INTRODUCTION
The chest radiograph remains the primary imaging investigation in the evaluation of diseases of the respiratory system. It is a low-radiation, cheap and easily available imaging technique, providing invaluable information regarding the lung parenchyma, pleura, mediastinum and chest wall. It has its share of limitations being a projectional two-dimensional (2D) imaging modality. Computed tomography (CT), a cross-sectional imaging modality provides excellent detail of the lung, pleura, mediastinum as well as chest wall to compensate for the limitations of chest X-ray. The chest X-ray as well as the CT scan suffice for all imaging needs in the chest. Ultrasonography (USG)/magnetic resonance imaging (MRI)/positron emission tomography (PET) have complementary roles in the evaluation of chest diseases.
CHEST RADIOGRAPHS
Even after 100 years of technological developments, the chest X-ray remains the primary imaging modality for diseases of the chest. It is obtained with the patient erect, facing the cassette, with the X-ray beam directed from behind the patient, from a distance of 6 feet to avoid magnification of mediastinal structures (Figs. 1 and 2). The X-ray is obtained at deep inspiration. A film obtained in expiration will result in alteration of the mediastinal contour as well as a misleading appearance of diffuse lung disease (Figs. 3A and B). It is important to position the patient well such that he or she is not rotated. A well-centered X-ray will demonstrate the medial ends of the clavicles to be equidistant from the spinous processes of the vertebrae. Rotation to the left results in the manubrium sternum, superior vena cava (SVC) and great vessels appearing prominent—this may simulate a mediastinal mass (Figs. 4A and B). Rotation may also result in one lung appearing more or less translucent (Figs. 5A to C). To minimize the shadow of the scapula on the lungs, the arms are placed on the sides and shoulders rotated forward so as to rotate the scapula laterally.
Fig. 1: PA view of the chest: Positioning for a PA view of the chest with patient facing the cassette and arms rotated forward to take the scapulae off the film.
A large part of the lungs on a frontal radiograph are obscured by the bony rib cage. To be able to visualize larger areas of lung parenchyma free from significant obscuration by the ribs, high kVp (peak kilovoltage) techniques are used. As the coefficient of X-ray absorption of soft tissue and bone approach each other at high kVp, 4the bony rib cage no longer obscures the lungs to the same extent as on lower kVp films. The mediastinum is also penetrated better in high-kVp films, thereby allowing more details to be viewed of the mediastinum and large airways (Fig. 6). Scattered radiation is higher at high kVp, causing significant degradation of image quality. To minimize this effect a grid or an air gap of 15 cm between the patient and cassette is used, thereby improving image quality. If an air gap is used, the distance between patient and X-ray beam is increased to 12 feet to avoid magnification of the mediastinum. A drawback of high kVp is a lack of demonstration of calcified lesions and small pulmonary nodules. Low-kVp films have the advantage of providing excellent detail in the unobscured lung, as there is excellent contrast resolution between vessels and aerated lung.
Fig. 2: PA view of the chest: Normal chest X-ray, note scapulae have been rotated off the chest so as to avoid obscuration of lung parenchyma.
Digital chest radiography has now nearly totally replaced analog radiography modalities. There have been compelling reasons for this shift. The availability of data in an electronic form makes it possible to postprocess the image data so as to present optimal image quality, view the images on large high-resolution workstations, archive as well as distribute images across a hospital network or to any remote location. Computed radiography or CR, the first commercially available digital X-ray imaging technique is still the most popular digital imaging technique available today. In this technique, conventional X-ray film is replaced by a phosphor plate. This phosphor plate when exposed to X-rays, stores the X-ray radiation as energy. This phosphor plate is read by a laser beam which releases the energy stored on the phosphor plate as light, producing an image. Recently, flat panel detectors have been introduced.
These do away with the need to have a cassette containing the phosphor plate. The images are instantly available as soon as the X-ray is exposed. The image quality is superior and as no cassette is involved, the work flow is much faster.
Figs. 3A and B: Inspiratory and expiratory views: PA view of the chest in inspiration (A) and in expiration (B) of same patient. Note change in mediastinal contour as well as diffuse haziness in both lung bases on expiratory view simulating interstitial lung disease.
Figs. 4A and B: Rotation: (A) To check for rotation on a PA view, a vertical line is drawn along the spinous processes of the vertebrae (blue). Horizontal line is drawn between the medial ends of the clavicles so as to cut the vertical line. The medial ends of the clavicles should be equidistant when there is no rotation (B) Note rotation to left as medial end of right clavicles rotates further away this results in a right paratracheal opacity representing SVC shadow. This opacity may simulate a mass or adenopathy.
Figs. 5A to C: (A) Chest X-ray reveals haziness in the left mid and lower zones. (B and C) Axial and coronal CT sections revealed absence of any pathology. Left sided haziness in the X-ray was due to the rotation to the left.
ADDITIONAL VIEWS
Lateral
The utility of this view is to check whether an equivocal frontal chest X-ray shadow is actually present, to position an abnormality seen on a frontal X-ray, and define as to which lobe it is located in. The patient stands perpendicular to the cassette with arms held high and well away from the thorax. The lateral chest X-ray is not of much use in evaluating the apices, as the shoulders overlap this region (Figs. 7 to 10).
Lateral Decubitus
Lateral decubitus is a useful view to demonstrate a small pleural effusion which is not visible on the PA view, or differentiate a free pleural effusion from loculated pleural fluid or pleural thickening (Fig. 11). A frontal radiograph is obtained with the patient lying in a decubitus position with the side suspected to have pleural effusion down. Free fluid gravitates along the dependent chest wall between the lungs and chest wall.6
Fig. 6: High-kVp X-ray demonstrates the lung fields well, the opacity of overlying ribs is reduced considerably; note the detail of the mediastinum and trachea. A disadvantage of this technique is a lower detection rate of pulmonary nodules and calcified granulomas as compared to low-kVp X-ray.
Fig. 7: Lateral view of chest and positioning for a lateral view: Left side of chest is in contact with the cassette, this reduces cardiac magnification as compared to right side; arms are held up.
Fig. 8: Lateral X-ray of chest: A normal lateral X-ray of the chest. Important points to note are: (1) Increasing lucency of the descending dorsal vertebrae. Loss of this progressive lucency is indicative of a pathological process in this location. (2) Homogenous cardiac opacity as well as aerated retrosternal region. Loss of homogeneity in this region would indicate the presence of a pathological process.
Lateral Shoot Through
This view is useful to demonstrate a small anterior pneumothorax in a supine patient. The X-ray beam is directed horizontally from one lateral chest wall and the cassette is placed along the other lateral chest wall.
Lateral Oblique
This view is used to demonstrate rib fractures and rib lesions. The axillary course of a rib is obscured on a frontal radiograph; on oblique view these are well visualized. The patient is rotated by 45° and a frontal radiograph is obtained.
Lordotic View
On a frontal radiograph the apices are often obscured by the clavicle and first rib thereby obscuring a lesion in this location. Subtle tubercular lesions hidden beneath the first rib/clavicle can be well-demonstrated on this view (Figs. 12A and B). Additionally, on a PA view it may be difficult to discern between a fibrotic tubercular lesion and costochondral cartilage; a lordotic view would be able to differentiate the two. The patient is positioned upright and the X-ray beam is angled 15° upward or alternatively the X-ray beam is kept horizontal and the patient arched backward resembling the posture of a “lord” (Figs. 13A and B).7
Figs. 9A and B: (A) PA view of the chest demonstrates a large mass lesion in the right upper and middle zone, silhouetting the right mediastinal border, with a small right pleural effusion; (B) Lateral X-ray demonstrates the large opacity overlying the upper cardiac silhouette as well as partly obliterating the retrosternal air space. The translucency over the lower dorsal vertebrae is lost due to presence of pleural fluid. Note well-defined lower zone pulmonary nodule overlying anterior end of lower dorsal vertebra. This lesion was not appreciated on the PA view.
Figs. 10A and B: Posterior mediastinal mass: (A) PA view of the chest reveals a large mass lesion occupying and extending beyond the confines of the mediastinum; (B) Lateral view localizes the mass to the posterior mediastinum. The mass lesion is seen as a homogenous opacity posterior to the trachea as well as displacing the trachea anteriorly.
PORTABLE RADIOGRAPHS
These are extremely useful as they are performed at the patient's bedside. They do have their share of limitations. Due to the shorter tube focus distance, there is mediastinal magnification. High-kVp techniques are not possible as the output of these machines is limited, the exposure time is longer, so that patients may be unable to hold their breath, resulting in motion artifacts. The positioning of these patients is also a challenge as they are often half upright or rotated. Patients also find it difficult to take a deep breath in a semi-erect position. Digital X-rays have fortunately helped considerably to improve image quality of portable X-rays. Similar to X-rays taken in the imaging department using CR, the same CR cassettes can be used in the intensive care unit (ICU), and processed in the same readers available in the imaging department. DR or digital radiography units which do not require a cassette and which are available for an imaging department are also available for portable radiography (Figs. 14A and B). These have a great advantage; they provide an instant image, thereby saving precious time—time taken to transport a cassette to the imaging department, process it, archive the image and transport it back. These however at present are extremely expensive. As a bridge, portable CR readers are being developed, so that at the bedside itself the CR cassette can be read, producing a quick image.
Fig. 11: Lateral decubitus: PA view of the chest had demonstrated a right basal opacity, ? collapse consolidation, ? pleural fluid. X-ray taken with patient lying on his right side; there is fluid layering along the chest wall indicating a free pleural effusion.
There are newer novel applications developing in digital radiography—Dual Energy, Tomosynthesis and Temporal Subtraction.
Dual-energy Subtraction Imaging
The absorption of X-ray by tissues depends upon the kilovoltage (kV) used, as well as on the consistency of the tissues. When kV is varied the response of tissues changes; as a result tissues can be separated from each other at different kVs. In the chest, bone and soft tissue both appear bright on low kV, so that a pulmonary nodule underlying a rib will be obscured due to their similar densities. At higher kV the attenuation of calcium and soft tissue to X-rays differs. This principle is used to generate images using different kVs. The images are subtracted to provide images with only soft tissue. This helps to improve detection of a solitary pulmonary nodule as only soft tissue is seen and no bone.
Figs. 12A and B: Lordotic view: (A) PA view of the chest reveals a questionable opacity underlying the first rib on the right side; (B) Lordotic view uncovers the first rib demonstrating ill-defined soft opacities in the right apex due to active tuberculous infection.
Figs. 13A and B: Lordotic X-rays demonstrate two methods of demonstration of the apices without overlap of first rib, in (A) the X-ray beam is horizontal, the patient is arched back simulating a “lord”. In the other method (B) the X-ray beam is angled upwards by 15° to the apex, the patient stands straight with back to the cassette.
Digital Tomosynthesis
Digital tomosynthesis is a technique where images of a certain depth in the chest are obtained. The tissues above and below this level are blurred, only tissue at that depth is visualized. This is similar to tomography of the olden days, now using digital techniques to enhance the evaluation.
Temporal Subtraction
This technique utilizes subtraction of a previous image from the present image. If there is any interval change it will be demonstrated. Inaccuracies do occur in terms of positioning as well as differences in breathhold.
Computer-aided Diagnosis
This is a technique which relies on a pattern recognition approach using artificial intelligence to help detect lesions which may be missed by radiologists. The main applications being evaluated at present are detection of pulmonary nodules, as well as pulmonary emboli (Fig. 15). These techniques are yet to become popular, as there is a high rate of false-positive detection; also the detection rate is similar to that observed by radiologists.
LIMITATIONS OF CHEST X-RAY
The limitations of a chest X-ray relate essentially to the fact that the chest X-ray is a 2D modality, imaging a three-dimensional (3D) structure. Nearly 75% of the lungs are covered by ribs, mediastinum and diaphragm; as a result a number of anatomical structures are superimposed reducing the detectability of lesions. From a technical aspect since the chest is a large region to be imaged, approximately 40 cm, as the whole of this area has to be radiated, there is significant scatter radiation resulting in degradation of image quality.
Figs. 14A and B: Portable chest radiograph: (A) PA view and (B) portable AP view of the chest. Note the change in cardiac outline between a PA view and an AP view. Commenting on cardiomegaly on an AP view may be hazardous.
Fig. 15: Computer-aided diagnosis (CAD): CAD demonstrates a pulmonary nodule colored in yellow, separate from adjacent vessels. The volume of this nodule can be easily determined. The nodule can be followed up on subsequent examinations to determine rate of growth. CAD helps in detecting lesions which may have been missed by radiologists; at present CAD has a high false-positive detection rate; however, it is extremely useful for volume measurements.
COMPUTED TOMOGRAPHY
CT has been heralded as the greatest discovery in medicine following the discovery of X-rays. The history of the development of the CT scanner is extremely unique. Electrical and musical industries (EMI) became famous in the 1960s as they were the record label for the Beatles. At their Abbey Road studios they recorded enough Vinyl for the Beatles to go around the earth's circumference. They became a cash-rich company. Godfrey Hounsfield, an eminent scientist with EMI who had already developed the first all-transistor computer, was keen to develop a product which would more effectively evaluate the attenuation of X-rays through soft tissues. This research was funded directly by profits from the Beatles. In 1972, Godfrey Hounsfield unveiled the first CT scanner to the world named as EMI. That scanner took 4 minutes to acquire a single slice and a further 7 minutes to reconstruct the image. CT has come a long way since those days with the entire thorax being scanned with a dual-source CT in under a second in 2010. Not only did the Beatles spawn an entire shift in musical tastes, outlook, physical appearance and hairstyles for nearly the entire globe, they contributed to one of the greatest advances in medicine since the discovery of X-rays.
Figs. 16A and B: Helical CT: (A) Demonstrates a conventional CT which obtained slices one by one; (B) Demonstrates a helical CT, all slices are obtained simultaneously in one breathhold.
CT scanners are based on the same principles as X-ray. Tissues attenuate X-rays differently depending on their composition, i.e. atomic number; thereby a CT scanner is able to detect minute differences in attenuation by tissues, providing extremely high anatomical detail. A CT scanner consists of an X-ray tube which emits X-rays, and a detector opposite to the X-ray tube. This combined assembly rotates 360° around the patient acquiring data. Data from one 360° rotation produces a single image. Present-day scanners are helical scanners; data is acquired simultaneously with the table moving and X-ray tube rotating during a single breathhold. This technique has significant advantages over the previous nonhelical scanners. As scans are acquired in a single breathhold, the possibility of missing a pulmonary nodule due to respiratory misregistration does not arise (Figs. 16 and 17). Data is acquired as a volume and therefore can be reconstructed at any slice thickness as well as in any plane which is desired. Additionally, as the scan time is shorter, less intravenous contrast medium is required. Helical scanners have advanced technologically from being single-detector to multidetector scanners (MDCT) (Figs. 18A and B). These MDCT scanners may have from 2 rows to 64 rows of detectors. Increasing the number of rows of detectors enables faster scans, reducing respiratory and motion artifacts.11
Figs. 17A and B: Multidetector CT: (A) Demonstrates a single-slice helical CT rotation; (B) Demonstrates a multidetector helical CT rotation.
