RADIOLOGY OF THE CHEST: INTRODUCTION

The chest radiograph is the most frequently performed radiographic study in the United States. It should almost always be the first radiologic study ordered for evaluation of diseases of the thorax. The natural contrast of the aerated lungs provides a window into the body to evaluate the patient for diseases involving the heart, lungs, pleurae, tracheobronchial tree, esophagus, thoracic lymph nodes, thoracic skeleton, chest wall, and upper abdomen. In both acute and chronic illnesses, the chest radiograph allows one to detect a disease and monitor its response to therapy. For many disease processes (e.g., pneumonia and congestive heart failure) the diagnosis can be established and the disease followed to resolution with no further imaging studies. There are limitations to the chest radiograph, and diseases may not be sufficiently advanced to be detected or may not result in detectable abnormalities. Other imaging methods are needed to complement the conventional chest radiograph. These imaging methods include computed tomography (CT), magnetic resonance (MR) imaging, ultrasound (US), and radionuclide studies. These techniques, their clinical uses, and case studies are included in this chapter.

TECHNIQUES

Conventional Radiography

THE POSTEROANTERIOR AND LATERAL CHEST RADIOGRAPH

The simplest conventional study of the chest is a posteroanterior and lateral chest radiograph taken in a radiographic unit specially designed for these studies. The x-rays travel through the patient and expose a receptor from which the image is recorded. Most commonly, the receptor is an intensifying screen and radiographic film, but several types of digital radiographic receptors are in use as well. Two of these types receptors are computed radiography and large field-of-view image intensifiers. The digital images may be printed on film by laser printers or viewed on monitors. The two views of a chest radiograph are taken in projections at 90 degrees to each other with the patient's breath held at the end of a maximum inspiration. The first view is obtained as the patient faces the film cassette with the x-ray beam source positioned 6 feet behind the patient. Because the x-ray beam travels in a posterior-to-anterior direction, this view is called a posteroanterior (PA) chest radiograph. Another view is then obtained with the patient turned 90 degrees, with the left side against the film cassette and arms overhead. The x-ray beam travels from right to left through the patient and this is called a left lateral view. Anatomic features of the chest that are readily identifiable on plain radiographs are shown in Figs. 4–1 and 4–2.

OTHER RADIOGRAPHIC PROJECTIONS

In some clinical situations, patients may not be able to stand or sit upright for the conventional PA and lateral radiographs, and a film must be taken with the patient's back turned to the film cassette and the x-ray beam traversing the patient in an anterior-to-posterior direction. These radiographs are called anteroposterior (AP) radiographs. They may be taken in the x-ray department but are more commonly obtained as portable studies at the patient's bedside.

Films may also be obtained with the patient lying on one side in a decubitus position with the x-ray beam traversing the patient either PA or AP along a horizontal plane. These films are designated lateral decubitus films. A left lateral decubitus radiograph indicates that the left side of the patient is dependent against the table. A right lateral decubitus radiograph indicates that the right side of the patient is dependent against the table.

THE PORTABLE CHEST RADIOGRAPH

If the clinical situation prevents the patient from coming to the radiology department, a chest radiograph may be obtained at the patient's bedside, and these are almost always AP radiographs. The AP portable radiograph does not provide as much information as PA and lateral chest radiographs for a number of reasons. Because it is a single view, lesions are not as easily or accurately localized along the AP axis of the thorax. The patients for whom these films are obtained are usually quite ill and cannot be positioned as well as patients traveling to the x-ray department. They frequently cannot cooperate by holding their breath at total lung capacity. A mobile x-ray generator is typically not as powerful as a fixed x-ray generator, and, therefore, longer exposure times are necessary to obtain sufficient film exposure. The quality of portable chest radiographs, therefore, is often inferior to that of PA and lateral radiographs, as a result of both respiratory and cardiac motion. X-ray grids are used to reduce scatter radiation and improve image quality. Grids are used for most conventional chest films done in radiology departments where fixed equipment is present. Grids are not usually used for portable radiographs, and the result is a high proportion of scattered x-rays that degrade the image. Paradoxically, the portable radiograph may be more expensive than a conventional PA and lateral chest radiograph, owing to extra labor and equipment costs in obtaining a bedside radiograph.

Computed Tomography of the Chest

Computed tomography is described in detail in Chapter 1. For CT examinations of the chest, intravenous contrast material is frequently administered for opacification of arteries and veins within the mediastinum and hila to facilitate the recognition of abnormal masses or lymph nodes. Anatomic features of the chest that are readily identifiable on CT scans are shown in Figs. 4–3 and 4–4.

Ultrasonography of the Chest

Ultrasound is described in detail in Chapter 1. Ultrasound of the chest is typically performed to evaluate fluid collections within the pleural space. Ultrasound may be used to guide thoracentesis, especially when the fluid collection is small or loculated.

Magnetic Resonance Imaging of the Chest

The principles and applications of MR are described in Chapter 1. Anatomic features of the chest that are readily identifiable on MR images are shown in Figs. 4–5 and 4–6.

Nuclear Medicine

Nuclear medicine techniques used in evaluating diseases of the thorax include ventilation-perfusion (V/Q) scanning, scanning for sites of inflammation with gallium-67 or indium-111–labeled white cells, and scanning with tumor-seeking radiopharmaceuticals for tumor staging. The V/Q scan is often the imaging study of choice for a patient with suspected pulmonary thromboembolism. The V/Q scan is noninvasive, and when results are negative, fewer than 10% of patients have pulmonary thromboembolism. The ventilation study is typically performed with the patient inhaling 10 to 30 mCi of xenon-133 while images are obtained with a scintillation camera (Fig. 4–7A ). Wash-in images are obtained for two consecutive 120-second periods, an equilibrium image is obtained, and then wash-out images are obtained over 30- to 60-second periods in posterior, and left and right posterior oblique projections. This portion of the study takes about 15 minutes. The perfusion scan is obtained by intravenously injecting 2 to 4 mCi of technetium-99m-labeled macroaggregated albumin containing 200,000 to 700,000 particles. The particles range in size from 10 to 100 m, and they lodge in capillaries and capillary arterioles, accurately reflecting pulmonary blood flow (Fig. 4–7B ). The scintillation camera is set so that it obtains anterior, posterior, both posterior oblique, and both anterior oblique projections for 750,000 counts per image. The perfusion study takes about 30 minutes to perform.

Other radionuclide scans used for the evaluation of suspected pulmonary disease include gallium-67 citrate scans, in which gallium accumulates in leukocytes and in some tumors. After 5 mCi of gallium-67 citrate is injected intravenously, scans are obtained at 24 to 72 hours, allowing time for blood background and colon activity to clear. Abnormal increase in activity in the lungs may be focal or diffuse and may correspond to disease activity in inflammatory diseases, including sarcoidosis, radiation pneumonitis, and idiopathic pulmonary fibrosis, as well as in pneumonia and lung abscess. Gallium activity within the lung is usually reported as a gallium index that is the product of an intensity of 0 to 4 (4=area of greatest activity, usually the liver) multiplied by the percentage of total lung area involved. The maximum gallium index is 400 (intensity of 4x100% involvement). Gallium has affinity for some tumors, including lymphoma, and can be used to detect occult sites of tumor either at presentation or during recurrence.

Another test that can be used to detect occult sites of infection is the indium-111–labeled white blood cell (WBC), or leukocyte, scan. The serous layer of an 80-mL blood sample taken from the patient is centrifuged to produce a white cell button. One to 2 mCi of indium-111 is added to the resuspended white cells. The labeled white blood cells are reinjected into a peripheral vein, and scanning is performed 24 to 48 hours after injection. The activity accumulates in sites of infection, and this test could be used to distinguish between pneumonia or lung abscess and noninfectious lung diseases. In practice, this test is infrequently obtained for pulmonary disease, because CT almost always localizes abnormalities precisely, and fiber-optic bronchoscopy is very effective for diagnosis of pulmonary abnormalities.

Tomography is also available for radionuclide imaging as two other techniques. Single photon emission computed tomography (SPECT) is used for photon emitters (99m Tc, 111 In,¹²³I). The primary advantage of SPECT is the ability to depict anatomy in three dimensions. SPECT may be used to improve the spatial resolution of radionuclide imaging, including perfusion scans, and gallium- and indium-111–labeled WBC scans. A positron emission tomography (PET) scanner resembles a CT scanner and uses positron emitters (fluorine-18, carbon-11). Today, the most widely used positron emitter is F-18-deoxyglucose (FDG), which is used as a metabolic tracer. The raised metabolic rate can be used to distinguish neoplasm and inflammation from normal tissue. Although PET provides tomographic images, the spatial resolution (0.7–1.0 cm) is somewhat inferior to that of CT.

TECHNIQUE SELECTION

The number of diseases and clinical situations for which a chest radiograph may be indicated is so large that an exhaustive listing of individual indications is prohibitive. As a general rule, however, conventional radiographs should be obtained for any patient with symptoms suggesting disease of the heart, lungs, mediastinum, or chest wall. In addition, a chest radiograph is indicated for patients with systemic diseases that have a high likelihood of secondary involvement of those structures. Examples of the former are pneumonia and congestive heart failure and of the latter are a primary extrathoracic neoplasm and connective tissue disease.

In an acutely ill patient, the portable chest radiograph is an invaluable tool for monitoring the patient's cardiopulmonary status. These radiographs are also used for monitoring of life-support hardware, such as central venous access catheters, nasogastric tubes, and endotracheal tubes.

