniscoid appearance (arrows) in a patient with a left pleural effusion resulting from mediastinal Hodgkin lymphoma.
In patients with suspected pleural effusion, a lateral decubitus film with the affected side down is the most sensitive technique to detect small amounts of fluid. With this technique, pleural fluid collections as small as 5 mL may be seen layering between the lung and lateral chest wall. While a moderate-size, free-flowing collection should be obvious on upright radiographs, a large pleural effusion can cause passive atelectasis of the entire lung, producing an opaque hemithorax. It may be difficult to distinguish the latter condition from collapse of an entire lung. While a massive effusion should produce contralateral mediastinal shift, a collapsed lung without pleural effusion will show shift toward the opaque side. In some patients, CT or US may be necessary to distinguish pleural fluid from collapsed lung.
CT is quite sensitive in the detection of free pleural fluid. On axial scans, pleural fluid layers posteriorly with a characteristic meniscoid appearance and has a CT attenuation value of 0 to 20 H. Small effusions may be difficult to
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differentiate from pleural thickening, fibrosis, or dependent atelectasis, and decubitus scans are useful in making this distinction. The pleural and peritoneal spaces are oriented in the axial plane at the level of the diaphragm. This may cause some difficulty in localizing the fluid to one or both spaces. Fluid in either the pleural or peritoneal space can displace the liver and spleen medially, away from the chest wall. A key to distinguishing ascites from pleural fluid on axial CT scans is to observe the relationship of the fluid to the diaphragmatic crus. Pleural fluid in the posterior costophrenic sulcus will lie posteromedial to the diaphragm and displace the crus laterally. In contrast, peritoneal fluid lies within the confines of the diaphragm and therefore will displace the crus medially. Another useful distinguishing feature is the quality of the interface of the fluid with the liver or spleen. Intraperitoneal fluid will show a distinct, sharp interface with the liver and spleen as it directly contacts these organs, whereas pleural effusions will have a hazy, indistinct interface with these viscera because of the interposed hemidiaphragms. Because the peritoneal space does not extend posterior to the bare area of the liver, right-sided fluid extending posteromedially must be pleural. A large effusion will allow the inferior edge of the adjacent atelectatic lower lobe to float in the fluid, creating a curvilinear opacity that can be misinterpreted as the diaphragm separating pleural fluid from ascites. This “pseudodiaphragm” is recognized as a broad band that does not extend far laterally or anteriorly and is contiguous superiorly with an atelectatic lung containing air bronchograms (Fig. 12.36). US is particularly useful in detecting free flowing pleural effusions, which are usually seen as anechoic collections at the base of the pleural space surrounding atelectatic lung (see Chapter 39).
Pleural fluid may become loculated between the pleural layers to produce an appearance indistinguishable from that of a pleural mass. Fluid loculated within the costal pleural layers appears as a vertically oriented elliptical opacity with a broad area of contact with the chest wall, producing a sharp, convex interface with the lung when viewed in tangent. CT is commonly utilized to detect and localize loculated pleural fluid collections. The characteristic finding is a sharply marginated lenticular mass of fluid attenuation conforming to the concavity of the chest wall that forms obtuse angles at its edges and compresses and displaces the subjacent lung. Multiple fluid locules can mimic pleural metastases or malignant mesothelioma radiographically; CT or US can confirm the fluid characteristics of these pleural “masses.”
Pleural fluid may extend into the interlobar fissures, producing characteristic findings. Free fluid within the minor fissure is usually seen as smooth, symmetric thickening on a frontal radiograph. Fluid within the major fissure is normally not visible on frontal radiographs, as the fissures are viewed en face. An exception is fluid extending into the lateral aspect of an incomplete major fissure, which produces a curvilinear density extending from the inferolateral to the superomedial aspect of the lung. Fluid loculated between the leaves of visceral pleura within an interlobar fissure results in an elliptic opacity oriented along the length of the fissure. These loculated collections of pleural fluid are termed “pseudotumors” and are most often seen within the minor fissure on frontal radiographs in patients with congestive heart failure. The tendency for these opacities to disappear rapidly with diuresis has led to the term “vanishing lung tumor.” Although a characteristic appearance on plain radiographs is usually sufficient for diagnosis, the CT demonstration of a localized fluid collection in the expected location of the major or minor fissure is confirmatory.