Figs. 18A and B: Multidetector CT: Comparison between a single-detector CT and a multidetector CT. (A) Single-detector (B) Multidetector CT. Note the increased coverage in a single rotation with a multidetector CT allowing for large volume coverage in shorter time with thinner slices.
Angiographic images may be obtained as well as larger volumes may be covered, with thinner sections obtained. A CT image is a 2D image, but there is a third dimension, depth or slice thickness. A thick slice contains different tissues within the section, which will be averaged to produce the final image. To obtain a high degree of anatomical detail as with high-resolution CT (HRCT) very thin sections are required, 1 mm or less, so that there is no averaging of tissues. These scanners have further revolutionized the diagnostic potential of CT, especially the 16, 64 slice scanners, as these produce thin slices (0.6–0.75 mm) which are isotropic, i.e. reconstruction of these slices in any plane results in no loss of resolution. These scanners have essentially converted CT from an axial cross-sectional technique to a true 3D technique allowing arbitrary selection of scan planes, and volumetric display of data. Newer scanners with 128 rows, 256 rows, 360 rows and dual-source CT have been introduced essentially to facilitate CT coronary angiography. The dual-source CT houses two CT scanners in one CT gantry. The advantage of this is in the performance of CT coronary angiograms without the need to use beta-blockers. As dual-source CT scanners have two X-ray tubes, they can fire at different energies resulting in dual-energy scans (Figs. 19 and 20). This is useful in obtaining lung perfusion scans. These help in the detection of pulmonary embolism. Segmental and subsegmental emboli may only be detected by demonstrating a perfusion defect on dual-energy scans (Figs. 21A and B).
Fig. 19: Dual-source CT: New generation of CT scanners with two CT tubes, providing faster scans and higher temporal resolution, of particular value in coronary angiograms as there is no need of beta-blockers, and images are of higher resolution.
Respiratory Misregistration
Conventional CT scanned the chest slice by slice. With every slice, the patient was asked to hold his or her breath, the table then moved to the next table position and 12another slice was obtained. The illustration demonstrates respiratory misregistration. In the first section, due to an increased inspiratory effort the nodule goes below the slice; in the next slice where the nodule should be visualized, it is not, as the patient has taken only a moderate inspiratory effort. This resulted in a lower accuracy for CT in detecting pulmonary nodules (Fig. 22).
Fig. 20: Dual-energy CT: Schematic diagram of a dual-energy CT scan, two tubes firing at different kVs, one at 80 kV and other at 140 kV simultaneously.
Multiplanar reconstructions (MPR) allow reconstruction of images in any plane such as the coronal, sagittal or any oblique plane (Figs. 23A to D). Curved multiplanar reconstructions are also possible where a curved structure such as a vessel or airway may be straightened out; its diameter as well as extent of stenosis may be quantified (Figs. 24 and 25).
Volume-rendering techniques (VRTs) are 3D techniques which provide a rendering of the surface of the organ. These are useful for demonstrating the tracheobronchial tree, as well as vasculature, especially the aorta and coronary arteries. An adaptation of this technique is virtual bronchoscopy. A 3D volume of the tracheobronchial tree is obtained, utilizing a fly-through software. The internal contents of the tracheobronchial tree can be visualized similar to an optical bronchoscopy, the advantages of a virtual bronchoscopy being the ability to demonstrate tracheobronchial stenosis, extrinsic compression, intraluminal masses, foreign bodies or intraluminal extension of extrinsic lesions. Internal measurements of the tracheobronchial tree are also possible (Figs. 26 to 31). This helps to determine the length and size of stents required in planning surgery. The main disadvantage is the inability to obtain biopsies and lavages.
Figs. 21A and B: Dual-energy CT: CT pulmonary angiogram (A) demonstrates bilateral pulmonary emboli, particularly on the right side. Dual-energy CT (B) demonstrates perfusion defects, particularly wedge-shaped defect in right mid-zone. Dual-energy CT provides a CT angiography with a perfusion scan, thereby increasing accuracy in detection of pulmonary embolism, especially subsegmental emboli. CT data in MDCT scanners is acquired as a data volume; this data can be postprocessed to provide a variety of different images(RTPA: Right pulmonary artery; LTPA: Left pulmonary artery).
Maximum Intensity Projections
The disadvantage of thin-section CT is the inability to differentiate small nodules from vessels. On thicker sections it is possible to differentiate these as the branching appearance of vessels is easily appreciated. Maximum intensity projections (MIPs) create a thicker slab of tissue and highlight structures with high intensity such as vessels and nodules. As the slab is thicker, the branching nature of the vessels is well-appreciated, the detection of nodules is much easier (Figs. 32A and B). The ideal thickness is 3 mm; an additional benefit beyond precise detection is an accurate characterization of the location of the nodules in relation to the vessels—whether centrilobular or perivascular. For detection of miliary nodules or pulmonary metastatic deposits this technique is ideal.
Figs. 23A to D: (A and B) Axial CT scans reveal an opacity in the right upper lobe. On the axial scans it is difficult to determine the etiology of the lesion; (C and D) Coronal and sagittal reconstructions demonstrate that the opacity represents fluid in the interlobar fissure. An example of how visualization of an abnormality in multiple planes may help establish the location, extent and etiology of the lesion.
Fig. 24: Curved multiplanar reconstruction (MPR): Curved MPR of aorta demonstrates displaced intimal flap separating true from false lumen, this is also well depicted on the volume rendering technique (VRT) image. The advantage of curved MPR is that a curvilinear structure can be straightened out.
Fig. 25: Curved multiplanar reconstruction (MPR) of pulmonary arteries: Curved MPR demonstrates main pulmonary artery and both right and left pulmonary arteries in one image. Note multiple pulmonary emboli in right and left pulmonary arteries. The advantage of a curved MPR is that the main, right and left pulmonary arteries can be demonstrated in a single image.
Minimum Intensity Projections
In emphysema, bronchiolitis obliterans, the contrast between normal and low-attenuation lung parenchyma may be subtle on inspiratory HRCT. Such subtle regional density differences can be highlighted by minimum intensity projections (MinIPs) (Figs. 33 and 34). MinIPs correlate excellently with pulmonary function tests. Another useful application of MinIP is demonstration of tracheobronchial tree stenosis/occlusions (Fig. 35). A window width of 350–500 HU and a window level of −750 to −900 HU is ideal (Fig. 36).
Fig. 26: Volume rendering technique (VRT) of trachea: Volume-rendered image of the trachea demonstrates an extrinsic mass lesion indenting the right main bronchus, causing significant narrowing of its lumen.
Fig. 27: Volume rendering technique (VRT) tracheobronchial tree. Volume-rendered 3D image of the tracheobronchial tree, no abnormality was detected. Note the visualization of not only the tracheobronchial tree, but also segmental and subsegmental bronchi.
Fig. 28: Volume rendering technique (VRT) tracheobronchial tree: Volume-rendered image of tracheobronchial tree and lung parenchyma. Mass lesion seen in left upper lobe infiltrates the left upper lobe bronchus causing significant narrowing of its lumen.
Fig. 29: Virtual bronchoscopy. Virtual bronchoscopy at the level of the carina reveals marked irregularity and narrowing of the right main bronchus due to a bronchogenic carcinoma.
Figs. 30A to C: Virtual bronchoscopy: (A) Chest X-ray reveals an area of collapse consolidation in right lower zone. (B) Virtual bronchoscopy reveals a well-defined foreign body in the right bronchus. (C) Post procedure, chest X-ray reveals clearing of collapse consolidation.
Window Settings
To visualize body structures the CT images are “windowed”. Two variables are used to select the densities to be viewed: window width and window level. CT density is measured in HU values. Arbitrarily, water is considered as zero and air as −1,000. Window width determines the number of Hounsfield units to be demonstrated. Any densities greater than the upper limit of the window width are displayed as white and any below are displayed as black. Between these two levels all densities are demonstrated in shades of gray.
CONTRAST MEDIA
Intravenous contrast enhancement is required to enhance mediastinal vasculature and separate vessels from mediastinal masses as well as demonstrate enhancement within mass lesions. Ionic contrast mediums which had a significant incidence of mild, moderate as well as severe reactions have now been nearly universally replaced by nonionic contrast media which are far safer. Other than anaphylactic reactions, contrast-induced nephropathy (CIN) is an important adverse event.16
Contrast-induced nephropathy is an exacerbation of previously demonstrated impairment in renal function occurring within 3 days following intravascular administration of contrast medium. This is in the absence of an alternative etiology for the deteriorating renal function. An increase in serum creatinine of more than 0.5 mg/dL or 25% above the baseline serum creatinine is considered the criterion to determine the presence of contrast-induced nephropathy. CIN is by no means uncommon. It is the third most common cause of acute renal failure in patients admitted to hospital. The incidence is estimated to be 1% with intravenous contrast medium, and 2–7% with intra-arterial contrast medium. In diabetics with normal renal function it rises to 16%. In patients with preexisting renal insufficiency prior to receiving contrast media, the incidence of developing CIN is 33%. Diabetics with associated renal insufficiency are at the greatest risk for developing CIN. Other risk factors for developing CIN are dehydration, hypotension, nephrotic syndrome, multiple myeloma, use of higher dose of contrast media, repeated doses of contrast media within 48 hours, use of higher osmolar contrast media and concurrent use of nephrotoxic drugs.
Fig. 31: Virtual bronchoscopy: Virtual bronchoscopy in an individual with carcinoma esophagus. The esophageal mass indents the posterior surface of the trachea as well as infiltrates into the lower trachea. Seen as nodular lesions projecting into the distal aspect of the trachea. This is an excellent non-invasive technique to determine local extension into the tracheobronchial tree.
To minimize the risk of CIN, universal use of nonionic contrast media, a volume expansion and the use of N-acetyl cystine are recommended. If the serum creatinine is greater than 1.4 mg/dL the possibility of another imaging modality should be considered. If a CT with contrast is considered imperative, the risk-benefit ratio should decide the issue.
SUPPORTIVE IMAGING TECHNIQUES
Sonography
This is a very useful imaging modality to demonstrate pleural fluid, especially at the bedside. Fluid manifests as an anechoic area separating the echogenic margin of lung and diaphragm. The contents of pleural fluid can also be estimated depending upon its echogenicity. Pleural fluid is usually anechoic; exudates are also anechoic but usually have internal septae (Fig. 37). Empyemas have echoes within and a hemothorax has echogenic fluid. Sonography is very useful to determine whether a basal opacity on an X-ray is due to pleural fluid or collapse consolidation.
Figs. 32A and B: Maximum intensity projection (MIP): (A) Routine high-resolution computed tomography (HRCT) reveals suspicious small nodules in the lung parenchyma. As the slice thickness is very thin, it is difficult to be certain whether these represent nodules or vessels. (B) MIP demonstrates vessels very well as branching structures. The fine nodules are seen well-separate from the vessels. This technique is very useful in detecting subtle miliary nodules.
Figs. 33A and B: Minimum intensity projection: (A) coronal and (B) axial minimum intensity projections demonstrate ill-defined areas of decreased attenuation in the lung fields representing areas of emphysema.
Fig. 34: Minimum intensity projections: High-resolution computed tomography (HRCT) demonstrates extensive emphysema; narrow window settings demonstrate emphysematous changes very well. Minimum intensity projections demonstrate the involvement extremely well, providing a global view.
Fig. 35: Minimum intensity projection of tracheobronchial tree. The entire tracheobronchial tree is demonstrated from the level of the pharynx. There is a mass lesion at the carina indenting the carina, extending to engulf the right lower lobe bronchus with resultant right lower lobe collapse; there is extension to the left to encase the left main bronchus narrowing and obliterating the left main bronchus. Note right lower lobe collapse with elevation of diaphragm.
Sonography is also an excellent guide for thoracocentesis, reducing the incidence of postaspiration pneumothorax.18
Fig. 37: Ultrasonography (USG) of the chest demonstrates a hypoechoic area representing a pleural effusion.
RADIONUCLIDE IMAGING
The main utility of radionuclide imaging in the respiratory system is in the detection of pulmonary embolism. Ventilation/Perfusion scans also known as V/Q scans simultaneously image the pulmonary blood flow as well as alveolar ventilation.
Perfusion imaging is performed by intravenous injection of microparticles or human protein-labeled technetium (Tc-99). These are trapped in the pulmonary capillaries on their first pass. In patients with a right to left shunt there is a small possibility of the particles occluding systemic vessels with resultant tissue ischemia/necrosis. Similarly, in patients with pulmonary hypertension there is a risk of further occlusion of an already depleted vascular bed. In both these situations the quantum of radiotracer particles injected should be reduced, though there is usually a wide safety margin. The radiotracer has a half-life of 6–8 hours; by 24 hours, most of the activity is only visible in the kidneys and gut. The radiotracer is injected with the patient in the supine position; this limits the effect of gravity on regional blood flow. The particles mix in the heart and consequently are trapped by pulmonary precapillary arterioles. The distribution of the particles is proportional to the regional blood flow. At least six views are obtained—anterior, posterior, right lateral, left lateral, right posterior oblique, left posterior oblique. Additionally, right anterior oblique and left anterior oblique views may be obtained, if required. Even though multiple projections are obtained, perfusion scans underestimate perfusion abnormalities. For example, the medial basal segment of the right lower lobe is completely surrounded by normal lung; consequently, a perfusion defect is not detected on planar perfusion imaging.
All parenchymal diseases cause a reduction in pulmonary blood flow in the affected lung zone. In pulmonary embolism, perfusion is reduced whereas ventilation is preserved. Parenchymal lung diseases cause both a ventilation defect and a perfusion defect. Tc-99m radio-labeled aerosols are used for ventilation scans. Approximately 30 mCi of radiotracer in 3 mL of saline is placed within a nebulizer. Oxygen is forced through the nebulizer at high pressure to form aerosolized droplets which are inhaled by the patient via a mouthpiece. The distribution of the radiotracer is proportional to regional ventilation. Images are obtained in multiple planes similar to perfusion imaging.
In pulmonary embolism there are perfusion defects which may be subsegmental, segmental or even involve an entire lobe or lung (Figs. 38 and 39). The ventilation scan in these patients is normal; thereby there are mismatched defects. In patients who have pulmonary embolism with infarcts there would also be a ventilation defect; however, the ventilation defect is smaller in size than the perfusion defect. Matched defects occur in chronic obstructive pulmonary disease (COPD) as there is a ventilation defect as well as reflex hypoperfusion.19
Fig. 38: Perfusion scan: Perfusions scans demonstrate multiple perfusion defects bilaterally, ventilation scan revealed no abnormality, indicative of ventilation-perfusion mismatch due to pulmonary embolism.