Fluoroscopy provides real-time imaging of the chest. Fluoroscopy may be used to evaluate the motion of the diaphragm in a patient with suspected diaphragmatic paralysis. A paralyzed hemidiaphragm has sluggish motion as the patient breathes, and as the patient takes in a quick breath of air, the air moves paradoxically upward as the normal hemidiaphragm moves downward ("sniff test"). Fluoroscopy and fluoroscopically positioned spot films are also useful for identification of calcification within a pulmonary nodule, within coronary arteries, or within cardiac valves. Fluoroscopic guidance is commonly used for percutaneous transthoracic needle biopsy of lung masses.

Because the three dimensions of the thorax are captured on a single two-dimensional chest radiograph, superimposition of structures within the thorax may result in confusing shadows. Because CT provides images without this overlap, it is frequently used to clarify confusing shadows identified on conventional radiographs (Table 4–1). These examinations are also used to detect disease that is occult because of small size or a hidden position. Because of its wider range of density discrimination, CT can demonstrate mediastinal and chest wall abnormalities earlier than is possible with conventional chest radiography. Abnormalities of hilar structures can be identified on CT scans because of the decreased overlap of the complex structures of the hilum. CT scans of the chest are routinely ordered for oncology patients, both for evaluation of the extent of disease at presentation and for monitoring response to therapy or progression of disease. CT is useful for evaluation of the lung parenchyma, because thin sections (1–2 mm thick) reveal great anatomic detail. Thin-section CT [or high-resolution CT (HRCT)] may enable detection of occult pulmonary parenchymal disease and may be used for following the course of known pulmonary disease. Because intravenous contrast material may be administered, vascular structures may be evaluated and the technique may be useful in patients with aortic dissection, aortic aneurysm, and superior vena caval obstruction. Because the cost of CT is approximately 10 to 20 times that of a PA and lateral chest radiograph, CT is not practical for monitoring the course of diseases on a daily basis.

Ultrasonography is useful for imaging the soft tissues of the chest wall, heart, and pericardium, as well as fluid collections within the pleural space. Large, mobile pleural effusions are usually aspirated without sonographic guidance, since these collect predictably within dependent areas of the thorax. On the other hand, loculated pleural fluid collections may be difficult to aspirate without guidance, and the most appropriate entrance site may be marked with sonography for easier access. Ultrasonography has been used for guidance for biopsy of peripheral lung lesions as well.

MR imaging of the thorax is most commonly used for cardiovascular imaging, but there are indications for MR imaging in mediastinal and pulmonary parenchymal imaging as well (Table 4–2). MR is helpful when bronchogenic carcinoma is suspected of invading vascular structures, including the cardiac chambers, pulmonary arteries and veins, and the superior vena cava. In a patient with suspected Pancoast's (superior sulcus) tumor, MR imaging is preferred to CT because of the ability to obtain images in coronal and sagittal planes. The apex of the lung can be difficult to evaluate on axial images alone because of partial-volume effects.

The diseases and situations for which nuclear medicine techniques are helpful are determined for the most part by the radioactive tracer, and these have been outlined in the technique section (Table 4–3).

EXERCISE 4-1: THE OPAQUE HEMITHORAX

Clinical Histories:

Case 4-1. A 40-year-old man with fever and dyspnea (Fig. 4–8)

Case 4-2. A 62-year-old man with dyspnea that increased over 2 days (Fig. 4–9)

Questions:

Radiologic Findings:

4-1. In this case, a frontal chest radiograph (Fig. 4–8) shows that the left hemithorax is opaque. Signs of mass effect are present and suggest a space-occupying lesion in the left hemithorax. There is shift of the mediastinum toward thecontralateral hemithorax, as evidenced by shift of the trachea and right heart border to the right. If a nasogastric tube were in place, esophageal shift could be inferred from the shift of the nasogastric tube. Space-occupying lesions also cause inferior displacement of the hemidiaphragm. Although the diaphragm itself is not visible, when the process is on the left, one can infer that the diaphragm is depressed by the inferior displacement of the gastric air bubble. Mass effect may also widen the distance between ribs. In this patient, the space-occupying lesion was a large left pleural effusion resulting from tuberculous empyema. A chest CT scan (Fig. 4–10) in this patient shows the large pleural effusion and complete collapse of the underlying left lung against the medial aspect of the left hemithorax. (A is the correct answer to Question 4-1.)

4-2. In this case, a frontal chest radiograph (Fig. 4–9) shows that the left hemithorax is also opaque. In contrast to the patient in Fig. 4–8, the patient in Fig. 4–9 has signs of volume loss within the left hemithorax. There is mediastinal shift toward the ipsilateral hemithorax, as evidenced by shift of the trachea and the right heart border into the left hemithorax. If more air were visible within the stomach, one would expect that it would be higher in the left upper quadrant of the abdomen than is normally seen, because of elevation of the left hemidiaphragm. The mediastinal window of the chest CT examination (Fig. 4–11A ) shows the mediastinal shift to the left and total consolidation of the left lung (arrows). There is a small left pleural effusion (arrowheads). The lung window of the chest CT examination (Fig. 4–11B ) shows that the right lung is aerated. In this patient, the left lung collapse is due to a bronchogenic carcinoma in the left main bronchus. This case exhibits the signs of volume loss, as opposed to mass effect. (B is the correct answer to Question 4-2.)

Discussion:

This exercise reviews the principal signs that allow one to distinguish mass effect from volume loss. The mass effect caused by a tumor or by a large pleural effusion expands the hemithorax and displaces the trachea, mediastinum, and diaphragm away from the mass. There may be a subtle increase in the distance between ribs. Volume loss, on the other hand, decreases the size of the hemithorax, and the trachea, mediastinum, and diaphragm move toward the involved hemithorax. The distance between the ribs on the abnormal side will be slightly decreased. In both chest radiographs (Figs. 4–8 and 4–9) the left lung is collapsed. In Fig. 4–8, the opacification of the left hemithorax occurs as a result of massive left pleural effusion, and the left lung is collapsed as a result of both compression by the fluid present within the left pleural space and a loss of the negative intrapleural pressure that keeps the lung in close juxtaposition to the chest wall. In Fig. 4–9, the collapse is due to obstruction of the left main bronchus, resulting in atelectasis (airlessness) of the left lung.

EXERCISE 4-2: LOBAR ATELECTASIS

Clinical Histories:

Case 4-3. A 61-year-old woman with dyspnea (Fig. 4–12A,B )

Case 4-4. A 45-year-old woman with chronic cough (Fig. 4–13A,B )

Case 4-5. A 62-year-old man with a cough productive of blood-tinged sputum (Fig. 4–14A,B )

Case 4-6. A 49-year-old woman with cough (Fig. 4–15A,B )

Questions:

Radiologic Findings:

4-3. In Fig. 4–12, there is opacity in the right upper lung that is sharply marginated on its inferior border. Volume loss is evidenced by the slight displacement of the trachea into the right hemithorax, the position of the right heart border further to the right of the thoracic spine than normal, and the slight elevation of the right hemidiaphragm, which is normally 1 to 1.5 cm higher than the left hemithorax. The pulmonary vessels of the right hilum are obscured by opacity in the right upper thorax. The configuration of the inferior margin of the opacity is that of a reverse S or an S on its side. The S sign of Golden describes the appearance of the minor fissure in right upper lobe collapse, which is due to bronchogenic carcinoma. In this case, bulky right hilar lymph node enlargement has caused extrinsic compression of the right upper lobe bronchus and has resulted in right upper lobe collapse. The right hilar mass tethers the medial aspect of the minor fissure to its normal midthoracic position, whereas the lateral aspect of the minor fissure moves freely and collapses superiorly. In patients in whom the minor fissure is incomplete, collateral air drift across the canals of Lambert and the pores of Kohn may allow a lobe to remain aerated despite complete obstruction of its bronchus. In Fig. 4–12A , hyperexpansion of the superior segment of the right lower lobe produces the ovoid lucency on the medial aspect of the collapsed right upper lobe. On the lateral radiograph, a V-shaped opacity is seen at the lung apex. A mass-like opacity is superimposed on the suprahilar area, corresponding to a combination of tumor and atelectatic lung. (B is the correct answer to Question 4-3.) In patients with right upper lobe collapse without a hilar mass, the fissure is able to rotate in a more straight line and does not result in the reverse S sign. The major fissure is oriented in a coronal plane and is not normally visualized on the frontal chest radiograph. Therefore, the major fissure would not account for the opacity seen on the frontal chest radiograph, either with or without a hilar mass.

4-4. In Fig. 4–13A,B , the right heart border is obscured by adjacent opacity on the PA radiograph. The heart is in the midthorax in approximately its normal position. The heart border has not been displaced to the left. On the lateral radiograph, a narrow triangular opacity is superimposed on the heart. The apex of the triangle points toward the hilum, and the base of the triangle is against the anterior chest wall. This is a collapsed right middle lobe. The right hemidiaphragm is slightly elevated, but there are no other signs of volume loss. Right middle lobe collapse may have minimal impact on the overall volume in the right hemithorax because it is the smallest of the pulmonary lobes, and the upper and lower lobes can expand to compensate for its volume loss. Right middle lobe collapse, unlike other lobar collapse, is often due to benign causes and results from extrinsic pressure because of enlarged lymph nodes, which totally surround the bronchus. This enlargement is most frequently due to granulomatous disease of an infectious or noninfectious nature. (D is the correct answer to Question 4-4.)