An uncommon appearance of pleural effusion is seen when fluid accumulates between the lower lobe and diaphragm and is termed a subpulmonic effusion. While small amounts of pleural fluid normally accumulate in this location, it is uncommon for larger effusions to remain subpulmonic without spilling into the posterior and lateral costophrenic sulci. A subpulmonic effusion may be difficult to appreciate on upright chest radiographs, because the fluid collection mimics an elevated hemidiaphragm. Clues to its presence on frontal radiographs include: apparent and new elevation of the diaphragm, lateral peaking of the hemidiaphragm that is accentuated on expiration, a minor fissure that is close to the diaphragm (right-sided effusions), and an increased separation of the gastric air bubble from the base of the lung (left-sided effusions). Despite the atypical subpulmonic accumulation of fluid with the patient upright, the effusion will layer dependently on lateral decubitus radiographs (Fig. 12.37).
The radiographic detection of pleural effusion in the supine patient can be difficult because fluid accumulates in a dependent location posteriorly. The most common finding is a hazy opacification of the affected hemithorax with obscuration of the hemidiaphragm and blunting of the lateral costophrenic angle. Fluid extending over the apex of the lung may produce a soft tissue cap with a concave interface inferiorly, while medial fluid may cause an apparent mediastinal widening.
Pneumothorax
The classic radiographic finding of pneumothorax on upright chest films is visualization of the visceral pleura as a curvilinear line that parallels the chest wall, separating the partially collapsed lung centrally from pleural air peripherally (Fig. 12.38). An expiratory radiograph aids in the detection of a small pneumothorax by increasing the volume of intrapleural air relative to lung, thereby displacing the visceral pleural reflection away from the chest wall and by exaggerating the differences in density of pneumothorax (black) to lung (gray) at the end of expiration. In a small
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percentage of patients, a pneumothorax will be visible only on a lateral or decubitus film or a frontal radiograph obtained in full inspiration. This suggests that when there is a strong clinical suspicion of pneumothorax and the frontal expiratory radiograph is normal, a lateral or inspiratory film may be beneficial for proper diagnosis.
FIGURE 12.36. Subpulmonic Pleural Effusion on CT. A. A CT scan through the lower chest shows fluid surrounding an enhancing broad curvilinear structure (asterisks). The fluid creates an ill-defined interface with the liver (arrows). B. A scan 1 cm more cephalad shows that the curvilinear density represents the tip of an atelectatic right lower lobe containing air bronchograms (arrows). C. More inferiorly, the crus of the diaphragm (dotted structure) is displaced laterally by posteromedial pleural fluid.
The detection of a pneumothorax is difficult when chest films are obtained in the supine position. Approximately 30% of pneumothoraces imaged on supine radiographs go undetected. Because many portable radiographs are obtained with the patient supine, the recognition of a pneumothorax on a supine film is particularly important in the critically ill patient, who is at high risk from iatrogenic trauma or barotrauma. In a supine patient, the most nondependent portion of the pleural space is anterior or anteromedial. Small pneumothoraces will initially collect in these regions and will fail to produce a visible pleural line. The affected hemithorax may appear hyperlucent. Anteromedial air may sharpen the borders of mediastinal soft tissue structures, resulting in improved visualization of the
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cardiac margin and aortic knob. The lateral costophrenic sulcus may appear abnormally deep and hyperlucent, a finding known as the “deep sulcus” sign. Visualization of the anterior costophrenic sulcus owing to air anteriorly and inferiorly produces the “double diaphragm” sign, as the dome and anterior portions of the diaphragm are outlined by lung and pleural air, respectively. When an anterior pneumothorax is suspected on a supine radiograph, an upright film, lateral decubitus film with the affected side up, or CT scan should be obtained (Fig. 12.39).
FIGURE 12.37. Bilateral Subpulmonic Pleural Effusions. A. An upright posteroanterior radiograph in a 41-year-old woman with ascites demonstrates apparent elevation of both hemidiaphragms. Right (B) and left (C) decubitus films demonstrate dependent layering of the subpulmonic pleural fluid (arrows).
Subpulmonic pneumothoraces are rare. Radiographically, a localized area of hyperlucency is seen inferiorly, with the visceral pleural line paralleling the hemidiaphragm. Loculated pneumothoraces develop as the result of adhesions between visceral and parietal pleura and may be found anywhere in the pleural space. CT is often necessary for diagnosis.