Fig. 39: Perfusion scan: Perfusion scan demonstrates no evidence of perfusion defect. A normal perfusion scan virtually rules out the possibility of a pulmonary embolism.
CT angiography has virtually replaced ventilation-perfusion scans as the modality of choice in the detection of pulmonary embolism (Table 1).
CT angiography has additional advantages. It is available at most institutions round the clock; many institutions may not have nuclear medicine facilities. Clinical mimics of pulmonary embolism such as aortic dissection and pneumonia can be detected by CT. Concurrent venous imaging to detect lower limb/pelvic venous thrombosis is possible with CT angiography, increasing the sensitivity of CT angiography, though at the cost of a higher radiation dose. The requirement to use contrast in CT angiography is a potential disadvantage, especially in individuals with renal impairment or in patients with a history of anaphylaxis to nonionic contrast media.20
Another debatable issue is the quantum of radiation dose in these two modalities. CT angiography has a higher radiation dose ranging from 2.7 mSev to 10.2 mSev depending on the type of scanner and technique used, as compared to radiation dose in V/Q, ranging from 1.2 mSev to 6.8 mSev. The newer dual-source CT scanners utilize a much lower radiation dose, 1.9–2.7 mSev, similar to the radiation dose of V/Q scan. In pregnancy the radiation dose to the fetus in V/Q scans is 0.1–0.8 mGy as compared to CT angiography, 0.01–0.6 mGy. CT angiography is thus preferred over V/Q scan in pregnancy. The dose to maternal breasts is much higher using CT angiography than V/Q scan; however, this can easily be minimized by using bismuth breast shields. In view of these significant advantages with a positive benefit over risk ratio, CT angiography is the preferred modality.
MAGNETIC RESONANCE IMAGING
Magnetic resonance imaging (MRI) is making rapid strides in the evaluation of the abdominal pathologies. Its utility in imaging the brain, spine, musculoskeletal system and pelvis is well established. Evaluation for pulmonary pathologies is limited by a number of factors—the lower proton density of lung, and by cardiac and respiratory motion. These limitations are magnified with increasing field strength; the recent shift to 3T by institutions has not helped. Outside the lung parenchyma, MRI can be a useful alternative to CT, especially when intravenous (IV) contrast is contraindicated such as in patients with renal failure or history of anaphylaxis to contrast media. MRI is useful in the evaluation of the chest wall and mediastinum, to detect mass lesions, as well as demonstrate their local extension (Figs. 40A to D). It is also useful to evaluate the pulmonary arteries, aorta and heart (Fig. 41). IV contrast may be used if serum creatinine is not elevated. Advances are occurring rapidly using newer sequences as well as experimenting with gases for ventilation scans.
POSITRON EMISSION TOMOGRAPHY-COMPUTED TOMOGRAPHY
Positron emission tomography-computed tomography (PET-CT) combines a PET scanner and a CT scanner in one gantry. Images acquired from both devices can be obtained sequentially in the same session and images superimposed in a single image.
Positron emission tomography imaging is based on the fact that metabolically active cells take up glucose. PET-CT fuses anatomical and functional data to provide an excellent correlation of anatomic and metabolic information. A radionuclide-labeled glucose analog Fluorine 18-deoxyglucose (FDG) is taken up by malignant tumors, inflammation/infection and active tissue repair. Sixty minutes after IV FDG, a CT is acquired over approximately 30 seconds, followed by a slow transit of the patient through the bore of the PET. This data acquisition takes 30–40 minutes. Standard uptake values can be calculated from the PET data. This is useful as a value above 2.5 SUV is considered significant. The main utilities of PET-CT in respiratory medicine are in the staging of neoplastic processes, including lymphoma and mesothelioma. It is also useful in the detection of inflammatory processes which are not detected by other imaging modalities (Figs. 42 and 43).
PULMONARY ANGIOGRAPHY
Pulmonary angiography is considered to be the gold standard in the evaluation of pulmonary thromboembolism. This is an invasive procedure with an incidence of 1.5% serious complications. Acute pulmonary emboli are demonstrated as intraluminal filling defects, peripheral occlusion of pulmonary vessels and/or wedge-shaped perfusion defects (Fig. 44). To improve the detection of small pulmonary emboli, dedicated techniques are now available, such as cine angiography, balloon occlusion angiography and superselective angiography.
Many studies using spiral CT angiography have demonstrated a sensitivity and specificity for spiral CT angiogram to match that of pulmonary angiogram. The limitations of both spiral CT angiography and pulmonary angiography are also comparable. It is reported that 10% of spiral CT examinations will be inconclusive compared to 12% for pulmonary angiograms. Three percent of spiral CT angiograms will be technically inadequate compared to 4% for pulmonary angiograms. In view of the less invasiveness and similar sensitivity and specificity of spiral CT angiogram as compared to pulmonary angiograms, spiral CT angiograms have by and large replaced pulmonary angiograms in the detection of pulmonary emboli (Fig. 44).21
Figs. 40A to D: Lipoma: (A) Chest X-ray demonstrates a large homogenous mass in the right lower zone with no shift of the mediastinum; (B) Lateral X-ray demonstrates opacity in an anterior location; (C and D) MRI characterizes the lesion as a lipoma, as the mass is of fat intensity.
BRONCHIAL ARTERY EMBOLIZATION
Bronchial artery embolization is performed to stop massive hemoptysis. The bronchial arteries arise from the intercostobronchial trunk which arises from the aorta at T5. There is a single bronchial artery on the right side and two on the left side. As with most anatomical structures there are variations in the anatomy of the bronchial arteries. These vessels are selectively cannulated and if on angiography, there is extravasation of the dye from an artery or its branch, that vessel is selectively embolized using polyvinyl alcohol or gel foam (Figs. 45A and B). Serious complications following bronchial artery embolization are rare. Patients mainly complain of occasional hemoptysis, transient fever and chest pain.22
Fig. 41: Mediastinal fibrosis: Contrast-enhanced MRI reveals bilateral superior pulmonary vein narrowing due to mediastinal fibrosis.
Fig. 42: Positron emission tomography-computed tomography (PET-CT) examination demonstrates uptake in right upper lobe mass lesion and in right paratracheal lymph node representing primary lung neoplasm with nodal spread.
APPEARANCES OF A NORMAL CHEST RADIOGRAPH
Lung Parenchyma
The lung markings seen on a chest X-ray represent vascular shadows. Occasionally, an accompanying bronchus may be visualized along with the vessels as an air-filled thin tube. Bronchi are best demonstrated end on with the accompanying vessel. In the erect position, the vascular markings are more prominent in the lower zones as the diameters of vessels are larger in the lower zones. In the supine position there is an equalization of the diameters of the vessels in the apices and bases. The vascular markings are a combination of pulmonary arteries and veins. In the upper zones it is not possible to differentiate these as they course similarly in a curvilinear fashion; in the lower zones they may be separated as veins course horizontally and arteries more vertically.
Fig. 43: Positron emission tomography-computed tomography (PET-CT) demonstrates a lesion in the left lingula with multiple bony lesions in sternum, ribs, vertebral body and soft tissue lesions in the spleen and left costal pleura representing a primary lung neoplasm with metastatic deposits.
Fig. 44: Pulmonary angiogram: Selective injection of left pulmonary artery demonstrates multiple filling defects in lower branch pulmonary arteries.
Figs. 45A and B: Bronchial artery angiogram: A patient with active tuberculosis presented with massive hemoptysis. Bronchial arteriogram (A) demonstrates large feeding vessels with extravasation of contrast, indicative of bleeding vessel; (B) The large feeder vessel was occluded with coils to stop the bleeding.
Trachea
The trachea enters the thorax 1–3 cm above the level of the suprasternal notch, the intrathoracic portion is 6–9 cm in length. The trachea contains 16–20 incomplete or horseshoe-shaped cartilage rings giving the trachea a corrugated outline—calcification of the cartilage rings occurs after the age of 40 years. The trachea deviates mildly to the right to accommodate the left-sided aortic arch. With unfolding and ectasia of the aorta the trachea deviates more to the right.
The trachea divides into the two mainstem bronchi at the carina, approximately at the level of the T5. The left main bronchus extends up to twice as far as the right main bronchus before giving off its upper lobe division. The right main bronchus is approximately 25 mm long; the left main bronchus is approximately 50 mm long. In children the angles between the bronchi are symmetric, but in adults the right mainstem bronchus has a steeper angle than the left. The segmental bronchi are not well demonstrated on the X-ray unless seen end on; they are well-demonstrated on CT.
Hilum
The hilar opacity is mainly due to pulmonary arteries and to a lesser extent due to the pulmonary veins. There is a small contribution by adenopathy, fat and bronchial walls. The left hilum is higher in position than the right hilum; this is because the left pulmonary artery arches over the left bronchus and descends posterior to the left bronchus while the right pulmonary artery extends directly inferiorly, anterior to the right bronchus. In 5% of individuals they may be at the same level. If the left hilum is found to be lower than the right hilum, it is useful to evaluate for left lower lobe collapse or a right upper lobe collapse. There is usually a wide variation in size of the hilum in normal individuals. If there is prominence of a hilar shadow, the possibility that this is due to a technical factor such as rotation or scoliosis should be first excluded. The margins of the hilum are usually smooth; if there is a lobulated contour a mass should be suspected.
The pulmonary arteries descend vertically downwards; the size of the descending vessels is relatively equal to a little finger. If the descending pulmonary artery is not visualized on the right side, always check for right lower lobe collapse. A mass lesion at the hilum in contact with 24the hilar vessels will result in a loss of the hilar silhouette. If the hilum is well-visualized through a mass lesion then the mass has not silhouetted the hilum, indicating that the mass is anterior or posterior to the hilum.
Diaphragm
The right dome is normally at the level of the sixth rib anteriorly. The left dome is usually about 1.5–2.5 cm below the right dome. There may be variations in the position of the diaphragm; they may be one interspace higher or lower, they may be at the same level or occasionally, the left is higher than the right but not more than 1 cm. During a respiratory cycle the diaphragm may move between 2.5 cm and 8.0 cm.
Nipples
These may be visualized as bilaterally symmetric dense well-defined spherical shadows with a sharp and a non-sharp margin (Fig. 46). If they are asymmetric they may be mistaken for a pulmonary nodule (Fig. 47). To clarify whether a shadow is a nipple or a pulmonary nodule, a marker may be placed on the nipple (Fig. 48), or in a female the breasts are manually elevated. If a nipple casts a shadow, the marker will be on the opacity; if the breasts have been elevated, the nipple will move up, the pulmonary nodule will remain in the same location.
Fig. 46: PA view of the chest demonstrates bilaterally symmetric dense well-defined rounded shadows with a sharp and a non sharp margin in the lower zones. These represent bilateral nipple shadows.
Fissures
Major fissures are present bilaterally and separate the upper from the lower lobes. The fissures run obliquely forward and downward crossing the hilum. They arise from the fifth thoracic vertebrae and end at the diaphragm approximately 3 cm behind the sternum. On a lateral radiograph, often parts or the whole of a fissure may be visualized. On a frontal radiograph the major fissures are rarely visualized.
A minor fissure is present on the right side dividing the upper and middle lobes (Fig. 49). The fissure extends from the hilum anteriorly and laterally. On a frontal radiograph it is seen in nearly 50% of individuals, contacting the lateral chest wall at or near the axillary portion of the sixth rib. It is also seen on the lateral chest radiograph in approximately 50% of individuals extending anteriorly from the hilum.
Azygous Lobe Fissure
This fissure develops due to failure of the azygous vein to migrate from the chest wall through the lung into its location at the tracheobronchial angle. The invaginated visceral and parietal pleura persist to form a fissure, at the bottom of which lies the azygous vein (Fig. 50). This may be occasionally seen on the left side with the left superior intercostal vein occupying the bottom of the fissure.
Fig. 47: Nipple shadow: PA view of the chest demonstrates a well-defined nodular lesion in the left lower zone, this may represent a nipple shadow or a nodular lesion.
Fig. 48: Nipple shadow: PA view of the chest shows a nipple marker coinciding with nodular lesion indicating that the shadow was a nipple.
Fig. 49: Minor fissure: Lateral view of chest reveals minor fissure as a horizontal line extending from the hilum anteriorly.
Mediastinum
The left mediastinal border above the level of the aortic arch is constituted by the left subclavian and carotid arteries. The left wall of the trachea is not visualized as it is in contact with the vessels. From the level of the aortic arch inferiorly the border is constituted by the aorta, main pulmonary artery, and heart (Fig. 51A). A small nodular well-defined opacity may be seen just below the aortic knuckle; this represents the left superior intercostal vein as it arches around the aorta before entering the left brachiocephalic vein. This should not be misinterpreted for a lymph node. The left border of the descending aorta is visualized through the main pulmonary artery and heart down to the aortic hiatus in the diaphragm.
The right mediastinal border is formed by the right brachiocephalic vein, SVC and right atrium. The right paratracheal stripe consisting of the tracheal wall and adjacent fat is seen through the brachiocephalic vein and SVC as the lung is in contact with the posterior wall of the trachea. The presence of this stripe excludes the possibility of a paratracheal mass lesion. This stripe is visible in two-thirds of individuals. At the lower end of this stripe is the azygous vein in the tracheobronchial angle.
Lateral View
On the lateral view there are three zones to observe. The vertebrae, each thoracic vertebra appears more translucent than the one above. The cardiac shadow is visualized as a homogenous opacity. The retrosternal space is well-aerated, any alteration in this pattern indicates an abnormality (Fig. 51B).
The two domes of the diaphragm overlap each other. It is fairly easy to separate the two. The right is visualized all the way from front to back. The left is only seen from the costophrenic recess posteriorly to the point where it meets the cardiac silhouette. Anterior to this point, it is not visualized as the lung/diaphragm interface is obliterated by the cardiac silhouette. Occasionally, it may be difficult to separate the two domes as they totally overlap. If the diaphragm silhouette is lost, an abnormality in the lower lobes should be suspected.26
It is difficult to differentiate the right from the left hilum as they totally overlap each other. The right pulmonary artery traverses anterior to the right bronchus and the left pulmonary artery hooks over and is posterior to the left bronchus. The bronchi are seen end on, the higher ring is the right and the lower the left bronchus. If the hilum is considerably prominent, large in size and lobulated in contour, a hilar mass should be suspected.
The mediastinal opacity is occupied by the heart. The portion behind the hila is the left atrium; the posterior border below the hilum is constituted by the left ventricle, the anterior surface of the shadow constitutes the right ventricle. If the cardiac silhouette does not appear to be homogenous, the possibility of a superimposed pulmonary pathology may be considered.