4-5. When the left lower lobe collapses, the result is a triangular opacity, which can be quite subtle, behind the heart. Secondary signs of volume loss, however, should prompt one to look closely for the collapse. These signs include shift of the trachea and heart to the left (note that the right heart border is now superimposed on the thoracic spine), inferior displacement of the left hilum, and elevation of the left hemidiaphragm. On the lateral radiograph, the right hemidiaphragm is visible along its entire contour. However, the left hemidiaphragm is obscured posteriorly because it is "silhouetted" by the collapsed left lower lobe. Because it is tethered medially by the inferior pulmonary ligament, the left lower lobe collapses posteriorly and medially (Fig. 4–16). The major fissure is displaced posteriorly, as well as rotated into a more sagittal orientation than the normal coronal orientation. All of the statements in Question 4-5 are correct except shift of the major fissure toward the anterior chest wall on the lateral view. (E is the correct answer to Question 4-5.) You may have noted the large lung volumes in this patient, which are due to centrilobular emphysema. In this patient, who has a long history of cigarette smoking, a squamous cell carcinoma in the left lower lobe bronchus was responsible for the collapsed left lower lobe.

4-6. The primary sign of volume loss in Fig. 4–15B is anterior displacement of the left major fissure on the lateral radiograph. The collapsed left upper lobe is opaque as a result of both airlessness and postobstructive pneumonitis. When there is little pneumonitis within the obstructed lobe, the left upper lobe can collapse completely behind the anterior chest wall, so that only a narrow band of opacity is visible behind the sternum. In this situation, the diagnosis may be suggested by the secondary signs of volume loss. Note the shift of the trachea to the left and the slight elevation of the left hemidiaphragm. The left lower lobe is hyperexpanded. The hyperexpanded superior segment of the left lower lobe produces a crescent of air around the transverse section of the aortic arch on the PA radiograph. A thin opaque line is visible at the apex of the left hemidiaphragm on the PA radiograph. Presence of this line, called ajuxtaphrenic peak, should prompt one to look for upper lobe collapse. The hilum may be displaced anteriorly in left upper lobe collapse, but it is never displaced inferiorly. Option E, inferior displacement of the left hilum, is therefore false. (E is the correct answer to Question 4-6.) Since the lingular bronchus arises from the left upper lobe bronchus, the lingular segment of the left upper lobe is collapsed as well in this patient. The lingula is adjacent to the left heart border and is responsible for the obscuration of the left heart border in left upper lobe collapse.

Discussion:

The term atelectasis refers to volume loss, or airlessness, within the lung. The term collapse is often used to describe complete atelectasis of an entire lobe or an entire lung. Atelectasis can occur as a result of several pathophysiologic processes. Obstruction of a bronchus by bronchogenic carcinoma should always be considered in an adult with lobar atelectasis. The tumor may be within the bronchus (endobronchial), as occurs with squamous cell carcinoma or small cell undifferentiated carcinoma. The tumor may be outside the bronchus, and enlarged lymph nodes may cause extrinsic compression of the bronchus. In a child, aspiration of a foreign body is a more likely cause of obstruction of a bronchus. Complete obstruction of a lobar bronchus may not always result in lobar collapse because pathways of collateral ventilation are present within the lung. The pores of Kohn and the canals of Lambert allow collateral air drift between adjacent areas of lung but do not extend across pleural surfaces. The visceral pleural surface that covers the lung creates the interlobar fissures (minor fissure, major fissure) that separate lobes of the lungs. These fissures are not always complete, however, and may not extend entirely across the lung. When the right upper lobe bronchus is occluded, for example, the right upper lobe may remain partially aerated as a result of collateral air drift from the right middle lobe, around an incomplete minor fissure. Obstruction of smaller airways can occur as a result of mucous plugs, which are often present in intubated patients and in patients with chronic small airway disease.

Passive atelectasis occurs as a result of a space-occupying process within the pleural space. This is also calledrelaxation atelectasis, since the lung is no longer exposed to the negative intrapleural pressure that normally keeps the lung apposed to the chest wall. Any space-occupying pleural process, including a large pneumothorax (air in the pleural space), pleural effusion, hemothorax (blood in the pleural space), or pleural tumor can cause atelectasis within the underlying lung. Compressive atelectasis is the term used to describe atelectasis caused by a space-occupying process within the lung itself. Cicatrization atelectasis describes the volume loss that occurs as a result of pulmonary scarring. Adhesive atelectasis occurs when there is a loss of the pulmonary surfactant that maintains the surface tension that keeps alveoli open. Adhesive atelectasis occurs with pulmonary embolism and with respiratory distress syndrome of the newborn. Atelectasis of small areas of lung is often referred to as subsegmental atelectasis and may be recognized as linear bands of opacity, often at the lung bases.

It is helpful to remember the normal positions of the hemidiaphragms, trachea, mediastinum, and hila so that displacement of these structures can be readily noted. In most patients, the left hilum appears slightly higher than the right, since the left hilar opacity is predominantly due to the left pulmonary artery arching over the left main bronchus. The right hemidiaphragm is usually 1.0 to 1.5 cm higher than the left hemidiaphragm. The trachea should be in the midline, and the spinous processes of the upper thoracic vertebrae should be superimposed on the center of the tracheal air column. The right heart border normally lies just to the right of the thoracic spine. Subtle signs of volume loss may be more readily appreciated by comparison of the patient's radiograph with baseline radiographs taken previously.

EXERCISE 4-3: AIRSPACE DISEASES

Clinical Histories:

Case 4-7. A 32-year-old man with fever, cough, and hemoptysis (Fig. 4–17A,B )

Case 4-8. A 57-year-old man with fever and a cough productive of purulent sputum (Fig. 4–18A,B )

Questions:

Radiologic Findings:

Both of these patients have opacity in the left upper lobe.

4-7. In this case (Fig. 4–17), the opacity is in the upper lung and obscures the margin of the aortic arch. The opacity extends down to the hilum but does not obscure the left heart border. (C is the correct answer to Question 4-7; see discussion.)

4-8. In this case (Fig. 4–18), the opacity is lower in the hemithorax and obscures the lateral margin of the heart. On the lateral view of each patient, the posterior margin is sharply demarcated by the major fissure, indicating the lobar nature of the process. Radiolucent structures that exhibit a branching pattern are noted to arborize through both opacities. (B is the correct answer to Question 4-8; see discussion.)

Discussion:

The patient in Fig. 4–17 has primary tuberculosis (Mycobacterium tuberculosis), manifested as pneumonia in the anterior and apicoposterior segments of the left upper lobe. The patient in Fig. 4–18 has pneumococcal pneumonia (Streptococcus pneumoniae) in the superior and inferior lingula segments of the left upper lobe. The opacity seen on both radiographs is best described as airspace disease. The alveoli, or airspaces, that are normally filled with air have become filled with exudate. The exudate-filled alveoli surround the bronchi, so that the air-filled bronchi are visible as radiolucent branching structures within the more radiopaque background (Fig. 4–19). Airspace disease is often either lobar, multilobar, or diffuse in distribution. The process may initially appear as multiple ill-defined nodules that rapidly coalesce. These nodules are the shadows of fluid-filled acini. They are 6 to 10 mm in diameter and always have ill-defined margins. The margins of these coalescing opacities are difficult to outline. Although there can be associated volume loss as the surfactant within the alveoli is lost, the signs of volume loss are often subtle and do not account for the opacity seen within the lung. Once airspace disease is identified, an attempt should be made to determine its cause. Airspace disease that appears suddenly or exhibits change over hours to days is due either to pulmonary hemorrhage or to contusion, pneumonia, or pulmonary edema (blood, pus, or water). The patient's clinical history, physical examination, and laboratory data help to determine the most likely diagnosis. In patients likely to have infectious disorders, the responsible organism is usually not identified at first treatment, and the patient is just given antibiotics. In patients who do not respond to this initial treatment, an attempt should be made to identify the organism.

In these two patients with fever and productive cough, pneumonia is likely. On the other hand, a patient with rib or sternal fractures as a result of blunt chest trauma is more likely to have pulmonary contusion. Pulmonary edema, which may occur as a result of either cardiogenic or noncardiogenic disease, is discussed later in this chapter.

A reticular pattern is one in which the opacities are linear in nature and the lines range from quite thin to several millimeters thick. The opacities are oriented in multiple directions and appear to overlap so as to create the appearance of a net. This pattern is not present.

EXERCISE 4-4: DIFFUSE LUNG INFILTRATES

Clinical History:

Case 4-9. A 69-year-old man with progressive dyspnea, orthopnea, and pedal edema and a history of hypertension (Fig. 4–20)

Question:

Radiologic Findings:

4-9. Frontal chest radiograph (Fig. 4–20) shows mild enlargement of the heart and indistinct vascularity, particularly at the lower lungs. Interlobular septal lines (arrowheads) are visible adjacent to both lower costophrenic angles.