Several entities produce a curvilinear line or interface or hyperlucency on chest radiographs and must be distinguished from a pneumothorax. Skin folds resulting from the compression of redundant skin by the radiographic cassette can produce a curvilinear interface that simulates the visceral pleural line. A skin fold produces an edge or interface with atmospheric air, in distinction to the visceral pleural line seen in a pneumothorax. The interface produced by a skin fold rarely continues over the lung apex and is often seen to extend beyond the chest wall. Pulmonary vascular opacities may be followed peripheral to the skin fold interface. Bullae may simulate pneumothorax by producing localized or unilateral hyperlucency. They are marginated by thin curvilinear walls that are concave rather than convex to the chest wall. The distinction of pneumothorax from bullous disease may be difficult but is usually evident by the clinical presentation. However, since this distinction has important therapeutic implications, certain patients may require CT.
CT is more sensitive than conventional radiographs in the detection of pneumothorax because of its cross-sectional nature and superior contrast resolution. The CT demonstration of linear parenchymal bands of tissue traversing large avascular areas helps distinguish bullae from loculated pneumothoraces. CT may be used to
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detect and drain loculated pneumothoraces in critically ill patients.
FIGURE 12.38. The Visceral Pleural Line in Pneumothorax. A cone-down view of an upright posteroanterior radiograph in a patient with a spontaneous pneumothorax demonstrates a curvilinear visceral pleural line (solid arrows) separating the lung medially from the chest wall laterally. Note the presence of thin-walled cysts (open arrows) from Coccidioides infection, which are most likely responsible for the pneumothorax.
Localized Pleural Thickening
Localized pleural thickening is seen as a flat, smooth, slightly raised soft tissue opacity extending over one or two intercostal spaces that displaces the lung from the innermost cortical margin of the ribs when viewed in tangent. Localized pleural thickening viewed en face is usually undetectable radiographically because the lesion does not significantly attenuate the x-ray beam and does not present a raised edge to be recognized as a distinct opacity. An exception is the presence of pleural calcification, which can usually be recognized as discrete thin linear or curvilinear calcific opacities paralleling the inner surface of the ribs when viewed end-on or as geographic areas of increased density with round or lobulated borders when viewed en face. Focal areas of pleural fibrosis are best appreciated on conventional and high-resolution CT scans, where they are easily distinguished from deposits of subpleural fat by their density.
There are two additional radiographic findings that mimic the appearance of focal pleural thickening. The apical cap is a curvilinear subpleural opacity <5 mm thick with a sharp or slightly irregular inferior margin which represents nonspecific fibrosis of the apical lung and adjacent visceral pleura. While it is usually bilateral and symmetric, slight asymmetry in thickness is common. Any growth of the opacity, significant asymmetry, inferior convexity of the opacity, rib destruction, or symptoms should prompt a CT or MR examination followed by biopsy to exclude an apical neoplasm (Pancoast or superior sulcus tumor). The companion shadows of the inferior aspects of the first and second ribs are smooth apical linear opacities that parallel the lower cortical margins of the first two ribs and represent the pleural layers and subpleural fat viewed in tangent. These are most prominent in obese individuals and should not be mistaken for pleural fibrosis.
Diffuse Pleural Thickening
Fibrothorax appears as a thin, smooth band of soft tissue with a sharp internal margin seen immediately beneath and parallel to the inner margin of the ribs and intercostal spaces. It is usually unilateral and extends over large areas of the dependent (posterior and inferior) portions of the pleural space. Anterior or posterior costal pleural thickening creates a veillike opacity without sharp margins when viewed en face on frontal radiographs. Blunting of the lateral costophrenic sulcus may be seen on frontal radiographs, while sparing of the posterior costophrenic sulcus and an absence of layering fluid on decubitus positioning help distinguish pleural fibrosis from a small effusion. Fibrothorax tends to spare the interlobar fissures and mediastinal pleura. CT and HRCT are more sensitive than conventional radiographs in the detection of pleural thickening. The diminished volume of the affected hemithorax seen with extensive fibrothorax is more easily appreciated on axial CT images than on frontal radiographs (see Fig. 19.9). CT and HRCT provide an unimpeded view of the underlying lung in patients with diffuse pleural thickening, allowing detection of associated interstitial pulmonary fibrosis. This is important in evaluating patients with suspected asbestosis and in assessing the extent of pulmonary disease in patients being considered for pleurectomy.