The aortic arch is well-visualized with the brachiocephalic artery often being visualized arising and extending anterior to the trachea. The left and right brachiocephalic veins are often visualized as an extrapleural bulge beneath the manubrium sternum and should not be mistaken for a sternal/chest wall mass. Similarly, in the inferior part of the chest, the anterior paracardiac fat may simulate a mass lesion posterior to the chest wall. This is because the two lungs do not meet in the midline, the heart and paracardiac fat being interposed.
The horizontal fissure is seen on most lateral chest X-rays. Oblique fissures appear like the blades of a propeller. The right oblique fissure at its most posterior position lies 4–5 cm behind the sternum, the left oblique is positioned slightly more superior (Figs. 49 and 52).
The IVC may be visible as a well-defined vertical line which meets the posterior and inferior aspect of the heart.
Interpreting Chest Radiographs
A systematic approach to the interpretation of a chest radiograph is very important. This is particularly so when an obvious abnormality is present. The PA view of the chest is printed as if the patient is facing the interpreter, with the right side facing the interpreter's left side. It is important first to evaluate the radiograph from a technical quality perspective. Important factors to evaluate are (Fig. 53).
Exposure: In a well-exposed radiograph the dorsal intervertebral disks should just be visible through the cardiac shadow. In an overexposed X-ray the vertebral bodies are well-outlined, the lung fields are darkened. The risk of overexposure is that parenchymal lung lesions may not be visible, though the retrocardiac regions are well-visualized. In an underexposed X-ray the mediastinum appears brighter than usual; also, there is no visualization of the dorsal intervertebral disks.27
Fig. 52: Lateral view of chest demonstrates the normal oblique fissures extending from the fifth dorsal vertebra posteriorly to the cardiophrenic angle crossing the hilum.
Fig. 53: Normal chest X-ray: A perfectly exposed X-ray as the dorsal interspaces are just visualized. There is no rotation as the clavicles are equidistant from the cervical spinous processes; the inspiratory effort is adequate, as the anterior ends of the sixth ribs are at the mid-diaphragmatic level.
Fig. 54: Tracheal deviation: PA view of the chest demonstrates tracheal deviation as a result of mass lesion in the neck arising from the thyroid causing significant displacement and compression to the left.
Inspiratory effort: Chest X-rays are obtained in deep inspiration; the midpoint of the right hemidiaphragm should be at the anterior end of the sixth rib.
Rotation: The medial ends of the clavicle should be equidistant from the spinous processes of the cervical vertebrae.
Evaluation of Different Structures on a Chest X-ray
Start with the trachea, note its position, mass effect, deviation and caliber (Fig. 54). Then evaluate the mediastinal silhouette, the right border, then the left border from above downwards. Note any loss of silhouette, cardiomegaly. Next evaluate the hilum, again one at a time, position of hilum, right in relation to left, equality in size and density. If a hilum appears larger or denser, a lateral view is very useful to confirm or exclude a mass lesion. For example, if the right hilum is prominent, presence of a mass will be seen on the lateral view as being posterior to the trachea, since the right pulmonary artery is anterior to the trachea. For the left, it is converse as the left pulmonary artery is posterior to the trachea. The lower lobe pulmonary vessels are well-visualized on a radiograph. Absence of this leash of vessels on a well-centered X-ray is a useful clue to lobar collapse. Evaluate the diaphragms for position, 28contour any loss of silhouette. Now evaluate the lungs. A useful method is to examine them in a zigzag fashion from below upward. Evaluate each zone from a size, transradiancy perspective. The position of the horizontal fissure if visible should be noted, as this may also be a clue toward lobar collapse. Finally, evaluate the ribs and chest wall. Before concluding, pitfall areas where abnormalities may lurk should be evaluated. These include the central mediastinum, lungs behind the diaphragm and heart, lung apices, lung and pleura along the inner surface of the chest wall.
CT Anatomy of Normal Mediastinum and the Lung
The normal mediastinal structures, heart, blood vessels, tracheobronchial tree, esophagus are always identified on cross-sectional imaging (Figs. 55A to D).
MEDIASTINAL VASCULATURE
The vertical portions of the ascending and descending aorta are well-visualized as spherical tubes, the diameter of the ascending aorta is 3.5 cm and of the descending aorta 2.5 cm. The descending aorta descends to the left of the vertebrae and then takes a more midline course to enter the abdomen anterior to the vertebrae. The arch of the aorta is seen in cross-section traversing from the ascending aorta to the descending aorta right to left, anterior to the trachea. Above the level of the aortic arch the great vessels are well-visualized in an arc anterior and to the left of the trachea. The left common carotid artery lies to the left of the trachea, left subclavian artery to the left or posterior to the trachea. The brachiocephalic artery is larger than the left common carotid and left subclavian artery. In 0.5% of the population the right subclavian artery has an anomalous origin arising distal to the left 29subclavian artery. It courses from left to right, posterior to the esophagus at the level of the aortic arch; it then ascends in the right paravertebral space to the root of the neck. The brachiocephalic in this situation becomes the right common carotid artery, with a size similar to that of the left common carotid artery. A barium swallow will demonstrate the posterior indentation of the esophagus caused by the anomalous right subclavian artery (Figs. 56A and B). Pressure on the esophagus by this artery may cause dysphagia.
The right subclavian and jugular vein unite to form the right brachiocephalic vein, which descends vertically in the mediastinum to continue as the superior vena cava (SVC) following its union with the left brachiocephalic vein. The SVC is usually half to two-thirds the diameter of the ascending aorta. The left brachiocephalic vein courses through the mediastinum from the left to the right, anterior to the great vessels. In 0.3–0.5% of the population a left SVC is present. This is more commonly seen in individuals with congenital heart disease. The left SVC is formed by the union of the left jugular and subclavian veins, and descends vertically in the left mediastinum to open into the coronary sinus. Due to the increased blood flow, the coronary sinus is increased in size in this situation.
The azygous vein ascends from the diaphragm in the prevertebral space to the right or posterior to the esophagus; it arches over the right main bronchus to open into the posterior wall of the SVC. In 1% of individuals the azygous penetrates the lung as it arches over the bronchus resulting in an azygous lobe. Occasionally, the IVC does not develop, the azygous becomes the conduit to drain blood back to the heart, and is then termed as the azygous continuation of the IVC. The hepatic veins then open directly into the right atrium and the azygous vein dilates. Variants in vascular anatomy such as left-sided SVC, azygous continuation of IVC, left superior intercostal vein, may be mistaken for a mass lesion or adenopathy on an unenhanced scan or chest X-ray. The hemiazygous and accessory hemiazygous veins ascend posterior to the descending aorta. The accessory hemiazygous may cross to the right to open into the azygous or open into the left superior intercostal vein. The left superior intercostal vein is a small vein, which arches around the aorta at the level of the arch and descending aorta to open into the left brachiocephalic vein. It is only occasionally identified on X-ray/CT.
Pulmonary Artery
The main pulmonary artery runs backward and upward obliquely to the left of the ascending aorta (Fig. 57). The right branch travels horizontally to the right between the ascending aorta and tracheobronchial tree; it then descends anterior to the right bronchus. The left branch curves upward and posteriorly over the left main bronchus and descends posterior to the left main bronchus. The main pulmonary artery diameter is approximately 2.8 cm. A main pulmonary artery/aortic ratio greater than 1 indicates pulmonary hypertension. The pulmonary artery branches are two-thirds the diameter of the main pulmonary artery.
Thymus
The thymus is best visualized in a section at the level of the aortic arch, anterior to the aorta and pulmonary artery, inferior to the left brachiocephalic vein, and superior to the right pulmonary artery (Fig. 58). Till puberty the thymus occupies most of the anterior mediastinum with a density of soft tissue. After puberty the gland starts to get replaced by fatty tissue; by 40 the gland is not visualized as it is replaced by fatty tissue. In individuals on chemotherapy the thymus may be visualized in adults, termed as thymic rebound.
Figs. 56A and B: Aberrant right subclavian artery: CECT chest demonstrates right subclavian artery arising distal to the left subclavian and courses from left to right, posterior to the trachea and esophagus.
Fig. 58: Thymus: CT scan chest demonstrates a normal thymus. Seen as a triangular well-defined soft-tissue density with internal fat densities.
Mediastinal Lymph Nodes
Ninety-five percent of normal mediastinal lymph nodes measure less than 10 mm in short axis diameter. Mediastinal lymph nodes are chiefly located in the paratracheal, prevascular, pretracheal, subcarinal and aortopulmonary regions.
Trachea
In cross-section, the trachea is round or oval with a flattened posterior margin formed by the fibromuscular membrane. On expiration there is a significant change in the diameter of the trachea. This is due to forward motion of the posterior wall of the trachea; there is consequent reduction in the AP diameter of the trachea.
The trachea divides into the two mainstem bronchi at the carina, approximately at the level of T5. The left main bronchus extends up to twice as far as the right main bronchus before giving off its upper lobe division. The right main bronchus is approximately 25 mm long, the left main bronchus is approximately 50 mm long. In children the angles between the bronchi are symmetric, but in adults the right mainstem bronchus has a steeper angle than the left. The segmental bronchi are well-demonstrated on CT.
The right upper lobe bronchus divides into the right apical, posterior and anterior segmental upper lobe bronchi (Fig. 59).
The right lower lobe bronchus divides into right lower lobe superior segment bronchus, (middle lobe medial and lateral) segmental bronchi and anterior, lateral, posterior and medial lower lobe segmental bronchi.
On the left side the upper lobe bronchus divides into apicoposterior and anterior upper lobe segmental bronchi as well as the lingular superior and inferior segmental bronchi. The left lower lobe bronchus divides into superior segmental and anterior medial basal, posterior and lateral basal segmental bronchi.
VARIATIONS
- Common origin of right upper/middle bronchus
- Tracheal bronchus—either a segmental or the entire right upper lobe bronchus arises from the trachea; there may be a displaced or supernumerary bronchus (Figs. 60A and B)31Fig. 59: Anatomy of tracheobronchial tree: AP view of branches of airways beyond the segmental bronchi.
- Accessory cardiac bronchus arising from the medial aspect of the right main bronchus, usually blind-ended but may supply a small lobule
- Lateral inversion of right and left-sided airways in “situs inversus”
- Situs ambiguus—airway has either bilateral right-sided or left-sided configuration
- Bridging bronchus—right lower lobe bronchus arises from the left main bronchus, crosses the mediastinum to reach the right lung.
The segmental bronchi divide progressively into smaller airways till after 6–20 divisions become bronchioles which further divide till terminal bronchioles. These are the last of the conducting airways. Beyond the terminal bronchioles lie the gas exchange units, the acini. The anatomy of the secondary lobule is discussed under the HRCT section of this chapter.
Diaphragm
The diaphragm consists of a large dome-shaped central tendon with radiating striated muscle attached to the xiphisternum and to the 7th to 12th ribs. The two crura arise from the first three lumbar vertebrae forming the lateral walls of the aortic hiatus. The aorta, azygous, hemiazygous veins and thoracic duct pass through this hiatus. There are two more hiatuses anterior to the aortic hiatus in the diaphragm—the esophageal hiatus through which pass the esophagus, esophageal arteries and vagus nerve, and the hiatus for the IVC.32
Fissures
The major fissures are well-visualized as thin white lines traversing from posterior to anterior and from cephalad to caudal. The minor fissure lies in the plane of the scanning, therefore, the fissure per se is not visualized. Its position can be inferred as there is an avascular zone in the subpleural regions (Figs. 61A and B).
An avascular zone in the right middle lobe points to the site of the minor fissure.
Interstitium: Normal HRCT Anatomy
The lung is supported by a network of connective tissue fibers known as the interstitium of the lung. The interstitium is divided into three components, the axial interstitium, the peripheral interstitium and the intralobular interstitium which communicates between the axial and peripheral interstitium. The peripheral interstitium is located beneath the visceral pleura; it envelops the lung like a fibrous sac from which connective tissue septae penetrate into the lung parenchyma. Between each interlobular septa lies a secondary lobule. The axial interstitium consists of the peribronchovascular interstitium which is strong connective tissue encasing the central bronchi and arteries. This interstitium extends from the level of the pulmonary hila to the periphery of the lung, encasing the centrilobular arteries and bronchioles in the secondary lobules (Fig. 62). The secondary lobule is the smallest unit of lung structure varying in size from 1 cm to 2.5 cm containing 10–12 acini. It is polygonal in shape, with its apex pointing to the hilum and base toward the pleural surface. Each is supplied by a small bronchiole and pulmonary arterial branch—centrilobular artery. This is visualized on HRCT sections as a small dot; however, the bronchus is not visualized as it is below the resolution of present-day HRCT scans (Fig. 63). The interlobular septae which marginate the secondary lobules contain pulmonary veins and lymphatics. At the level of the secondary lobule all three connective tissue systems are present.
Anatomy of Bronchi and Pulmonary Vessels
The bronchi and pulmonary arteries run parallel to each other. Their appearances depend upon the scan plane they are sectioned in. If the scan plane is perpendicular to their course they will appear as well-defined round structures adjacent to each other. If sectioned in the same plane, they will appear as tubular structures running parallel to each other. The artery is seen as a well-defined round homogenous white structure. The accompanying bronchus has a thin well-defined wall with a lucent center containing air resembling a pipe with air in its lumen. The outer surface of these structures is smooth. The inner diameter of the bronchus to accompanying arterial diameter is usually 0.65/0.7:1. A bronchoarterial ratio of 1:1 is considered normal; greater than this is considered as bronchiectasis (Fig. 64). An increased bronchoarterial ratio greater than 1 may be seen in patients who reside at a high altitude; the mild hypoxemia induces mild bronchial dilatation as well as vasoconstriction, resulting in an altered bronchoarterial ratio. Bronchi are visualized till the peripheral 2 cm of the lung. It is rare to see normal bronchi in the peripheral 2 cm of the lung. Normal bronchi may extend till 1 cm of the mediastinal surface.
Figs. 61A and B: Fissures: (A) Axial and (B) sagittal reconstructions demonstrate major interlobar fissures. The minor fissure is not seen on the axial scan as it is in the same plane as the slices. The position of this fissure is inferred on the axial images as a zone of avascularity.
Fig. 62: Normal anatomy of interstitium: Schematic diagram demonstrates peribronchovascular interstitium in green extending to the secondary lobules. In secondary lobules it forms centrilobular interstitium (blue). The periphery of the secondary lobule is bounded by the interlobular interstitium (yellow). Within the secondary lobule the fine bands in brown represent the intralobular interstitium.
Fig. 63: Anatomy of secondary lobule—schematic diagram demonstrates polygonal secondary lobules. The secondary lobules share common walls with lymphatics and pulmonary veins in their walls. The center of the secondary lobule contains the centrilobular artery and bronchus.