Discussion:

Pulmonary edema can be divided into two major categories: cardiogenic edema and noncardiogenic edema.Cardiogenic edema occurs as a result of elevation of pulmonary capillary pressure, which is usually due to pulmonary venous hypertension. Noncardiogenic edema occurs as a result of disorders that increase pulmonary capillary permeability. With both types of edema, there is a net movement of fluid out of the microvasculature and into the pulmonary interstitium and alveoli. The most common cause of pulmonary edema is left ventricular failure, which may be due to atherosclerotic coronary artery disease, mitral or aortic valvular disease, myocarditis, or cardiomyopathy. Cardiogenic edema is preceded by pulmonary venous hypertension, which is associated with redistribution of pulmonary blood flow from dependent regions of the lung to nondependent regions. In the erect patient, the radiographic sign of this redistribution is an increase in size of vessels in the upper lungs and a decrease in the caliber of pulmonary vessels in the lung bases. Radiographically, it is often difficult to distinguish pulmonary arteries from pulmonary veins, but for purposes of determination of flow redistribution, the distinction is ignored and multiple vessels are measured at equal distances from the hilum or chest wall.

When seen end-on, normal bronchoarterial bundles may appear as adjacent circles of equal diameter, with the artery opaque and the bronchus lucent. The pulmonary arteries and bronchi are located together in the same interstitial space and arborize adjacent to each other. The pulmonary veins return blood to the heart in a separate interstitial space and have a slightly different arborization pattern. As the pulmonary venous pressure increases, fluid leaks from the pulmonary capillaries into the adjacent interstitium. This interstitial pulmonary edema may be identified by peribronchial cuffing, indistinctness of the perivascular margins, perihilar haziness, and thickening of the interlobular septa and interlobar fissures. As the pulmonary capillary pressure increases further, fluid spills into the alveoli, producing a symmetrical appearance of airspace filling that is predominantly perihilar (central) and basilar in distribution. Cardiogenic edema is greatest in dependent regions of the lungs. In supine patients, the dependent regions are the posterior segments of the upper lobes, and the superior and posterior basilar segments of the lower lobes. The central pattern of pulmonary edema has been called "bat wing" edema. As the pulmonary edema worsens, the pulmonary and pleural lymphatics clear fluid from the lungs, and pleural effusions will develop. In congestive heart failure, the pleural effusions are generally small to moderate in size, and there is typically more fluid within the right pleural space than the left. Isolated left pleural effusion is unlikely to be due to congestive heart failure. In cardiogenic edema, the heart size will be increased. The cardiothoracic ratio is a guide to determining cardiac enlargement. The transverse dimension of the heart is divided by the transverse diameter of the thorax at the same level. When the cardiothoracic ratio is greater than 0.5, cardiomegaly is often (but not always) present. When possible, both the PA and lateral projections should be used to determine cardiac volume. Cardiomegaly may be more readily recognized when comparison is made with prior radiographs. Comparison requires a similar depth of inspiration and similar positioning of the patient (AP versus PA, supine versus erect).

Noncardiogenic edema, or "capillary leak" edema, may be due to a number of conditions, including adult respiratory distress syndrome, fat embolism, amniotic fluid embolism, drug overdose, near drowning, and acute airway obstruction. The cause of pulmonary edema in patients with intracranial injury or tumor (neurogenic pulmonary edema) is uncertain. Similarly, the etiology of high-altitude pulmonary edema is incompletely understood. The common radiographic findings in noncardiogenic edema are symmetric, diffuse areas of airspace filling that is often patchier in appearance and more peripheral in distribution. The heart size is usually normal; pleural effusions and septal lines are typically absent.

Renal failure and volume overload may result in pulmonary edema, which may be chronic. When the amount of edema is small to moderate, patients are often reasonably well compensated and are able to carry out many activities of daily living.

EXERCISE 4-5: AIRWAY DISEASE

Clinical History:

Case 4-10. A 22-year-old man who has had chronic cough and copious mucous production since childhood (Fig. 4–21A,B )

Question:

Radiologic Findings:

4-10. In this case, the most prominent radiographic finding in Fig. 4–21A is coarse thickening of the bronchovascular bundles as they radiate from the hila. Thickened bronchial walls may be identified as tram-track lines in the left lower lobe behind the heart and just medial and caudal to the interlobar pulmonary artery on the right. Tram-track lines refer to the appearance of the nearly parallel walls of bronchi oriented longitudinally. Careful inspection shows that these are present throughout both lungs and are located near the hila. Bronchial walls also project as ring-shaped opacities near the hila. (Note that one projects into the middle of the left interlobar pulmonary artery.) Both of these structures represent the thick walls of dilated bronchi (bronchiectasis). The hila themselves are slightly enlarged as a result of a combination of enlarged hilar lymph nodes and mild pulmonary arterial hypertension. The lung volume is significantly increased. The diaphragms are flatter than normal, especially on the lateral radiograph. The anterior clear space (retrosternal area) is larger and more radiolucent than normal. The right paratracheal stripe, on the other hand, is normal, and there is no evidence of right paratracheal lymphadenopathy. (D is the correct answer to Question 4-10.)

Discussion:

The cause of this patient's bronchiectasis is cystic fibrosis. The mucus in patients with cystic fibrosis is thickened, and these patients do not have normal tracheobronchial clearance. This abnormal clearance may cause mucoid impaction, and atelectasis and pneumonia are frequent complications. Bronchiectasis can also occur as a result of pneumonia in patients without cystic fibrosis. In these patients, the bronchiectasis is more likely to be confined to a single lobe, often a lower lobe. Bronchiectasis is divided into three groups: cylindrical, fusiform (or varicose), and saccular (or cystic). These three groups not only describe the appearance of the abnormal bronchi, but also give an indication as to its severity. Cylindrical bronchiectasis, the mildest form, is reversible, and appears as thick-walled bronchi that fail to taper normally. The more severe forms, fusiform and saccular, are irreversible. Fusiform bronchiectasis has a beaded appearance, whereas the bronchi in saccular bronchiectasis end with clubbed, cystic areas. If the severe forms are localized, surgical resection may be curative. Medical therapy with bronchodilator and, when necessary, antibiotics is used when surgery is not indicated.

Bronchography was formerly the standard method of diagnosing bronchiectasis (Fig. 4–22A,B ). Currently, CT is the method of choice for determining the presence and extent of bronchiectasis. It has the advantages of being less invasive and more readily tolerated by the patient. When the bronchus is perpendicular to the CT plane of section, bronchiectasis is identified as ring shadows adjacent to an opaque circle. The ring represents the thickened, dilated bronchial walls. The opaque circles represent the pulmonary artery adjacent to the dilated bronchus. Images from the patient show a combination of varicose and cystic bronchiectasis (Fig. 4–23A, B ). When the bronchus lies within the plane of section of the CT scan, the dilated bronchial walls project as roughly parallel lines near a vessel (Fig. 4–23C ).

EXERCISE 4-6: SOLITARY PULMONARY NODULE

Clinical History:

Case 4-11. A 53-year-old man scheduled for coronary artery bypass grafting; Close-up view of left upper lobe from a preoperative chest radiograph is shown (Fig. 4–24).

Question:

Radiologic Findings:

4-11. Close-up view in Fig. 4–24 of the left upper lobe shows a nodule that is smoothly marginated and has a region of central opacity, indicating a calcified central nidus.

Discussion:

Bronchogenic carcinoma, particularly adenocarcinoma, frequently presents as a solitary pulmonary nodule in the periphery of the lung. A new solitary pulmonary nodule or nodule of indeterminate age, therefore, should be considered a possible malignancy. The most common cause of a solitary pulmonary nodule is a granuloma, typically the result of prior granulomatous infection, such as tuberculosis or histoplasmosis. These can frequently be identified as granulomata because of characteristic patterns of calcification.

In attempting to determine whether or not a nodule is benign, the characteristics to consider are the age of the patient, any history of previous malignancy, and the nodule's growth rate, density, shape, and edge characteristics. The most important of these are the growth rate and density. If a nodule has had no growth over a 2-year period and has calcification of the types associated with benign causes, then the nodule is almost certainly benign. Because of the importance of time in assessing growth, comparison with old films is the most important test and the least expensive method of determining whether a nodule is benign. A 2-year interval is approximately four doubling times for an average lung carcinoma; therefore, an increase in diameter of one-third to one-half of the nodule would be expected. The absence of growth over a 2-year period is evidence that the nodule is stable is size and must, therefore, be benign. If radiographs demonstrate growth over this 2-year interval, then the nodule should be assumed to be malignant.

If the nodule is diffusely and completely calcified (Fig. 4–25), if it is calcified centrally (Fig. 4–26), or if it has a laminated pattern (Fig. 4–27), then the nodule may be assumed to be benign. Calcification may not be apparent on the initial radiograph because the most commonly used technique for chest radiography obscures subtle calcification. Demonstration of calcification may require fluoroscopy or repeated chest radiography with low kVp (kiloVoltage* peak) technique to enhance its depiction. When it is not clear from these studies whether calcification is present, CT should be used to identify it. CT has an extended range of tissue discrimination in comparison to plain films. The presence of calcification within a pulmonary nodule can be determined by evaluating the attenuation values within a region of interest (ROI) centered over the nodule (Fig. 4–28A–C ). Air within the lung measures –800 Hu, noncalcified nodules measure 30 to 100 HU, and calcified nodules measure greater than 200 HU. Nodules with somewhat dense calcification can be easily identified, but subtle amounts of calcification may require a special phantom for accurate determination. Nodules with attenuation values between 0 and 200 are not necessarily malignant; they just do not have enough calcification to be categorized unequivocally as benign.