Pleural and Extrapleural Lesions
The shape and margins of a peripheral opacity as seen on conventional radiographs help define the opacity as parenchymal, pleural, or extrapleural. Pleural masses form
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obtuse angles with the adjacent normal pleura, in distinction to peripheral lung lesions, which usually contact the normal pleura at acute angles. Pleural and extrapleural masses are usually vertically oriented elliptic opacities. Pleural lesions tend to have smooth, well-defined margins as they compress normal lung. These smooth margins are best appreciated on radiographic projections with the x-ray beam tangent to the interface between the mass and the lung. Another feature of pleural lesions is the clarity of the margin of the lesion on frontal and lateral radiographs; a mass sharply outlined by lung on one view but poorly marginated on the orthogonal view should suggest a pleural or extrapleural process. In contrast, intraparenchymal lesions are surrounded by air and will have similar margins on both views. Pleural lesions, unlike parenchymal lesions, do not change position with respiratory motion. Lung disease is often confined to a lobe, while pleural disease may extend across fissures. Pedunculated pleural lesions such as fibromas are rare but can present with radiographic features of both pleural and parenchymal lesions.
FIGURE 12.39. Deep Sulcus Sign in Supine Patient With Pneumothorax. A. A supine chest film obtained following placement of a left internal jugular central venous catheter shows a deep sulcus sign at the left base (arrows), representative of a pneumothorax. B. Film obtained after placement of a left thoracostomy tube shows that the deep sulcus sign has resolved.
Despite the aforementioned features, the distinction of pleural from peripheral parenchymal lesions may be difficult. This distinction has important diagnostic implications; while parenchymal processes are best evaluated by examination of expectorated sputum or by bronchoscopy, pleural lesions will require thoracentesis or pleural biopsy. CT is often used to help distinguish between pleural and parenchymal disease (see Chapter 19). A peripheral lesion that is completely surrounded by lung on CT is intraparenchymal, with the exception being the rare pleural lesion arising within an interlobar fissure. Peripheral lung masses generally have irregular margins and may contain air bronchograms. Those parenchymal lesions that contact the pleura will form acute angles with the chest wall, as on plain films. The CT appearance of pleural and extrapleural or chest wall lesions are similar. Both pleural and extrapleural lesions are sharply defined and form obtuse angles with the chest wall (see Fig. 19.10); rib destruction or subcutaneous mass are the only findings that localize an extrapulmonary lesion to the chest wall. When a peripheral parenchymal lesion invades the pleura, determining the origin of the mass may be impossible. CT can further characterize peripheral lesions by their density; a smooth fatty mass is almost certainly a pleural lipoma (see Fig. 19.10), whereas a homogeneous pleural or extrapleural soft tissue mass is most likely a fibroma or neurogenic tumor (see Fig. 19.11). The signal intensity on T1W and T2W spin-echo MR images may be useful in the characterization of focal pleural masses. On T1WIs and T2WIs, loculated fluid collections will show homogeneous low and high signal respectively. Lipomas will show homogeneous high signal intensity on T1WI and intermediate signal intensity on T2WI, while fibromas are typically of intermediate and high signal intensity, respectively, as a result of the high cellularity of these tumors.
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Chest Wall Lesions
Chest wall lesions become evident radiographically when (1) they extend into the thorax and become outlined by displaced lung, (2) there is bone displacement or destruction by the mass, or (3) they protrude externally from the skin surface to be outlined by air in the atmosphere. CT, MR, and US are all useful in assessing the characteristics of chest wall lesions. While CT and MR are most useful in determining the extent of intrathoracic involvement by chest wall lesions, US is the least expensive and simplest method of characterizing the nature of palpable chest wall lesions, particularly if they are thought to be vascular or cystic in nature. The radiographic findings of chest wall lesions related to specific bony or soft tissue components of the chest wall are detailed in the section on chest wall disease in Chapter 19.
Diaphragm
Radiographic findings of diaphragmatic disorders include elevation and depression of the diaphragm and abnormalities of diaphragmatic contour. The diagnostic considerations of diaphragmatic disease are reviewed in Chapter 19.
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