RADIOGRAPHIC PATTERNS OF DISEASE PROCESSES
The most important aspects of imaging are to determine the anatomic location of a lesion, whether in the lungs, mediastinum, pleura or chest wall as well as the nature of the lesion. The most common abnormality visualized on a radiograph is a pulmonary opacity (Table 2). An opacity is often ill-defined and is more opaque than the surrounding lung. It is useful to categorize the patterns of pulmonary opacities as it helps to narrow the differential diagnostic possibilities.
Consolidation/Air-space Opacities
Air-space opacities represent one or more ill-defined areas of increased density in the lung parenchyma. When they abut the pleura they have a sharp margin. Vascular shadows are obscured by the air-space opacity, as the air-filled dark lung does not contrast with the soft tissue density of vessels.
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Similarly, intrapulmonary airways are rarely visible on chest X-rays. With air-space opacification the air in the airways contrasts with the air-space opacity, so that the airways become visible. This appearance is known as an air bronchogram sign. It also confirms the opacity is intrapulmonary. Another useful sign is the silhouette sign. The borders of the heart and domes of the diaphragm are well-visualized as they are contrasted by the interface with the dark lung. If a pulmonary opacity is in contact with the margins of the heart/diaphragm there is an interruption of the margins resulting in a loss of silhouette. This helps in detecting and localizing the abnormality. Conversely, presence of an opacity with preservations of the silhouette would indicate that the pulmonary abnormality is not in contact with the heart border or diaphragmatic surface. Cavitation may occur within air-space opacities. The cavity results following expulsion or drainage of necrotic contents via the bronchial tree. A gas-filled space with or without an air-fluid level is seen in the air-space opacity. CT is more sensitive in detection of air-space opacities; it may detect opacities even when the chest X-ray is normal. The causes of air-space opacities are numerous; any pathological process which results in filling of alveoli will result in an air-space opacity. The differential diagnosis of air-space opacities includes pneumonia, atelectasis, infarction, hemorrhage, neoplasm, and edema (Figs. 65 to 74).
Important points which may help in the differential diagnosis of air-space opacities:
- Opacities over half a lobe with no loss of lung volume are virtually diagnostic of pneumonia.
- Widespread pneumonia is invariably accompanied by cough and fever.
- Lobar consolidation with lobar expansion causing bulging of the fissure is most often seen in infection due to Klebsiella pneumoniae. It is also occasionally seen following infection with Streptococcus pneumoniae, staphylococcus, and other gram-negative bacteria.
- Neoplastic obstruction of a lobar bronchus usually causes some degree of atelectasis. However, bronchoalveolar carcinoma and lymphoma may appear as lobar pneumonia with no evidence of atelectasis, as the neoplastic process spreads in the alveolar spaces without involvement of the bronchi.
- Aspiration should be suspected with a history of alcoholism, seizures, unconscious state. Air-space opacities with evidence of associated loss of volume are seen in patients with aspiration pneumonia. Air-space opacities with well-marked hemoptysis may occur in intrapulmonary hemorrhage.
- Cavitation within a consolidated lobe could represent tuberculosis or a necrotizing pneumonia (Fig. 72). The latter is commonly caused by Klebsiella (Kl.) pneumoniae, Pseudomonas (Ps.) aeruginosa, Staphylococcus aureus and anaerobic bacteria. Cavitation could also arise in relation to noninfectious etiologies such as Wegener's granulomatosis, other forms of vasculitis and in neoplasms (Figs. 75 to 77).
- Lucencies seen within an air-space opacity could be due to overlying uninvolved lung, areas of centrilobular emphysema within the abnormal lung, necrosis of tissue with cavitation, pneumatoceles.
- Rib or vertebral body destruction in the absence of a mass points to a metastatic lesion, though tuberculosis or fungal infections can also present similarly, as destructive bone lesions.
Fig. 65: Right upper lobe pneumonia: PA view of the chest demonstrates a consolidation in the right upper zone with loss of silhouette of right aortic border. Note there is no loss of volume and silhouette of right cardiac border. There is no shift of mediastinal structures. This is a feature of pneumonia.
Fig. 66: Right middle lobe pneumonia: PA view of the chest demonstrates ill-defined air space opacities in the right lower zone which has an ill-defined inferior margin and sharp superior margin. Air space opacities are ill-defined, however, when they about the pleura in this case, they have a sharp margin. Note there is loss of silhouette of right cardiac border but silhouette of right aortic border is preserved.
Fig. 67: Right upper and middle lobe pneumonia: Large area of consolidation is seen in the right lung with loss of silhouettes of both right cardiac and right aortic borders and with subtle bronchograms within; note there is no evidence of loss of volume or mediastinal shift.
Fig. 68: Right lower lobe pneumonia. PA view of the chest demonstrates an ill-defined consolidation in the right lower zone preserving silhouette with cardiac margin but loss of silhouette with diaphragm.
Fig. 69: Right lower lobe pneumonia. PA view of the chest demonstrates an ill-defined area of consolidation in the right lower zone; there is no loss of the silhouette of the cardiac as well as diaphragmatic surface indicating this consolidation is not in contact with either the diaphragm or cardiac surface.
Fig. 70: Right upper lobe pneumonia with collapse consolidation: PA view of the chest reveals a triangular shaped consolidation with air bronchograms in the right upper zone associated with elevation of the minor fissure and mild deviation of trachea to the right representing a right upper lobe consolidation with partial collapse.
Fig. 71: Consolidation. CT chest demonstrates a large consolidation in the right middle lobe with an air bronchogram pattern. There is an associated pleural effusion.
Fig. 72: Consolidation with cavitation: PA view of the chest reveals ill-defined area of consolidation with cavitation in the right upper zone. Causative organism—Staphylococcus aureus.
Fig. 73: Pulmonary infarct. PA view of the chest reveals a wedge-shaped area of consolidation in the right lower zone abutting the pleura. The appearance of a wedge-shaped consolidation should raise the possibility of a pulmonary infarct.
BAT WING PATTERN OF PULMONARY OPACITY
This is a term used to describe diffuse parahilar opacities which have ill-defined margins. These may be symmetric or asymmetric, being larger on one side. The most common cause for this opacity is pulmonary edema, especially if associated with cardiomegaly/pleural effusion/Kerly A/B lines. Another feature of pulmonary edema is the rapid appearance and disappearance of opacities (Figs. 78 and 79). Other conditions which may present with this type of opacities are aspiration pneumonias, and inhalation exposure to noxious gases. Immunocompromised patients, especially Pneumocystis jirovecii pneumonia can have a similar appearance (Fig. 80). Bat wing opacities unchanged over a long period of time with nonspecific symptoms, suggest the possibility of alveolar proteinosis (Fig. 81) or a neoplastic process such as lymphangitic carcinomatosis.
Peripheral air-space consolidations are considered as a photographic negative of pulmonary edema as the opacities are in the lung periphery. Especially when present in the upper zones the most common possibility is chronic eosinophilic pneumonia.37
Figs. 74A and B: (A) X-ray chest in a febrile patient demonstrates no abnormality; (B) CT chest reveals multiple bilateral cavitating and subpleural nodular lesions. CT is more sensitive than chest X-rays in detection of focal lesions, as well as demonstrating internal morphology of focal lesions, such as cavitation, necrosis, calcification, and air bronchograms.
Fig. 75: Lung abscess: PA view of chest reveals thick-walled cavitatory lesions with air-fluid level in the left upper zone as well as in the right lower zone. These lesions represent lung abscesses.
Fig. 76: Wegener's granulomatosis: PA view of the chest X-ray reveals multiple well-defined rounded nodular lesions in both the mid and lower zones. Some appear solid, some cavitatory and some with air-fluid levels. c-ANCA was strongly positive in this patient confirming Wegener's granulomatosis.
If the opacities are not predominantly in the upper zones, the possibilities include cryptogenic organizing pneumonia, viral pneumonia or a mycoplasmal pneumonia. Fleeting shadows, shadows which come and go, or appear in different regions of the lungs, raise the possibilities of pulmonary edema, eosinophilic pneumonia, asthma, ABPA and vasculitis (Figs. 82A to D).
White-out lungs are typical for acute respiratory distress syndrome (ARDS), especially with associated air bronchograms (Fig. 83). Sarcoid may present with patchy opacities in the lungs which may be spherical and have associated mediastinal adenopathy.38
COLLAPSE/ATELECTASIS
Often the words collapse and consolidation are used interchangeably. Consolidation is essentially due to replacement of alveolar air by an exudate, transudate or cellular debris resulting in a homogenous opacity with no loss of volume. Atelectasis or its synonym “collapse” indicates volume loss. The atelectatic/collapsed segment or lobe of the lung will therefore demonstrate a homogenous opacity with accompanying volume loss. Atelectasis is caused by bronchial obstruction which is either due to an intrabronchial pathology, foreign body or extrinsic compression of the bronchus (Figs. 84A and B). Compression atelectasis can be due to compression of adjacent lung by tumor, bulla, pneumothorax or pleural effusion.
Fig. 77: Tuberculosis: PA view of the chest reveals ill-defined fibrocavitatory lesion in left upper and mid zones as well as patchy nodular consolidation with cavitation in right mid zone. Incidentally note is dextrocradia. The presence of upper/mid zone cavitation in the Indian subcontinent favors the diagnosis of tuberculosis.
Cicatrization Atelectasis
Following resolution of an inflammatory/infective process there may be localized atelectasis. This is due to either direct destruction of lung parenchyma or fibrotic contraction, termed as cicatrization fibrosis. This is commonly seen in tuberculosis, radiation fibrosis, interstitial pulmonary fibrosis, and bronchostenosis (Figs. 85 and 86).
Pulmonary fibrosis can cause significant loss of volume due to fibrotic contraction of lung parenchyma.
Plate or Discoid Atelectasis
This is a form of atelectasis, which is due to hypoventilation, leading to alveolar collapse. The alveoli in the lung bases as well as posterior aspects of the lung fields are the most prone to collapse. These appear as linear plate or disk-like opacities in the lower zones, occasionally extending across the whole breadth of the lower lobe (Fig. 87). As these are due to hypoventilation they are seen mainly in hospitalized patients, post general anesthesia and in patients with an acute abdomen where the diaphragm is splinted, resulting in reduced respiratory excursion.
Figs. 78A and B: Pulmonary edema. AP view portable X-ray. (A) demonstrates ill-defined fluffy opacities in both lung fields; within a few hours, on a follow-up X-ray; (B) the opacities regressed.
Figs. 79A and B: Pulmonary edema. Portable chest X-rays in a patient with left centralvenous catheter in situ. X-ray (A) reveals an ill-defined opacity in the right lower zone; (B) subsequent X-ray a few hours later reveals increasing opacities in the both lungs. This feature of rapidly appearing and disappearing shadows is highly suggestive of pulmonary edema.
Fig. 80: Pneumocystis jirovecii pneumonia (PCP): Immunocompromised patient with diffuse ill-defined air-space opacities. In the setting of immunocompromise, the most likely etiology would be Pneumocystis jirovecii pneumonia.
Fig. 81: Alveolar proteinosis. PA view of the chest demonstrates ill-defined airspace opacities in both lung fields sparing the right upper lobe. Intercostal drainage (ICD) seen in situ following thoracoscopic biopsy which revealed pulmonary alveolar proteinosis. Patient presented with cough, fever and mild dyspnea over 3 months. This is an example of bilateral white-out lungs with subacute to chronic symptoms.
Figs. 82A to D: Fleeting opacities. Serial high-resolution computed tomography (HRCT) chest performed in 30-year-old patient with blood eosinophilia reveal (A) multiple ill-defined areas of consolidation seen in right upper lobe on 30/8/13. (B) resolution of previously seen consolidation with reappearance of lesions of less severe extent on 25/11/13. (C) ill-defined areas of peribronchovascular and subpleural consolidation with air bronchogram and adjacent areas of ground-glass attenuation involving right upper and middle lobes on 17/09/18. (D) regression in the right lung consolidation on 27/09/18. CT-guided biopsy performed on 30/08/13 revealed Churg-Strauss syndrome with vasculitis.
Lobar Collapse/Atelectasis
The imaging features of lobar collapse are a pulmonary opacity with evidence of volume loss. The pulmonary opacity is due to loss of air in the alveoli of the collapsed segment/lobe and/or due to retained mucous secretions. The loss of volume is demonstrated by a shift of normal structures such as the hilum, interlobar fissures, mediastinum, with crowding of ribs, and of bronchovascular structures and elevation of the dome of the diaphragm. There is hypertranslucency of the normal ipsilateral lung due to compensatory overexpansion, with pulmonary vessels within it being more widely separated when compared to the opposite lung. It is important to note that when there is severe/total collapse of a lobe it may not always be possible to demonstrate the shadow of the lobar collapse on an X-ray, as the signs are too subtle. A shift of the hilum, fissure or the mediastinum should always suggest an underlying atelectasis.41
Figs. 84A and B: Obstructive atelectasis. Chest X-ray (A) demonstrates an opaque left hemithorax with a shift of the mediastinum to the left indicative collapse of left lung. The most likely cause would be an obstruction to the left main bronchus. Bronchoscopy revealed a mucus plug obstructing the left main bronchus; (B) after aspirating the mucus plug the lung expanded with few residual opacities.
Fig. 85: Fibrocalcareous tuberculosis (TB). PA view of the chest reveals bilateral apical fibrotic lesions with calcified nodular lesions in both apices. These features of reticular opacities with calcified nodules and loss of volume are typical of old healed tuberculosis.
GOLDEN S-SIGN
When there is obstructive collapse by a central neoplasm with consequent peripheral collapse—the shape of the fissure assumes an “S” shape, as the fissure is concave peripherally and convex centrally.
Fig. 86: Radiation fibrosis. PA view of the chest reveals an ill-defined opacity in the right apical region with associated loss of volume, shift of trachea to the right, with the right hilum pulled up. Patient had received radiation for cancer of the esophagus with resultant radiation fibrosis.
Lower Lobe Atelectasis
The appearances of right and left lower lobe atelectasis are similar. The lobes collapse posteromedially in the lower part of the chest. Left lower lobe atelectasis is often difficult to detect as the collapsed lobe is hidden 42by the cardiac silhouette (Fig. 88). A penetrated X-ray would reveal the opacity of the collapsed lower lobe (Figs. 89A and B). As the lobe collapses posteromedially, the oblique fissure rotates backward and medially, the upper portion of the oblique fissure swinging downward. The collapsed lobe is seen as a triangular opacity lying against the mediastinum. On the right side the medial aspect of the diaphragm is obscured, the lateral margin of the adjacent vertebrae is effaced, the ipsilateral hilum is depressed and the ipsilateral lower lobe pulmonary artery is not visualized (Figs. 90 and 91). Lower lobe atelectasis is better demonstrated on a lateral view (Fig. 92). The lung collapses posteriorly, therefore is seen as an opacity overlying the vertebrae. Normally, the vertebrae on a lateral view demonstrate increasing transradiancy of the lower dorsal vertebrae. On CT the collapsed lobe is seen plastered along the vertebral column in a posteromedial location. The major fissure rotates to lie obliquely.