If a nodule is not calcified or if it has shown growth over a 2-year period, it should be considered as a possible malignancy and further assessment should be dictated by the clinical circumstances. Most patients will need evaluation for possible surgical resection and tissue biopsy to determine the cause.

Note that the margins of the lesion, whether smooth or spiculated, are of no value in determining the benignity or malignant potential of a lesion. Only uniform or central calcification, absence of growth over a 2-year period, or CT attenuation values greater than 200 HU throughout the nodule are reliable noninvasive indicators of benignity. (D is the correct answer to Question 4-11.)

EXERCISE 4-7: PULMONARY NEOPLASM

Clinical History:

Case 4-12. A 64-year-old man with cough and weight loss and a 50-pack-per-year history of tobacco use (Fig. 4–29A,B )

Question:

Radiologic Findings:

4-12. In this case, the chest radiographs show a round opacity projecting just laterally and cephalad to the left hilum. Because the medial margin of the opacity can be seen, a mediastinal mass is excluded. The left pulmonary artery can be seen through the opacity and is normal in size. On the lateral view the opacity maintains a round shape and projects over the anterior portion of the chest. The opacity is smaller than the volume of the left upper lobe, and no air bronchograms are present; this excludes consolidation of the lung as an answer. The posterior margin of the opacity is not a long straight or gently curving line, as is the major fissure, and therefore left upper lobe atelectasis is not the correct answer. The one best description of the radiographic findings is mass in the left upper lobe. (A is the correct answer to Question 4-12.) In a patient with cough, weight loss, and a history of tobacco use, bronchogenic carcinoma should be the primary consideration. A CT examination in this patient (Fig. 4–30) shows the mass in the anterior segment of the left upper lobe, which is contiguous with the superior left hilum. A CT-guided percutaneous biopsy of this mass was positive for squamous cell carcinoma.

Discussion:

More than 150,000 new cases of lung cancer, or bronchogenic carcinoma, are diagnosed in the United States each year. Bronchogenic carcinoma is the more appropriate term, because most of them arise from the epithelium of the airways and not the lung per se. Because early recognition and surgical resection offer the patient the best chance for cure, it is important to be familiar with the variety of radiographic appearances of lung cancer. Four major cell types account for almost 90% of all lung cancers. The major cell types are squamous cell, adenocarcinoma, large cell, and small cell. For therapeutic purposes, lung cancer is divided into small-cell and non-small-cell carcinoma. This distinction is necessary because small-cell bronchogenic carcinoma is almost always widespread at the time of diagnosis and is best treated by chemotherapy and radiation therapy. Non-small-cell bronchogenic carcinoma, on the other hand, is best treated by surgical resection when the tumor is confined to one lung and regional lymph nodes. The typical radiographic appearance of small-cell carcinoma is bulky hilar or mediastinal lymph nodes or both; and the primary tumor sometimes is visible as a nodule within the lung.

Non-small-cell bronchogenic carcinoma includes adenocarcinoma, squamous cell carcinoma, and large-cell carcinoma. Adenocarcinoma, the most common cell type, typically appears as a solitary pulmonary nodule in the periphery of the lung. Bronchioalveolar cell carcinoma is a subtype of adenocarcinoma that may present as either lobar airspace disease or as diffuse ill-defined pulmonary nodules (Fig. 4–31). Bronchioalveolar cell carcinoma may rarely present as a solitary pulmonary nodule. The second most common cell type, squamous cell carcinoma, is associated with cigarette smoking and most often is found as an endobronchial tumor resulting in lobar collapse (Fig. 4–9). The endobronchial tumor is visible bronchoscopically, and sputum cytology is frequently diagnostic in this tumor. Squamous cell carcinoma can also appear radiographically as a solitary cavitary mass (Fig. 4–32) or noncavitary mass. Large-cell carcinoma is the least frequent cell type. Its appearance is that of a bulky lesion within the lung.

When non-small-cell lung cancer is diagnosed, the patient undergoes a series of clinical and radiologic studies to determine the stage of the tumor. In the TNM staging system (Table 4–4), the categories of disease are stage IA, IB, IIA, IIB, IIIA, IIIB, or IV (Table 4–5). Stages I, II, and IIIA are surgically resectable. Patients with either stage IIIB or stage IV disease are not surgical candidates, but are treated with chemotherapy, radiation therapy, or both. In addition to helping define which treatment the patient should receive, the stage of the tumor helps provide prognosis. Patients with stage I disease have a 60% 5-year survival rate. Patients with stage IV disease have a 10% 5-year survival rate.

EXERCISE 4-8: MULTIPLE PULMONARY NODULES

Clinical History:

Case 4-13. A 70-year-old woman with uterine carcinoma treated with surgical resection 3 years previously. Chest radiograph obtained as part of a routine follow-up examination is shown (Fig. 4–33).

Question:

Radiologic Findings:

4-13. In this case, the chest radiograph shows multiple, smoothly marginated, solid nodules in both lungs. These are water-density nodules that are distributed diffusely and have varying sizes. The heart is normal in size and shape.

Discussion:

The radiographic pattern of multiple pulmonary nodules is frequently encountered. The clinical setting has considerable influence on the differential diagnosis in such cases and should always be taken into account when assessing patients with this pattern. However, the differential diagnosis may be narrowed by assessing the absolute size of the nodules, the uniformity of their size, their marginal characteristics, whether or not they are calcified, and whether or not they are cavitary. In adults the most common causes of multiple nodules are metastatic neoplasm and infectious disease. Metastatic neoplasm may result from carcinoma, sarcoma, or lymphoma. Pulmonary metastases may be of any size and number. In contrast to inflammatory nodules, nodular pulmonary metastases are often of variable diameters. Metastases are usually of soft-tissue density similar to muscle or blood. Metastases may be calcified if the patient has a sarcoma that makes bone or cartilage (e.g., osteosarcoma). Calcified pulmonary nodules are more frequently encountered in patients with healed fungal or mycobacterial disease. Differentiation is most commonly made by the clinical setting or review of old films, but determination of the correct diagnosis may require tissue confirmation.

Multiple pulmonary nodules may also be due to infectious disease, most commonly fungal or mycobacterial infections. In the United States the most common fungus is histoplasmosis (Fig. 4–34), although there are regional variations. Infectious nodules are often not as sharply defined as metastases. This is especially true if the nodules represent acinar shadows. In these instances, the nodule is approximately 5 to 10 mm in diameter and is ill defined or fuzzy on its margin. Acinar nodules develop in patients with viral pneumonias such as herpes pneumonia or chickenpox pneumonia.

Multiple pulmonary nodules may also develop in a wide variety of other disorders, including Wegener's granulomatosis and arteriovenous malformations. (A is the correct answer to Question 4-13.)

EXERCISE 4-9: CAVITARY DISEASE

Clinical History:

Case 4-14. A 27-year-old man with a history of intravenous drug usage and a 2-week history of fever and malaise (Fig. 4–35A,B )

Question:

Radiologic Findings:

4-14. A close-up view of the chest radiograph (Fig. 4–35A ) and CT image (Fig. 4–35B ) of the left upper lobe show multiple thin-walled cavitary lesions. A left pneumothorax is also present. There is no hilar or mediastinal lymph node enlargement. The heart and skeleton are normal.

Discussion:

Inflammatory lesions are the most common cause of lung cavities. The number of cavities may range from one to many. A wide variety of infecting organisms may result in cavitation, and the radiograph is nonspecific as to etiology. There is considerable overlap in appearances from the various organisms, so that culture or histologic evaluation is the only satisfactory means of identifying the etiology. If the lesion is single, a cavitating pneumonia should be the first consideration, especially if the patient is febrile. If multiple cavities are present, the infection is likely due to hematogenous dissemination, and a source for this dissemination should be sought. The source could be right-sided endocarditis or infected venous thrombi. Staphylococcus aureus pneumonias are frequently seen in intravenous drug users and usually appear as multiple cavities. These usually have thin walls (2–4 mm) that are slightly indistinct on their outer borders.

As the AIDS epidemic has progressed, it has been recognized that patients with Pneumocystis carinii may develop cavitary lesions in the lungs. These cavities may be reversible and result from pneumatoceles or they may be due to a slowly progressive granulomatous reaction. The cavities are usually in the upper lobes and are thin walled. Pneumothorax can result when a peripheral cavity ruptures through the visceral pleura, into the pleural space.

Cavities may result from pulmonary vasculitis, of which Wegener's granulomatosis is the prototype. Neoplasia, either primary or secondarily involving the lung, may also cavitate (Fig. 4–36A,B ). This patient is rather young to have neoplasia. If he did have AIDS and Kaposi's sarcoma, it would be unusual for that to cavitate. (E is the correct answer to Question 4-22.)

EXERCISE 4-10: OCCUPATIONAL DISORDERS

Clinical Histories:

Case 4-15. A 64-year-old man, who previously worked in a naval shipyard, with a cough productive of blood-tinged sputum (Fig. 4–37A,B )

Case 4-16. A 55-year-old man who worked as a coal miner for 30 years (Fig. 4–38A,B )

Questions:

Radiologic Findings:

4-15. The dense radiopaque lines projecting adjacent to the left diaphragmatic surface on the PA radiograph and over both diaphragmatic surfaces on the lateral radiograph represent calcified pleural plaques. These are better seen on the oblique radiograph (Fig. 4–39A ) and on the CT (Fig. 4–39B ). When the pleural plaques are seen en face on the PA radiograph, they produce irregular opacities over the left midlung. These opacities have been described as having a holly leaf appearance. At the lung bases, a network of fine lines is superimposed over the normal vascular shadows. These reticular markings represent interstitial pulmonary fibrosis, which almost certainly represents asbestosis. Also present is a 3.5-cm mass in the anterior segment of the right upper lobe. This is a primary bronchogenic carcinoma. (C is the correct answer to Question 4-15.) The oval convexity in the lower right paratracheal region represents regional metastasis to the lower right paratracheal lymph node.

4-16. The patient in Fig. 4–38A,B has a myriad of small, rounded pulmonary opacities (nodules) that in some areas have coalesced to form larger pulmonary masses. The nodules are predominantly located in the upper lobes. There is also bilateral hilar lymph node enlargement, which is more evident on the lateral radiograph. Bilateral upper lobe volume loss is indicated by upward displacement of the hila. The superior lateral margin of the large opacity is relatively straight, and there is emphysema lateral to it. Nodular diseases that have an upper lobe preponderance include silicosis, sarcoidosis, and eosinophilic granuloma. In this patient with a history of working in coal mines, the most likely of these is silicosis, or coal worker's pneumoconiosis. (A is the correct answer to Question 4-16.)

Discussion:

The two most commonly encountered occupational lung diseases in the United States are asbestosis and silicosis. Development of these diseases is dose dependent, and there is a latent period of many years between exposure and disease. Asbestos-related diseases occur after exposure to asbestos particles, which are found in many types of insulation, fireproofing materials, concrete, and brake linings. The patient with asbestos exposure is at an increased risk of developing lung cancer. If the patient also smokes, there is an additive risk, and these patients may be as much as 100 times more likely to develop lung cancer than the nonsmoking individual with no asbestos exposure.

The term asbestosis is used to refer to the pulmonary fibrosis that may be incited by the presence of the mineral and is not used in reference to the pleural disease. The pulmonary fibrosis is predominantly distributed in the lung bases. When severe, it is detected with plain chest radiography. When it is more subtle, CT is required for its demonstration (Fig. 4–40). When confined to the pleura, the process is called asbestos-related pleural disease. There are five manifestations of asbestos-related pleural disease: asbestos-related pleural effusion, diffuse pleural thickening, pleural plaques, rounded atelectasis, and malignant mesothelioma. Asbestos-related pleural effusion occurs from 7 to 15 years after exposure. It is self-limited and may resolve without sequelae or result in diffuse pleural thickening. Pleural plaques are fibrous plaques that occur predominantly on the parietal pleural surfaces of the lower thoracic wall and diaphragmatic surfaces. Pleural plaques may be up to 8 to 10 mm thick, but are not easily visualized when seen en face. Oblique radiographs (Fig. 4–39A ) may show plaques that are projected en face on the PA chest radiograph. The plaques usually occur 10 years or more after exposure. Early in the development of pleural disease, the plaques are not calcified, but with time, the incidence of calcification increases. CT is the most sensitive method of identifying pleural plaques (Fig. 4–39B ). Diffuse pleural thickening may result from the scarring of a previous benign asbestos-related pleural effusion or it sometimes is due to confluent pleural plaques. Rounded atelectasis is a piece of folded lung tissue that appears as a mass adjacent to the chest wall. The parietal pleura adheres to an area of lung, usually in the posterior lower lobes, and gradually produces a spiraling folded area of lung, which mimics lung cancer. The comet-tail appearance of bronchi and vessels spiraling into the mass may suggest the correct diagnosis, but because there is such a great increase in the risk of lung cancer in the asbestos-exposed individual, the mass should be closely followed. Surgical resection is often necessary to distinguish the mass of rounded atelectasis from lung cancer. The final asbestos-related disease of the pleura is malignant mesothelioma. This is a malignant tumor of the pleura that usually presents as pleural masses or pleural effusion (Fig. 4–40).

Silicosis is another form of pulmonary fibrosis that occurs after prolonged exposure to silica. Historically, it has most often developed in coal miners. Because of improved ventilation standards and the increased automation of coal mining, silicosis is less commonly encountered today. There is an increased incidence of tuberculosis in coal miners, but no increased risk of lung cancer has been reported. For reasons that are unexplained, silicosis is predominantly an upper lobe process. It appears as small pulmonary nodules, and as the fibrosis progresses, the hila are retracted upward over a period of years. The small granulomatous nodules of simple silicosis coalesce to form larger conglomerate masses. When these reach at least 1 cm in diameter, the disease is called complicated silicosis, and as they become larger still, it is designated progressive massive fibrosis. Very early disease may be seen only on CT, although in the later stages of the process, the small nodules and conglomerate masses are readily seen on either plain films or CT images (Fig. 4–41A,B ). Hilar and mediastinal lymph nodes may calcify in the periphery of the lymph node, a type of calcification known as eggshell calcification (Fig. 4–42). An acute form of silicosis can occur in sandblasters who inhale a massive amount of sand. This type of silicosis radiographically resembles pulmonary edema. Coal worker's pneumoconiosis is a similar process that results from inhalation of coal of a relatively pure carbon content. This dust is relatively more inert than silica and incites less fibrosis. The nodules are less well defined on their periphery, and there is less tendency to develop progressive massive fibrosis. These distinctions are rather artificial, because rock dust is usually not very pure and contains a mixture of silica, carbon, and other minerals.

EXERCISE 4-11: MEDIASTINAL MASSES AND COMPARTMENTS

Clinical Histories:

Case 4-17. An asymptomatic 37-year-old woman, routine chest radiograph (Fig. 4–43A,B )

Case 4-18. A 55-year-old man with multiple subcutaneous nodules (Fig. 4–44A,B )

Case 4-19. A 25-year-old woman with a nonproductive cough (Fig. 4–45A,B )

Questions:

Radiological Findings:

4-17. A spherical mass 4 cm in diameter is present in the subcarinal region on the frontal radiograph (Fig. 4–43A ) and superimposed on the hilar region on the lateral radiograph (Fig. 4–43B ). CT (Fig. 4–46) shows that the lesion is of fluid attenuation (greater attenuation than the subcutaneous fat, but less attenuation than muscle). This mass is in the middle mediastinum. (B is the correct answer to Question 4-17.) In an asymptomatic individual, this most likely represents a congenital bronchogenic cyst. These masses can grow to sufficient size to cause symptoms such as dyspnea or dysphagia owing to compression of the trachea or esophagus. Bronchogenic cysts may also occur within the lungs and are often surgically resected because of the likelihood of pulmonary infection. The differential diagnosis of a middle mediastinal mass also includes lymphoma, esophageal tumor, hiatal hernia, and aortic arch aneurysm.

4-18. The frontal radiograph (Fig. 4–44A ) shows a lobulated mass to the left of the lower thoracic vertebrae. Note that the lateral wall of the descending thoracic aorta remains visible, suggesting that this mass is either anterior or posterior to the aorta, but does not displace lung from the wall of the aorta. The mass is not visible on the lateral radiograph. The residual myelographic contrast material visible within the spinal canal hints at the neural nature of these masses. The axial CT images in Fig. 4–47A,B show that the masses are bilateral and paraspinal in location. These masses are in the posterior mediastinum. (C is the correct answer to Question 4-18.) Neurogenic tumors are the most common cause of posterior mediastinal masses. In this patient with multiple subcutaneous nodules, they most likely are neurofibromas. The differential diagnosis of posterior mediastinal masses also includes paraspinous abscess, descending thoracic aorta aneurysm, Bochdalek hernia, and lymphoma.

4-19. In Fig. 4–45, the frontal chest radiograph (Figs. 4–45A and 4–48A ) shows a mass projecting over the left hilum (long arrow, Fig. 4–48A ) without obscuration of the interlobar pulmonary artery (short arrow, Fig. 4–48A ). Because the mass does not obliterate the margins of the vessel, it must be either anterior or posterior to the hilum. On the lateral view (Fig. 4–48B ), the anterior clear space is somewhat opaque, and there is a suggestion of margins of the mass (arrows). The CT scan (Fig. 4–48C ) shows the mass, surrounded by fat, in the anterior mediastinum. (A is the correct answer to Question 4-19.) The mass is cystic, and the contents have rather low density, suggesting that the mass contains some fat. Notice the thick, irregular wall of the mass. No other abnormalities are present. This is consistent with a teratoma. The differential diagnosis of anterior mediastinal masses also includes lymphoma, thyroid mass, thymoma, and ascending aortic aneurysm.

Discussion:

Two methods of dividing the mediastinum for radiographic purposes are in common use. The radiographic divisions are arbitrary and are intended to provide the most appropriate differential diagnosis for abnormalities that occur in these locations. Neither of the divisions follows the divisions used by anatomists. In the older system, the mediastinum is divided into three compartments. The anterior mediastinum is that portion of the mediastinum that is anterior to the anterior margin of the trachea and along the posterior margin of the pericardium and inferior vena cava. The posterior mediastinum lies behind a plane that extends the length of the thorax behind a line drawn 1 cm posteriorly to the anterior margin of the vertebral column. The middle mediastinum is the region between these two boundaries. This system has been superseded by a four-compartment model, which designates a superior mediastinal compartment as the space that lies above a plane extending from the sternomanubrial junction to the lower border of the fourth thoracic vertebra. The anterior mediastinum is just caudad to the superior compartment and is anterior to a plane extending along the anterior aspect of the tracheal air column and along the anterior pericardium. Note that the heart shifts from the anterior to the middle mediastinum as the system changes. The middle mediastinum occupies the area from the anterior pericardium backward to a plane 1 cm posterior to the anterior margin of the vertebral column. The addition of the fourth compartment occurred when CT was developed and it became easier to identify structures in each compartment.