Fig. 87: Plate atelectasis. PA view of the chest in a postoperative patient reveals a central line in situ. Plate atelectasis is seen in the left lower zone with evidence of loss of volume as evidenced by elevation of left dome of diaphragm.
Fig. 88: Lower lobe collapse: Schematic diagram of left lower lobe collapse. The lower lobe collapses behind the cardiac silhouette on the PA view. The diaphragm is mildly elevated and the left lung volume is reduced. The diagram of the lateral view demonstrates the posterior collapse of the lower lobe, and a shift of the oblique fissure posteriorly.
Figs. 89A and B: Left lower lobe collapse. (A) PA view of the chest demonstrates a homogenous opacity with a smooth margin behind the cardiac silhouette due to the collapse of left lower lobe. Note the evidence of volume loss in the left lung. (B) Lateral view of the chest demonstrates obscuration of the density of lower dorsal vertebral bodies due to the posteriorly collapsed left lower lobe.
Fig. 90: Right lower lobe collapse: Schematic diagram—PA view demonstrates collapsed segment along the right heart border abutting the diaphragm. There is elevation of the right dome of diaphragm, loss of volume in the right lung and a shift of mediastinum to the right. Lateral view reveals the collapsed lung posteriorly with shift of the oblique fissure posteriorly.
Fig. 91: Right lower lobe collapse. PA view of the chest demonstrates a homogenous opacity in the right paracardiac region with loss of the cardiac and diaphragmatic silhouette. There is evidence of loss of volume, as the right dome of the diaphragm is elevated and the right lung is smaller in size as compared to the left.
Fig. 92: Right lower lobe collapse. Lateral view demonstrates an ill-defined haze overlying the lower dorsal vertebrae. There is loss of normal increasing translucency of lower dorsal vertebrae due to the collapsed right lower lobe opacity overlapping the vertebrae. Note the elevated right dome of the diaphragm.
Fig. 93: Right middle lobe collapse. Schematic diagram demonstrates right lower zone opacity abutting the cardiac silhouette with elevation of the diaphragm, and reduction in right lung volume. Lateral view demonstrates minor and major fissure approximate with each other, with a triangular opacity representing the collapsed middle lobe within.
Right Middle Lobe Atelectasis
The atelectatic right middle lobe on a chest X-ray is seen as an opacity along the right heart border resulting in a loss of the silhouette of the right cardiac border (Figs. 93 and 94A). There is no significant change in the vasculature; the right hilum does not change in position. Right middle lobe atelectasis is best demonstrated on a lateral view as the horizontal fissure descends with increasing atelectasis (Fig. 94B). The atelectatic lobe is seen as an opaque wedge extending from the hilum anteriorly. Occasionally, when the atelectasis is very severe the appearances may resemble a thickened fissure. On CT, right middle lobe atelectasis is seen as a triangular wedge atelectatic lung, bound by the major fissure posteriorly and minor fissure anteriorly (Fig. 95).44
Figs. 94A and B: Right middle lobe collapse. (A) PA view demonstrates an ill-defined opacity in the right lower zone; (B) Lateral view of the chest reveals a homogenous opacity overlying the cardiac silhouette bounded by the interlobar fissures representing right middle lobe collapse. Note the marked downward shift of the lesser fissure.
Fig. 95: Collapse of the lateral segment of the right middle lobe. CT chest reveals a mass lesion in the right hilum causing collapse of the lateral segment of the right middle lobe, seen as a band-like shadow in the right middle lobe.
Fig. 96: Right upper lobe collapse: Schematic diagram demonstrates on PA view right upper lobe opacity, elevation of minor fissure, right hilum and right dome of diaphragm. Lateral view demonstrates elevation and backward rotation of minor fissure with collapsed right upper lobe opacity within the two fissures.
Right Upper Lobe Collapse
The right upper lobe collapses against the mediastinum and lung apex (Fig. 96). As the lobe collapses the silhouette of the superior vena cava is lost. When there is total collapse a wedge of tissue is seen in the right upper zone along the mediastinum (Fig. 97). The right middle and lower lobes demonstrate compensatory expansion and there is elevation of the right hilum. The major and minor 45fissures move upward and toward each other. This is well seen on the lateral view. The collapsed lobe on the lateral view silhouettes the ascending aorta. On CT, the collapsed right upper lobe appears as a triangular soft tissue density lying against the mediastinum and anterior chest wall.
Left Upper Lobe Atelectasis
The pattern of collapse is complex, as there is no horizontal fissure. As the lobe collapses it pulls the major fissure forward and the lower lobe expands posterior to the major fissure (Figs. 98A to C). As the left lower lobe expands posterior to the collapsing left upper lobe, on PA radiographs the atelectatic left upper lobe appears as a diffuse haze overlying the left hilum often extending to the lung apex, but fading inferiorly and laterally (Figs. 99A and B). The left cardiac and mediastinal silhouette is lost. As the lower lobe expands the aortic knuckle may be visible and consequently the left apex and upper mediastinum may be visible as the expanded lung occupies these regions.
Fig. 97: Right upper lobe collapse: PA view of the chest demonstrates triangular opacity in the right apical region with the deviation of the trachea to the right and loss of volume in right hemithorax. This is due to the right upper lobe collapse.
On the lateral view the collapsed lung is seen anteriorly with the major fissure moving anteriorly to be relatively parallel to the chest wall. As the lower lobe overexpands air may be seen between the sternum and the atelectatic lung. The appearances on CT are very similar to those seen with right upper lobe atelectasis (Fig. 99C).
Right Middle and Lower Lobe Atelectasis
This type of atelectasis is rare considering the distance between the two bronchi. It may however occur due to separate occlusions of the right middle and lower lobe bronchi. The appearances resemble a right lower lobe atelectasis; the extent of involvement is more extensive, extending to the lateral costophrenic angle on the PA view and to anterior chest wall on the lateral view.
Linear and Band-like Opacities
Linear opacities are linear densities less than 5 mm and bands are considered to be linear densities more than 5 mm in thickness (Fig. 100). The causes are tabled in Table 3.
Figs. 98A to C: Left upper lobe collapse (A) Schematic diagram (B and C) PA views demonstrate an ill-defined haze overlying the left upper lobe. A homogenous opacity is not seen as in other lobar collapses as the compensatory expansion of the left lower lobe occurs posterior to the collapsed left upper lobe. These opacities are summated on a PA view resulting in only a hazy opacity. On the lateral view the opacity of the collapsed left upper lobe is better visualized, though with marked expansion of the lower lobe, the expanded lower lobe may intersperse between the sternum and collapsed left upper lobe. Note the major fissure has moved anteriorly parallel to the anterior chest wall.
Figs. 99A to C: Left upper lobe collapse. PA view of the chest (A) demonstrates an ill-defined opacity in the left suprahilar region. Lordotic view (B) demonstrates a well-defined opacity plastered against the mediastinum. CT chest (C) demonstrates collapsed lobe abutting mediastinum.
Fig. 100: Plate or Discoid atelectasis. PA view of the chest reveals linear bands in the right mid and left lower zone due to plate atelectasis, following general anesthesia.
Mucoid impaction appears as one or more band-like opacities pointing toward the hilum, usually 1.0 cm or more in diameter (Fig. 101). The margins are usually sharply demarcated and smooth with a finger-in-glove appearance. This appearance is mainly seen in ABPA but may also be seen as a result of bronchial obstruction in bronchial carcinoid, lung Ca, bronchostenosis, broncholithiasis, and bronchial atresia. If the lung distal to the obstructed segment is consolidated or collapses, the linear bands of mucoid impaction will not be visualized as they are now silhouetted by the collapse/consolidation.
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Fig. 101: Mucoid impaction chest X-ray reveals well-defined nodular opacities in left lower zone. CT demonstrated the nodular opacities to be due to mucoid impaction. The nodular opacities seen on X-ray are due to end on dilated bronchi with mucoid impaction.
Septal Lines
Interlobular septa of normal lungs are not visible on chest radiographs or even HRCT. When septa become thickened they become visible. Kerley first described septal lines especially in pulmonary edema. They were named ABC, “A” referred to septal lines which ranged up to 4.0 cm radiating from the hila into the central portions of the lung, more visible in the upper/mid zones of lung. These are now referred to as deep septa. The “B” lines are short, less than 1.0 cm in length, are parallel to each other and at right angles to the pleura. They are referred to as peripheral interlobular septa, and are seen most frequently in the lung bases. Kerley “C” lines have been dropped, as they actually represent many B lines superimposed on each other. It is important to differentiate septal lines from vascular shadows. Kerley B lines are essentially visualized in the last 1 cm of lung parenchyma; lung vessels are not seen in the last 1 cm of the lung. Kerley A lines are differentiated from lung vessels as they are much thinner and do not branch (Figs. 102A and B).
Figs. 102A and B: Septal lines: (A) Chest X-ray demonstrates cardiomegaly, right pleural effusion and prominent lung markings; (B) CT chest demonstrates smooth septal thickening with ground-glass densities due to pulmonary edema secondary to congestive cardiac failure.
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Unilateral Transradiancy of the Lung
The causes for unilateral transradiancy of the lung are:
- Radiographic artifact: The radiographic output is usually adjusted to increase the output in the region of the bases as compared to the apices. This is known as a heel-toe effect. If this heel-toe effect is horizontally oriented rather than vertically, it will result in one hemithorax being overpenetrated. A similar effect occurs when the patient is rotated. This can be detected by observing the soft tissue in relation to the shoulders; the penetration will be different.48Fig. 103: Interstitial pneumonia: Chest X-ray reveals extensive reticular opacities and ill-defined areas of consolidation more on right mid zone as result of an interstitial pneumonia.
- Thoracic wall and soft tissue abnormalities: Unilateral mastectomy or congenital absence of pectoralis muscle (Poland syndrome) (Fig. 111).Fig. 105: Miliary tuberculosis. PA view of the chest reveals multiple small nodules in both lung fields as a result of miliary tuberculosis.
- Overexpansion or increased translucency of one lung:
- Obstructive emphysema due to a foreign body, or intrabronchial mass lesion
- Compensatory emphysema due to severe lobar collapse or lobectomy
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Fig. 107: Alveolar microlithiasis: CT chest in a relatively asymptomatic patient reveals extensive small nodular high-density calcified lesions in both lung fields as a result of alveolar microlithiasis.
- Pleural effusion in a supine patient, causing an ipsilateral increase in density of the hemithorax, consequently the opposite hemithorax appears to be hypertranslucent (Fig. 112)
- Macleod's or Swyer-James syndrome.Fig. 109: Progressive massive fibrosis: PA view of the chest reveals bilateral ill-defined parahilar mass lesions with multiple small ill-defined nodular lesions along the periphery of the lesion.
- Increased translucency of both lungs:
- Widespread transradiancy of both lungs may be seen in airway disease such as constrictive bronchiolitis, asthma and emphysema
Fig. 111: Unilateral mastectomy: PA view of the chest, note right lung appears more translucent than left lung. This is due to mastectomy on the right side.
Solitary Pulmonary Nodule
A pulmonary nodule is referred to as a spherical opacity with relatively well-defined margins with a diameter of up to 3 cm (Fig. 113). Lesions more than 3 cm in size are considered as mass lesions. A well-defined spherical opacity below 1 cm in diameter is referred to as a small SPN.
With increasing use of MDCT and its high spatial resolution, small nodules are being detected with an increasing frequency. Though most are benign in etiology, it is important to remember that 20–30% of lung cancers present as a solitary pulmonary nodule. One of the primary roles of imaging, beyond detection is to accurately differentiate malignant from benign lesions. It is important to obtain 3/5 mm sections as well as thin 1-mm sections through the lung on CT. The thinner sections help to reduce partial volume averaging so as to provide an accurate assessment of the internal contents and margins of the nodule. The thicker 3/5 mm sections are important as it is difficult to differentiate small SPN from vessels in thin 1 mm sections.
The first step in the radiological evaluation is to determine whether the nodule is pulmonary or extrapulmonary, as the chest X-ray gives a 2D image. Skin, pleural or rib lesions can appear as an intrathoracic lesion. Lateral, oblique X-rays or a CT scan would help to localize the lesion (Figs. 114 to 116). Once the lesion is confirmed to be intrapulmonary, the possibilities would essentially be an infective lesion, benign lesion or a malignant lesion. There is a significant overlap in the imaging appearances. To help differentiate, it is useful to look at the clinical and morphological features.
Fig. 112: Unilateral translucency: Frontal chest X-ray in supine position reveals uniform haziness of right hemithorax with transradiancy of left hemithorax. This is due to a right pleural effusion layering along the chest wall contributing to the right hemithorax opacity and consequent transradiancy of left hemithorax.
Fig. 113: Solitary pulmonary nodule: Chest X-ray demonstrates a well-defined nodular lesion with calcification along its medial aspect in the right upper zone. The lateral margins of the lesion appear to have obtuse angles with the chest wall, a sign suggesting that the lesion is extrapulmonary.
Fig. 114: Solitary pulmonary nodule: CT demonstrates that the nodule demonstrated on the chest X-ray is not intrapulmonary. It arose from the posterior end of the rib with calcification along its anterior aspect. The histopathology revealed an enchondroma.
Nodule Morphology
Calcification: Presence of calcification in a pulmonary nodule is a useful sign to differentiate benign from malignant nodules. However, 13% of all lung carcinomas demonstrate calcification; only 2% less than 3 cm in size demonstrate calcification. The different types of calcification which may be visualized in a pulmonary nodule are—concentric, popcorn, punctate/eccentric and uniform.
Concentric: The calcification occupies the entire SPN or the entire periphery of the SPN in a laminated manner. This calcification is mainly seen in tuberculous and fungal infections.
Popcorn calcification: Multiple small rings or nodules of calcification which overlap are seen in hamartomas/cartilage tumors (Fig. 117).
Punctate/Eccentric calcification: Punctate/Eccentric calcification is suspicious as it may be seen in infections and malignancies. A malignancy may engulf a calcified focus representing an old-healed granuloma, with calcification appearing on the periphery of the lesion (Fig. 118).
Figs. 115A and B: Solitary pulmonary nodule (A) PA view demonstrates a solitary pulmonary nodule in right lower zone; (B) lateral view demonstrates nodule is subcutaneous (arrow). This case demonstrates the paramount importance of a lateral X-ray of the chest in determining the location of a nodular opacity.
Figs. 116A and B: (A) Chest X-ray reveals solitary pulmonary nodule in right lower zone. (B) Lateral view demonstrates nodule in posterior, pleural base with a wide pleural attachment and with obtuse angles against the chest wall. These features favor pleural/extrapleural mass lesion rather than an intrapulmonary lesion.
Fig. 117: Solitary pulmonary nodule: CT chest demonstrates a well-defined nodule in the right upper lobe. There is a popcorn type of distribution of calcification typical of a hamartoma.
Uniform calcification: The entire SPN is calcified; this is typical of calcified granulomas (Fig. 119).
Fig. 118: Solitary pulmonary nodule: CT chest reveals a nodular mass lesion in the left lower lobe with a calcific speck along its periphery, an example of an eccentric type of calcification. CT-guided biopsy revealed an adenocarcinoma. The calcific density represented an old granuloma which healed with calcification and was engulfed by the neoplasm.
Size
Most malignant nodules are larger than 2 cm in size, however 40% are less than 2 cm, 15% are less than 1 cm, 1% of malignant lesions are less than 7 mm in size. Most 53lesions above 3 cm are likely to be either bronchogenic carcinoma, lung abscess, Wegener's granulomatosis, lymphoma, round atelectasis, focal pneumonia, or hydatid cysts. It is difficult to detect a lesion less than 5 mm in diameter on a chest X-ray. If a lesion which is 5 mm or less is seen on a chest X-ray, it is invariably calcified.
Shape
A spiculated margin is very suggestive of carcinoma; the spicules represent spread into the interstitium of the lung (Figs. 120 and 121). Lobulation and notching which indicate unequal growth are suggestive signs for malignancy but may be seen in inflammatory lesions. There is considerable overlap in the findings between benign and malignant. A spiculated lesion though has a predictive value of 90% to be a malignant lesion. An inflammatory lesion with fibrosis may however have a similar appearance. Benign lesions usually have smooth margins. Conversely 20% of primary lung tumors have smooth margins; most metastatic lesions also have smooth margins.
Cavitation
Cavitation occurs in inflammatory as well as primary and metastatic tumors. Benign lesions tend to have thinner and smoother walls as compared to malignant lesions, which have thicker and irregular walls (Figs. 122 and 123).
Fig. 119: Solitary pulmonary nodule: CT chest demonstrates a well-defined pulmonary nodule in the right upper lobe. The nodule is densely calcified, representing a uniform type of calcification, indicating with certainty that the nodule is benign.
Fat
Demonstration of fat within a solitary pulmonary nodule is pathognomonic of a hamartoma, (50% of hamartomas demonstrate fat in the lesion) (Fig. 124). Rarely, lipoid pneumonia/metastatic liposarcoma or renal cell carcinoma metastasis may demonstrate fat densities.
Fig. 120: Solitary pulmonary nodule: Chest X-ray demonstrates a nodule in the left upper lobe. Note its spiculated margin, a relatively specific sign to indicate malignancy.
Fig. 121: Solitary pulmonary nodule: CT chest demonstrates a nodular lesion in the left apex. There are multiple radiating bands arising from the surface of the nodule resulting in a spiculated appearance. This is typical of a malignant lesion. Rarely, an inflammatory lesion may demonstrate spiculation.
Fig. 122: Solitary pulmonary nodule: CT chest reveals a well-defined nodular lesion in the right upper lobe abutting the pleura with internal cavitation, the margins of which are smooth. CT-guided biopsy revealed this lesion to be due to Mycobacterium tuberculosis.
Fig. 123: Solitary pulmonary nodule: CT chest reveals a large nodular lesion with internal necrosis and cavitation in the right lower lobe. The inner margins of the cavitation are irregular: CT-guided biopsy revealed a squamous carcinoma.
Satellite Nodules
Multiple small peripheral nodules around an SPN are very useful signs indicating a benign lesion, especially inflammatory in etiology. It has a positive predictive value of 90%.
Air Bronchogram
Presence of an air bronchogram does not exclude a neoplasm as this may be seen in a bronchoalveolar carcinoma or in lymphoma. Presence of an air crescent is useful to diagnose an aspergilloma (Fig. 125).
Fig. 124: Solitary pulmonary nodule: CT chest reveals a small pulmonary nodule in the right chest anteriorly. There is a fat density within the lesion; this is typical of a hamartoma.
Fig. 125: Solitary pulmonary nodule: Well-defined solitary pulmonary nodule in right mid-zone with an air crescent along superior surface of nodule. The air crescent indicates that the nodule represents a fungal ball in a cavity—aspergilloma.
CT Halo Sign
Lung cancers can have a halo around them, though such halos may also be seen in inflammatory lesions, especially in invasive aspergillosis (Fig. 126).
Rate of Growth
Lung cancers take from 1 month to 18 months to double in volume, the average time being 4.2–7.3 months. Volume doubling faster than 1 month suggests an infection/infarction/aggressive lymphoma. Doubling 55after 18 months is seen in granuloma/hamartoma/carcinoid/round atelectasis. A lesion which has not grown or has reduced in size in 2 years is likely to be benign. For a nodule to double in volume, the change in nodule diameter is approximately 26% (Figs. 127A and B). A 4 mm nodule which increases to 5 mm would have doubled in volume. Thus accurate measurements are critical in deciding doubling time. There is significant inter- and intraobserver variation in measurements, especially in spiculated lesions. The ideal method to evaluate growth is to evaluate volume, as an irregular-shaped structure is being measured. Automated volume measuring techniques are very useful in this setting. The problems of inter-/intraobserver variations are minimized, as all spiculated and irregular margins are taken into consideration for measurements. Most modern CT workstations have automated software that enables accurate measurements.
Fig. 126: Solitary pulmonary nodule: High-resolution computed tomography (HRCT) demonstrates a well-defined nodule in the apical segment of the right lower lobe with an ill-defined halo of ground-glass around the nodule. This appearance is seen in invasive aspergillosis.
Figs. 127A and B: Solitary pulmonary nodule: CT chest studies done 6 months apart reveal progression in size of nodule. CT-guided fine-needle aspiration cytology (FNAC) of lesion revealed a non-small-cell cancer; this is the most important sign in the evaluation of a pulmonary nodule (its progression in a short-period of time). It indicates the need for further intervention, FNAC, biopsy or surgical excision.
Nodule Enhancement and Metabolism
There are numerous reports in Western literature on the utility of contrast enhancement to differentiate between benign and malignant SPN. If the enhancement of a nodule following contrast enhancement exceeds 20 HU then it is most likely malignant, whereas if less than 15 HU it is most likely benign. Enhancement is determined by measuring HU values, postcontrast after 1, 2, 3, 4 minutes. The peak HU value is subtracted from the precontrast HU value. Sensitivities of 98%, specificity of 73%, positive predictive value of 77%, and negative predictive value of 98% have been reported. However, these findings do not apply to patients in the Indian subcontinent as the most likely differential diagnosis of a malignant SPN is an inflammatory lesion (in particular a tuberculous lesion). A tuberculoma will enhance to a similar extent as a malignant 56nodule. For the same reason the FDG PET is insensitive in differentiating a malignant from a tuberculous or other inflammatory pathology. Further, PET can be quite insensitive in detecting pulmonary nodules, especially metastatic nodules, less than 1 cm in diameter.
High-resolution Computed Tomography Patterns of Diffuse Lung Disease
The detection and diagnosis of diffuse lung diseases is based on the demonstration and recognition of specific abnormal findings. These findings can be classified into essentially two groups, those with increased lung attenuation and those with decreased lung attenuation. Those with increased lung attenuation can be further subdivided into reticular opacities, nodular opacities and parenchymal opacification. Those with decreased lung attenuation can be subdivided into cystic lesions, emphysema, bronchiectasis, mosaic perfusion/attenuation and air trapping.
RETICULAR OPACITIES
Thickening of the interstitial fiber network of the lung by inflammation, fluid, fibrous tissue or neoplastic infiltration results in linear/reticular opacities. Thickening of the axial interstitium results in thickening of the interstitium along the walls of the bronchovascular structures (Fig. 128). Since bronchial walls and vessels have similar densities, it is difficult to differentiate the interstitial thickening from the underlying bronchovascular structures. Consequently, the appearances are of thickening of the bronchial wall and an increase in the vessel diameter.
Thickening of the peripheral interstitium is easy to demonstrate, as septal thickening is seen in the subpleural regions, marginating the secondary pulmonary nodule, and interlobular interstitium. This is manifested as radiating bands extending perpendicular to the pleural surface (Figs. 129 and 130).
Fig. 128: Peribronchovascular interstitial thickening: The vessels appear to be prominent in size with irregular surfaces. This is due to peribronchovascular interstitial thickening. There is extension of the interstitial thickening peripherally into the subpleural regions.
Fig. 129: Interlobular interstitial thickening: Schematic diagram of secondary lobules demonstrates thickening of walls of secondary lobule as well as centrilobular interstitium.
Fig. 130: Interlobular interstitial thickening: HRCT in a patient with lymphangitis carcinomatosis reveals smooth thickening of the interlobar interstitium. The walls of the secondary lobule are thickened, and the internal architecture is preserved, demonstrating the anatomy of the secondary lobule very well.
Thickening of the intralobular interstitium, which lies within the secondary lobule, is seen as a fine haze of linear opacities or may appear as ground-glass opacities (Fig. 131).
The interstitial thickening may be smooth, nodular or irregular. Smooth thickening is seen in pulmonary edema, lymphangitis carcinomatosis (Figs. 132A and B). Nodular thickening is seen in lymphangitis carcinomatosis, sarcoidosis. Irregular septal thickening is seen mainly in patients with lung fibrosis (Fig. 133). Extensive peribronchovascular fibrosis can result in large conglomerate masses of fibrous tissue as seen in sarcoidosis, silicosis, tuberculosis and talcosis. Subtle peribronchovascular interstitial thickening may be difficult to detect.
Fig. 131: Intralobular interstitium: HRCT demonstrates ill-defined reticular ground-glass densities in the right middle lobe and left lingula associated with traction bronchiectasis. These features are due to intralobular interstitial thickening.
Involvement of the peribronchovascular interstitium predominantly is seen in nonspecific interstitial pneumonias (NSIPs) (Figs. 134A and B) as compared to predominantly subpleural interstitial thickening seen in usual interstitial pneumonia. Another differentiating feature is the lack of honeycombing, seen typically in UIP. Also in UIP, there are no significant ground-glass densities and parenchymal opacification which are seen in the cellular variety of NSIP (Fig. 135).
Axial Interstitium
In patients with irregular interstitial thickening, fibrotic tissue along the bronchial walls causes traction resulting in “traction bronchiectasis” (Figs. 136 and 137). A similar involvement of the peripheral bronchioles is termed traction bronchiolectasis. The dilated bronchi have a varicose or a corkscrew appearance.
When there is involvement of the terminal bronchioles, the bronchioles may dilate to occupy the entire secondary lobule, resulting in honeycomb cysts. On HRCT, honeycomb cysts are usually 1.0 cm or more in diameter with thin walls in the subpleural regions.
Figs. 132A and B: Smooth interstitial thickening: CT chest (A) demonstrates an ill-defined mass lesion in the lingula flush with the pericardium. CT-guided fine-needle aspiration cytology (FNAC) revealed an adenocarcinoma. HRCT (B) reveals smooth septal thickening from the surface of the mass lesion, this represents lymphatic infiltration by the mass lesion. Smooth septal thickening is also present in the right middle lobe with preservation of the secondary lobule. This is due to lymphangitis carcinomatosis secondary to hematogenous spread.
These honeycomb cysts share their walls and occur in several contiguous layers (Figs. 138 and 139). Honeycombing indicates end-stage lung disease. The location of honeycombing is important in the differential diagnosis of chronic ILD. If the honeycombing is basal and posterior with associated significant fibrosis and architectural distortion, the diagnosis is UIP. If honeycomb cysts are seen in the upper zones the possibility of sarcoid should be considered; if in the mid-zone with a patchy distribution, the diagnosis of chronic hypersensitivity pneumonitis should be entertained. Anterior honeycomb cysts with fibrosis are seen in ARDS since the posterior portions of the lungs are protected by collapse/consolidation and are therefore not exposed to the deleterious effects of mechanical ventilation.
Fig. 133: Irregular septal thickening: HRCT demonstrates irregular interstitial thickening in both lung bases posteriorly in a subpleural and peribronchovascular location as seen in usual interstitial pneumonia.
Nodular Opacities
A nodule is defined as a rounded opacity which can be well- or ill-defined. A small nodule is one which is less than 1.0 cm; a large nodule varies in size between 1.0 cm and 3.0 cm; nodules above 3.0 cm are termed as masses.
Small nodules are of two types: (1) interstitial and (2) air-space. Interstitial nodules are well-defined and discrete, as seen in sarcoidosis, miliary tuberculosis, silicosis and metastatic lesions. Air-space nodules tend to be ill-defined and conglomerative. Airspace nodules may have a soft tissue density or demonstrate a diffuse ground-glass haze. Examples of air-space nodules are seen in exudative bronchiolitis. Despite these differences in appearance, it is often difficult to differentiate interstitial from air-space nodules on HRCT. The distribution of nodules is extremely useful in establishing the differential diagnosis. Nodules may be perilymphatic, random or centrilobular in distribution. Perilymphatic nodules occur in relation to the lymphatics/interstitium (Figs. 140 and 141), i.e. in relation to the perihilar bronchovascular interstitium, interlobular septae, subpleural interstitium.
Figs. 134A and B: Fibrotic nonspecific interstitial pneumonia (NSIP): Extensive interstitial thickening in the lungs anteriorly in the upper lobes and posteriorly in the lung bases. The predominant interstitial thickening is in the peribronchovascular interstitium and not in the subpleural regions.
Fig. 135: Cellular nonspecific interstitial pneumonia (NSIP): HRCT demonstrates ill-defined areas of air-space opacification in the peribronchovascular and subpleural regions of both lung bases. There are no honeycomb changes. In view of the parenchymal opacification, lack of honeycomb changes, and significant fibrotic lesions this would represent the cellular variety of nonspecific interstitial pneumonia.
Fig. 136: Traction bronchiectasis: HRCT demonstrates peribronchovascular interstitial thickening as evidenced by thickening and irregularity of the vessel and bronchial wall. There is dilatation and irregularity secondary to peribronchial interstitial thickening, representing traction bronchiectasis.
The subpleural distribution of nodules is best demonstrated in relation to fissures. These small nodules in the subpleural regions may coalesce to form pseudoplaques along the pleura. These nodules may also coalesce to form large conglomerative masses. Satellite nodules may be seen in relation to these conglomerative masses giving the appearance of a galaxy (Fig. 142). This pattern is seen in sarcoidosis, silicosis/coal workers pneumoconiosis, lymphangitic carcinomatosis, lymphoproliferative disorders. These diseases demonstrate different patterns of perilymphatic involvement, allowing a distinction.