The differential diagnosis of lesions occurring in each compartment is in part dependent on the structures that exist there. Note that there are vascular structures and lymph nodes in each of the compartments. Therefore, abnormalities of the blood vessels (e.g., aneurysms) and lymph node diseases (e.g., lymphoma) would have to be included in the differential diagnosis of diseases in all mediastinal compartments. The most common mass to occur in the superior mediastinum is an enlarged substernal thyroid, which may become large enough to extend into the anterior or middle mediastinum (Fig. 4–49A–D ).

EXERCISE 4-12: PLEURAL ABNORMALITIES

Clinical History:

Case 4-20. A tall, 21-year-old man who noted the sudden onset of dyspnea, and right-sided pleuritic chest pain (Fig. 4–50A,B )

Question:

Radiologic Findings:

4-20. In Fig. 4–50A, there is increased radiolucency in the periphery of the right hemithorax. On the close-up of the right lung (Fig. 4–50B ), there is a thin white line (arrows) paralleling, but displaced from, the right lateral chest wall. The thin line represents the visceral pleura. There is air-filled lung medial to this thin white line, and there is air within the pleural space lateral to this line. Note the absence of pulmonary vessels lateral to the pleural line. (C is the correct answer to Question 4-20.) Note the rounded, thin-walled blebs at the apex of the right lung on the close-up view in Fig. 4–50B .

Discussion:

Pneumothorax is the presence of air in the pleural space. The lung collapses away from the chest wall because of its normal elastic recoil. In some instances, a ball valve mechanism is present, and air continues to enter the pleural space and further collapses the lung and displaces the mediastinum away from the side of the pneumothorax. The relationship of the air in the pleural space to the lung and chest wall can be clearly seen on the CT scan of a patient with a left pneumothorax (Fig. 4–51). Note that air rises to the highest point in the thorax, the anterior thorax in a supine patient and the lung apex in an upright patient. The visceral pleura covering the lung is visible as a thin white line on both chest radiographs and CT scans. No pulmonary vessels may be seen extending beyond the pleural line, and the air in the pleural space appears more radiolucent than the adjacent lung.

The most common mimic of a pneumothorax, particularly in a supine patient, is a skin fold. The film cassette for portable AP chest radiographs is placed behind the patient's back. Skin folds may be pressed between the patient's back and the film cassette. Radiographically, a skin fold produces an interface, or an edge of thick tissue outlined by the greater radiolucency of the superimposed lung. If you can distinguish an edge from a line, then you can distinguish a skin fold from a pneumothorax. The absence of pulmonary markings beyond the pleural line is supporting evidence for a pneumothorax. Because the vessels taper as they approach the lung periphery, the vessels in the extreme periphery of the lung may be too tiny to see.

Pneumothorax is spontaneous if it occurs in the absence of trauma (including barotrauma). Spontaneous pneumothorax may be primary and occur in the absence of significant other lung disease, or it may occur secondarily because of lung disease. Apical blebs are present in a high percentage of patients with primary spontaneous pneumothorax, and their rupture is thought to be the most frequent cause of spontaneous pneumothorax. For unknown reasons, it occurs most frequently in tall young men. Secondary spontaneous pneumothorax may occur in association with any cavitary lesion that lies in the periphery of the lung, as well as in emphysema, in bullous disease, and in pulmonary fibrosis of a variety of etiologies.

EXERCISE 4-13: PLEURAL EFFUSION

Clinical History:

Case 4-21. A 45-year-old man with increasing dyspnea and abdominal swelling of 1-week duration (Fig. 4–52A,B )

Question:

Radiologic Findings:

4-21. The frontal chest radiograph (Fig. 4–52A ) shows opacity at the lower left hemithorax, which has a concave border curving upward laterally adjacent to the chest wall. The overall lung volume is low in both the right and left lungs. There is separation of the gastric bubble from the inferior margin of the lung by several centimeters. On the lateral examination (Fig. 4–52B ), the opacity obscures the posterior heart margin and has a margin curving slightly upward to the posterior chest wall. The findings are those of a pleural effusion on the left. The patient is noted to have slight abdominal protusion that is seen on the lateral examination. This was due to ascites in this patient with cirrhosis.

Discussion:

The visceral pleura is the outer lining of the lung, and the parietal pleura is the lining of the chest cavity. Normally, these surfaces are smooth and are separated by a minimal amount of pleural fluid. This provides a nearly friction-free environment for movement of the lung within the thorax. The pleural space, therefore, is a potential space that, in the normal individual, contains no more than 3 to 5 cm³ of pleural fluid. Fluid may accumulate within the pleural space as a result of conditions that (1) increase pulmonary capillary pressure, (2) alter thoracic vascular or lymphatic pathways, (3) alter pleural capillary or lymphatic permeability, or (4) affect diaphragmatic peritoneal and pleural surfaces.

Pleural effusions are usually approached clinically according to whether the effusion develops because of alterations of the Starling equation, which controls fluid flow and maintenance in body compartments, or whether the pleura is affected primarily by a disease process. Processes resulting from alterations of the Starling equation include congestive heart failure, hypoproteinemia, fluid overload, liver failure, and nephrosis. These effusions are usually transudates (clear or pale yellow, odorless fluid without elevation of the ratios of pleural fluid: serum protein and LDH). Processes that alter pleural capillary or lymphatic permeability include infections, inflammation, pulmonary embolism, and neoplasms. These effusions are usually exudates (clear, pale yellow or turbid, bloody, brownish fluid; pleural fluid protein: serum protein greater than 0.5; and pleural fluid LDH: serum LDH greater than 0.6). Enlarged lymph nodes or masses within the hila or mediastinum may obstruct lymphatic fluid flow and cause pleural exudates. Abdominal conditions that may produce pleural effusions include pancreatitis, subphrenic abscesses, liver abscesses, ovarian tumors, peritonitis, and ascites.

The most common radiographic sign is pleural meniscus. The volume of fluid necessary to produce a pleural meniscus within a costophrenic angle varies from individual to individual. Approximately 100 cm³ of pleural fluid will cause appreciable blunting of the posterior costophrenic angle on the lateral view; and 200 cm³ will cause blunting of the lateral costophrenic angle on the PA projection in an upright patient (Fig. 4–53A–C ). A lateral decubitus chest radiograph, with the side containing the pleural effusion placed down (dependent), will demonstrate even smaller amounts of free-flowing pleural effusions (Fig. 4–54). Each millimeter of thickness of pleural fluid in the lateral decubitus projection corresponds to approximately 20 cm³ of pleural fluid. Large pleural effusions may usually be aspirated without guidance other than the chest radiograph. Small effusions are more difficult to aspirate and, if thoracentesis is planned, additional imaging guidance with ultrasonography or CT may be used. The effusion may simply be marked and aspirated by the clinical physician, or the effusion may be aspirated by a radiologist. If thoracentesis is attempted and fails for a large pleural effusion, it may be loculated, and further imaging guidance is usually helpful.

When pleural adhesions develop, fluid in the pleural space becomes loculated (Fig. 4–55A,B ) and may be trapped in nondependent areas of the thorax. The appearance of pleural fluid may change and, rather than a meniscus shape, may assume the shape of a convex margin away from the chest wall. If fluid is trapped in the fissures, it will assume a biconvex lens shape. If a bronchopleural fistula develops, the patient will have a hydropneumothorax that may be recognized by air-fluid levels of different lengths on the PA and lateral chest radiographs. When cavities develop in the lung, the fluid levels are usually of the same length. (All of the options in Question 4-21 are correct.)

EXERCISE 4-14: PULMONARY VASCULAR DISEASE

Clinical History:

Case 4-22. A 62-year-old woman with worsening shortness of breath and mild hemoptysis 1 day after receiving intravenous chemotherapy for ovarian cancer. A PA and lateral chest radiograph (Fig. 4–56A,B ) and a CT scan with intravenous contrast were obtained (Fig. 4–56C,D ).

Question:

Radiologic Findings:

4-22. The CXR shows small bilateral pleural effusions. These cause blunting of the lateral costophrenic angles on the PA view of the chest (Fig. 4–56A ) and of the posterior costophrenic angles on the lateral view of the chest (Fig. 4–56B ). The size of the pleural effusions is not sufficient to explain the patient's symptoms. The CT scan (Fig. 4–56C ) demonstrates filling defects within the pulmonary arteries bilaterally (arrows). At the level shown, thromboemboli are visible within the right interlobar (descending) pulmonary artery and within the basilar segmental arteries on the left. (C is the correct answer to Question 4-22.) The lung windows (Fig. 4–56D ) show peripheral areas of increased attenuation (arrows), consistent with areas of pulmonary infarction.

Discussion:

Pulmonary thromboembolism can occur as a result of deep-venous thrombosis, typically from the veins of the pelvis and lower extremities. These thrombi dislodge (embolize) and travel via the inferior vena cava and right heart chambers to become trapped in the tapering branches of the pulmonary arterial system. Because pulmonary embolism often occurs without pulmonary infarction, the appearance of the chest radiograph is usually normal. The areas of lung deprived of pulmonary arterial flow are perfused by bronchial arterial collateral vessels. The chest radiograph may demonstrate subtle signs of volume loss or a small pleural effusion. Pulmonary opacities develop because of microatelectasis within the region of lung that has had an embolus or from hemorrhage within a pulmonary infarction. Pulmonary infarction may occur if the pulmonary venous pressure is elevated or the bronchial arterial supply to a region is deficient for some reason. The cone-shaped area of pulmonary infarction has been called a Hampton's hump after its original descriptor. An area of radiolucency, corresponding to diminished pulmonary vascularity distal to a pulmonary embolism, is occasionally seen and is called the Westermark sign. There may also be an increase in the size of the pulmonary artery proximal to a large central pulmonary embolus.

Two imaging modalities are widely used in the evaluation of a patient with suspected pulmonary embolism: radionuclide perfusion scan and chest CT. The radionuclide perfusion scan may be the more appropriate examination in the patient with a normal chest radiograph and no preexisting cardiac or pulmonary disease. In the patient with an abnormal chest radiograph, or preexisting cardiopulmonary disease, the V/Q scan is more likely to be interpreted as "indeterminate" and a chest CT becomes the preferred imaging modality. The chest CT also has the advantage of demonstrating unsuspected abnormalities, such as pericardial effusion, emphysema, esophagitis, or aortic dissection, which are responsible for the patient's chest pain or dyspnea.

On chest CT, thromboemboli are visible as filling defects within the contrast-filled pulmonary arteries. These are typically several centimeters long and often are seen draped across the bifurcation of an artery (saddle emboli). In patients with acute pulmonary embolism, the filling defects are seen within the center of the arterial lumen, although they may also completely occlude the artery. In patients with chronic pulmonary embolism, the filling defects are more likely to be found against the wall of the artery. Calcification within the thrombus also confirms the chronic nature of the thrombus.

In some patients, the diagnosis of pulmonary embolism remains uncertain after either a V/Q scan or a chest CT. These examinations can be inadequate for a number of both technical and clinical reasons. The chest CT can be difficult to interpret unless the patient is able to suspend respiration for the duration of the scan. Fortunately, helical CT scans are able to scan the entire thorax in under 30 seconds. Many patients with severe dyspnea, however, are unable to achieve this. Pulmonary angiography can be obtained to further evaluate the pulmonary arterial circulation when either the V/Q scan or chest CT are nondiagnostic.

GLOSSARY OF TERMS IN CHEST ROENTGENOLOGY

Adapted from "Terms Used in Chest Radiology" in Fraser RS, Muller NL, Colman N, Pare PD. Fraser and Pare's diagnosis of diseases of the Chest. 4th ed. Philadelphia: WB. Saunders Co.; 1999: xvii–xxxi.

Acinar pattern (synonyms: alveolar pattern, airspace disease, consolidation) A collection of round or elliptic, ill-defined, discrete or partly confluent opacities in the lung, each measuring 4 to 8 mm in diameter and together producing an extended, inhomogeneous shadow.

Air bronchogram A branching lucency that represents the roentgenographic shadow of an air-containing bronchus peripheral to the hilum and surrounded by airless lung (whether by virtue of absorption of air, replacement of air, or both), a finding generally regarded as evidence of the patency of the more proximal airway.

Air-fluid level A local collection of gas and liquid that, when traversed by a horizontal x-ray beam, creates a shadow characterized by a sharp horizontal interface between a gas density above and liquid density below.

Airspace The gas-containing portion of lung parenchyma, including the acini and excluding the interstitium and purely conductive portions of the lung.

Anterior junction line A vertically oriented linear opacity approximately 1 to 2 mm wide, produced by the shadows of the right and left pleural surfaces in intimate contact between the aerated lungs anterior to the great vessels. It is usually obliquely oriented, projected over the tracheal air column, below the level of the clavicles.

Aortopulmonary window A zone of relative lucency seen on both the PA and lateral chest radiographs bounded medially by the left side of the trachea, superiorly by the inferior surface of the aortic arch, and inferiorly by the left pulmonary artery. The pleural surface of the aortopulmonary (AP) window is normally concave; convexity of the AP window suggests lymphadenopathy.

Atelectasis Less than normal inflation of all or a portion of lung with corresponding diminution in volume. Qualifiers are often used to indicate extent and distribution (linear or platelike, subsegmental, segmental, lobar), as well as mechanism (resorption, relaxation, compressive, passive, cicatricial, adhesive).

Azygoesophageal recess On the frontal chest radiograph, a vertically oriented interface between air in the right lower lobe, and the adjacent mediastinum containing the azygos vein and esophagus. It projects in the middle of the heart and spine on the frontal view.

Bleb A thin-walled lucency within or contiguous to the visceral pleura.

Bulla A sharply demarcated area of a vascularity (lucency) within the lung measuring 1 cm or more in diameter and possessing a wall less than 1 mm in thickness.

Carina The bifurcation of the trachea into right and left main bronchi.

Cavity A gas-containing space within the lung surrounded by a wall whose thickness is greater than 1 mm and often irregular in contour.

Fissure The infolding of visceral pleura that separates one lobe, or a portion of a lobe, from another. Radiographically visible as a linear opacity normally 1 mm or less in width. Qualifiers: minor (horizontal), major, accessory, azygos, anomalous.

Ground-glass pattern A finely granular pattern of pulmonary opacity such that pulmonary vessels remain visible. The degree of opacity is not sufficient to result in air bronchograms.

Hilum (plural: hila) Anatomically, the depression or pit in that part of an organ where the vessels and nerves enter. On chest radiographs, the term hilum represents the composite shadow of the bronchi, pulmonary arteries and veins, and lymph nodes on the medial aspect of each lung.

Honeycomb pattern A number of ring shadows or cystic spaces within the lung representing airspaces 5 to 10 mm in diameter with walls 2 to 3 mm thick that resemble a true honeycomb. The finding implies interstitial fibrosis and end-stage lung disease.

Interface (synonyms: edge, border) The boundary between the shadows of structures of different opacity (e.g., the lung and the heart).

Interstitium A continuum of loose connective tissue throughout the lung consisting of three subdivisions: (1) bronchoarterial (axial), surrounding the bronchoarterial bundles; (2) parenchymal (acinar), between the alveolar and capillary basement membranes; and (3) subpleural, between the pleura and lung parenchyma and continuous with the interlobular septa and perivenous interstitial space.

Line A longitudinal opacity no greater than 2 mm in width.

Lobe One of the principal divisions of the lungs (usually three on the right, two on the left) enveloped by the visceral pleura except at the hilum. The lobes are separated in whole or in part by pleural fissures.

Lucency (synonym: radiolucency) The shadow of tissue that attenuates the x-ray beam less effectively than surrounding tissue. On a radiograph, the area that appears more nearly black, usually applied to areas of air density or fat density.

Lymphadenopathy (synonym: adenopathy) Enlargement or abnormality of lymph nodes.

Mass Any pulmonary or pleural lesion greater than 3 cm in diameter.

Miliary pattern A collection of tiny (1–2 mm in diameter) discrete opacities in the lungs, generally uniform in size and widespread in distribution.

Nodular pattern A collection of innumerable small, discrete opacities (2–10 mm in diameter), generally widespread in distribution.

Nodule A sharply defined, discrete, circular opacity up to 3 cm in diameter within the lung.

Opacity The shadow of tissue that attenuates the x-ray beam more than surrounding tissue. On a radiograph, areas that are more white than the surrounding area are said to be more opaque.

Posterior junction line A vertically oriented, linear opacity approximately 2 mm wide, produced by the shadows of the right and left pleurae in intimate contact between the aerated lungs, representing the plane of contact between the lungs posterior to the trachea and esophagus, and anterior to the spine; the line may project above and below the suprasternal notch.

Posterior tracheal stripe A vertically oriented linear opacity 2 to 5 mm wide, extending from the thoracic inlet to the bifurcation of the trachea, visible on the lateral radiograph, representing the posterior tracheal wall and contiguous mediastinal tissue (anterior, and often posterior, walls of the esophagus).

Primary complex The combination of a focus of pneumonia due to a primary infection (e.g., tuberculosis or histoplasmosis), with granulomas in the draining hilar or mediastinal lymph nodes. (Synonym: Ranke complex. The term Ghon focus describes the pulmonary lesion that has calcified. Ranke complex is the term to describe the combination of the Ghon focus and calcified hilar lymph nodes.)

Reticular pattern A collection of innumerable small, linear opacities that together produce the appearance of a net.

Reticulonodular pattern A collection of innumerable small, linear, and nodular opacities that together produce the appearance of a net and superimposed small nodules.

Right tracheal stripe A vertically oriented linear opacity 2 to 3 mm wide, extending from the thoracic inlet to the right tracheobronchial angle. It represents the right tracheal wall and contiguous mediastinal tissue (visceral and parietal pleurae of the right lung).

Septal line (synonym: Kerley line) A linear opacity, usually 1 to 2 mm in width, produced by thickening of the interlobular septa, and often due to either edema or cellular infiltration.

Silhouette sign The effacement of an anatomic soft-tissue border by either a normal anatomic structure or a pathologic state, such as airlessness of adjacent lung or accumulation of fluid in the contiguous pleural space.

Stripe A longitudinal opacity 2 to 5 mm in width.

Tramline shadow Parallel or slightly convergent linear opacities that suggest the projection of tubular structures, generally representing thickened bronchial walls.

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