Fig. 137: Traction bronchiectasis: HRCT demonstrates peribronchovascular interstitial thickening with consequent traction bronchiectasis and multiple ground-glass opacities.
Fig. 138: Honeycomb cysts: Extensive honeycomb cysts are seen in both lung fields especially the left.
Sarcoidosis
Nodules are seen essentially in relation to the peribronchovascular interstitium and subpleural regions.60
Figs. 139A and B: Dependent densities: Supine HRCT reveals ill-defined opacities in the lung bases posteriorly. (A) These appear as reticular opacities due to interstitial fibrosis. Prone scans at the same level; (B) demonstrate that the opacities have resolved. These opacities in the lung base on a supine scan represent basal atelectasis. It is important to obtain prone scans in all patients with basal posterior opacities to exclude basal atelectasis.
Fig. 140: Perilymphatic nodules: HRCT demonstrates extensive nodules in a peribronchovascular location along the vascular surfaces as well as the fissures. As the vessels are white and the nodular areas also white, the appearance is of a nodular surface of the vessels.
The central bronchovascular structures and fissures have a nodular appearance. An upper lobe preponderance is common, with the lung involved in a patchy asymmetric fashion, groups of nodules occurring in one region, normal lung in other regions.
Silicosis/CWP
Nodules are distributed in a subpleural and centrilobular location, rarely in a peribronchovascular location as compared to sarcoidosis. Nodules tend to be more evenly distributed as compared to sarcoidosis (Fig. 143).
Fig. 141: Perilymphatic nodules: HRCT demonstrates multiple small well-defined nodules along the surface of the bronchi and vessels. The vessels have a beaded appearance. These represent interstitial nodules along the peribronchovascular interstitium.
Lymphangitic Carcinomatosis
There is smooth thickening of the peribronchovascular and interlobular interstitium. Nodules are seen in relation to these thickened septae. The involvement may be unilateral, patchy or bilateral and symmetric.
Patterns of Distribution of Nodules
Random
The distribution is uniform with no predilection for any anatomic structures, bilateral and symmetric as seen in miliary tuberculosis (Fig. 144), hematogenous metastasis, and fungal infection.61
Fig. 142: Sarcoidosis: HRCT demonstrates multiple small nodules in an interstitial location, along the fissures, vessels and bronchi as well as in the subpleural regions. The distribution is asymmetric and essentially perilymphatic. The nodules are seen to conglomerate in the right middle lobe with a number of satellite nodules resulting in an appearance akin to a galaxy. This distribution pattern is typical of sarcoidosis.
Fig. 143: Silicosis: HRCT demonstrates multiple small well-defined nodules distributed evenly in both lung fields. These nodules are along the vessels, fissures and in the subpleural regions, i.e. perilymphatic in location. As compared to the asymmetric distribution of nodules in sarcoidosis the distribution is uniform in silicosis.
Centrilobular
Ill-defined small nodules are centered on the centrilobular structures of the secondary pulmonary lobule.
Fig. 144: Miliary tuberculosis: HRCT demonstrates multiple small nodules in a random distribution. There is no predilection for any anatomic structure; the distribution is uniform. This is typically seen in the miliary tuberculosis.
Nodules which are predominantly centrilobular in location are most likely secondary to bronchiolar/peribronchiolar inflammation resulting in infiltration or fibrosis of the surrounding interstitium and alveoli (Figs. 145A and B). Angiocentric diseases may also manifest as centrilobular nodules. Bronchiolar diseases manifesting as centrilobular nodules are endobronchial spread of tuberculosis, nontuberculous mycobacterial infections, granulomatous infections, bronchopneumonia, panbronchiolitis, bronchiectasis, ABPA, hypersensitivity pneumonitis (Fig. 146), Langerhans’ cell histiocytosis, respiratory bronchiolitis (Fig. 147), endobronchial spread of neoplasm. Angiocentric nodules are due to pulmonary edema and pulmonary hemorrhage.
Centrilobular nodules due to bronchiolar inflammation may have a tree-in-bud appearance; as the bronchioles dilate and are filled with inspissated mucus, a branching pattern is visualized (Figs. 145A and B).
Parenchymal Opacification
Diffuse or multifocal increase in lung attenuation is a common finding on HRCT in patients with chronic lung disease. Increased lung opacity may be ground-glass or consolidation. These represent varying degrees of parenchymal opacification, depending upon whether the vessels are obscured or not by the parenchymal opacification.62
Figs. 145A and B: Centrilobular nodules: HRCT demonstrates multiple small ill-defined nodular lesions in centrilobular location.
Fig. 146: Hypersensitivity pneumonitis: HRCT demonstrates multiple small nodules in both lung fields distributed uniformly, evenly spaced, representing centrilobular nodules due to hypersensitivity pneumonitis.
Ground-glass opacity is an area of parenchymal opacification not associated with obscuration of the underlying vessels (Fig. 148). Parenchymal consolidation obscures the vessels (Fig. 149).
Ground-glass opacity results from either fluid, inflammatory material within the alveoli/interstitium or the presence of fine interstitial fibrosis in the intralobular interstitium of the secondary lobule. The distribution is usually geographic with areas of spared lung interspersed with areas of affected lung. Detection of ground-glass opacity is of significance as this indicates an ongoing active as well as potentially treatable process. Since ground-glass opacity may also be a manifestation of intralobular interstitial thickening, presence of significant areas of fibrosis/lung destruction in other regions would indicate that the ground-glass densities are more likely due to intralobular fibrosis.
Fig. 147: Respiratory bronchiolitis: HRCT demonstrates multiple small pulmonary nodules in both lung fields. These nodules are evenly spaced at the centers of the secondary lobule. These represented nodules due to respiratory bronchiolitis.
Pitfalls in Diagnosis of Ground-Glass Opacity
There is a reduction in the amount of air in the alveoli during expiration; consequently there is an increase in lung attenuation, mimicking the appearance of ground-glass densities. It is useful to check the shape of the trachea to determine whether the scan has an adequate inspiratory effort. If the posterior tracheal surface is seen to bulge into the tracheal lumen, it is an expiratory scan rather than inspiratory (Figs. 150A and B). The diagnosis of ground-glass opacity is essentially subjective, based on quantitative assessment of lung attenuation. It is important to maintain consistent window settings. Using too low a window mean with a narrow window width may give an appearance of ground-glass densities. Similar appearances may occur with a wider window width without changing the window mean. A useful tip is to see the air in the trachea or bronchi. If the air appears gray rather than black, the apparent increase in attenuation of lung parenchyma is usually not genuine. In patients with patchy areas of emphysema or air-trapping, normal lung regions may appear as areas of increased attenuation due to the contrast with darker areas. This can be avoided by using consistent window settings. Additionally in regions of normal lung attenuation, air bronchograms are not visualized as seen in areas of ground-glass density. Expiratory images are also useful in confirming lucent areas to represent areas of emphysema or air-trapping (Figs. 151A and B).
Fig. 149: Computed tomography (CT) chest showing consolidation in the left lower lobe with air bronchogram.
Differential Diagnosis of Ground-Glass Densities
A large number of diseases may be associated with ground-glass opacities on HRCT as the pathological processes in the early stages are similar (Fig. 152). These disease processes may be acute, subacute or chronic.
Figs. 150A and B: Pitfall in diagnosis: HRCT (A) reveals ill-defined ground-glass densities in both lung fields. Note shape of trachea; the posterior wall is bulging inwards showing that this is an expiratory scan; (B) HRCT in deep inspiration in same patient at same level. Note trachea is well-distended and there are no ground-glass densities.
Fig. 151A and B: Hypersensitivity pneumonitis: HRCT reveals ill-defined areas of ground-glass densities in the inspiratory (A) and expiratory phases (B). Note the accentuation of air trapping in the expiratory phase.
Fig. 152: Pneumocystis jirovecii pneumonia (PCP): Seropositive patient presented with fever and dyspnea. HRCT revealed diffuse ground-glass densities indicative of PCP. confirmed on bronchoalveolar lavage.
Acute disease processes manifesting as ground-glass densities include acute interstitial pneumonia (Figs. 153 and 154), diffuse alveolar damage (Fig. 155), pulmonary edema, ARDS, pulmonary hemorrhage (Fig. 156), pneumonia and early radiation fibrosis. Subacute/chronic disease processes include interstitial pneumonias, especially NSIP, DIP (Fig. 157), respiratory bronchiolitis, interstitial lung disease, hypersensitivity pneumonitis, drug reactions, chronic eosinophilic pneumonia, Churg Strauss syndrome, lupoid pneumonia, sarcoidosis and alveolar proteinosis (Fig. 158).
Figs. 153: Acute interstitial pneumonia: HRCT chest demonstrates ill-defined areas of increased lung attenuation in an acutely breathless patient.
Decreased Lung Attenuation
Pathological processes with decreased lung attenuation may be due to lung cysts, emphysema, bronchiectasis, mosaic attenuation or air-trapping.
Emphysema
This is a result of permanent abnormal enlargement of air-spaces with destruction of their walls distal to terminal bronchioles. On HRCT emphysema appears as focal or diffuse areas of decreased attenuation compared to normal lung parenchyma. By modifying the window settings of HRCT (600–800 window mean) emphysema can be very well-demonstrated (Figs. 156 and 158). Emphysema is essentially of four types:65
Fig. 154: Acute interstitial pneumonia: HRCT of the chest with coronal reconstruction in an acutely breathless patient demonstrates ill-defined areas of ground-glass opacification and consolidation.
Fig. 155: Diffuse alveolar damage: Drug-induced diffuse alveolar damage seen on HRCT as diffuse ill-defined areas of increased lung attenuation in both lung fields.
- Centrilobular: This occurs predominantly in the upper lobes with lung destruction around the centrilobular arterial branches resulting in lucencies grouped around the centers of the secondary pulmonary lobule. With more severe destruction the appearances resemble panlobular emphysema. Centrilobular emphysema occurs in cigarette smokers due to enzymatic destruction of lung parenchyma as there is an imbalance between lung proteases and antiproteases (Figs. 159 and 160).Fig. 156: Alveolar hemorrhage: HRCT in a patient with hemoptysis demonstrates ill-defined areas of ground-glass density in right middle lobe as well as right lower lobe. The ground-glass densities were due to alveolar hemorrhage.
- Panlobular emphysema: This is characterized by uniform destruction of the pulmonary lobule leading to widespread areas of low attenuation. The pulmonary vessels appear fewer and thinner in appearance, termed as a diffuse simplification of lung architecture. Panlobular emphysema occurs in individuals with alpha-protease inhibitor deficiency and as an extension of centrilobular emphysema in cigarette smokers (Figs. 161A and B).66
- Paraseptal emphysema: The area of destruction involves the alveolar ducts and alveolar sacs marginated by the interlobular septa. On HRCT there are subpleural cysts which share thin walls. These cysts may become fairly large and reach up to a size of 1.0 cm. Paraseptal emphysema may be confused with honeycomb cysts, as both are in a subpleural location. Honeycomb cysts tend to be in several contiguous layers as compared to paraseptal emphysema which tends to occur in a single layer. Additionally, lung fibrosis usually accompanies honeycomb cysts, whereas other forms of emphysema such as centrilobular and panacinar may be present with paraseptal emphysema. Honeycomb cysts tend to be in the lung bases as compared to paraseptal emphysema which tends to be in the upper lobes.
- Bullous emphysema is characterized by large bullae, often associated with centrilobular/paraseptal emphysema (Fig. 162).
Fig. 158: Alveolar proteinosis: HRCT reveals ill-defined ground-glass densities in both lung fields with a background of septal thickening. This appearance simulates a crazy pavement appearance, most commonly seen in alveolar proteinosis.
Bulla represents a sharply demarcated area of emphysema measuring 1.0 cm or more in diameter with a thin wall not more than 1 mm. They may range up to 20 cm in diameter but generally range between 2 cm and 8 cm in diameter (Fig. 163).
Bleb—Bleb refers to a gas-containing space within the visceral pleura.
Pneumatocele is a thin-walled gas-filled space within the lung, occurring from lung necrosis and bronchiolar obstruction. It usually occurs in an acute setting following an acute pneumonia and is often transient. Pneumatocele has a similar appearance to lung cyst or bulla.
Differential Diagnosis of Cystic Lesions
The differential diagnosis of diffuse cystic lung diseases includes pulmonary Langerhans’ cell histiocytosis, usual interstitial pneumonia, and centrilobular emphysema. Langerhans’ cell histiocytosis chiefly involves the upper lobes and also shows the presence of nodules (Fig. 164). UIP chiefly involves the lower lobes with cysts subpleural in location. The cystic spaces in centrilobular emphysema do not have well-defined walls. Lymphangioleiomyomatosis occurs in young females with evenly distributed cysts in both lung fields. Cystic bronchiectasis may also enter into the differential diagnosis and is generally easily identified.
Figs. 159A and B: Centrilobular emphysema: (A) multiple thin-walled air spaces in both lung fields due to centrilobular emphysema (B) These are well-demonstrated on minimum intensity projection.
Mosaic Attenuation
The lung may have an inhomogenous attenuation pattern with ill-defined areas of increased and decreased lung attenuation intermixed. This may be due to infiltrative diseases with areas of ground-glass density, increased lung attenuation with areas of normal lung attenuation intermixed (Figs. 165A and B).
Fig. 160: Centrilobular emphysema: Multiple well-defined air spaces are seen with a central vessel within. These findings are typical for centrilobular emphysema. Lung destruction is seen to be occurring around the centrilobular vessel.
Mosaic perfusion is characterized by areas of decreased lung attenuation with areas of normal lung attenuation. Lung density is partially determined by the amount of blood present in lung tissue. Regional perfusion differences may occur due to airway abnormalities or vascular abnormalities. If there is reduced ventilation of a portion of the lung due to narrowing of the airways, there is reflex vasoconstriction resulting in hypoperfusion of the hypoventilated region. This is seen in bronchiolitis obliterans, bronchiolitis, bronchiectasis, and cystic fibrosis. If there is vascular obstruction there would be areas of hypoperfusion resulting in areas of low attenuation as seen in acute and chronic pulmonary thromboembolism.
Airway Diseases
Upper Airways Obstruction
Tracheal stenosis: Tracheal stenosis can be related to inflammatory or neoplastic causes and is sometimes due to Wegener's granulomatosis. The lesion may occur anywhere within the trachea and may involve the major bronchi also (Figs. 166A and B).
Figs. 161A and B: Panacinar emphysema: (A) Axial and (B) coronal HRCT images demonstrate large area of lung destruction seen in right lower zone. The density of the lung parenchyma is reduced and there is considerable thinning and separation of the vessels.
Fig. 162: Bullous emphysema: HRCT demonstrates extensive bullae in both lung fields, especially right with consequent compression of the lung parenchyma. There is extensive centrilobular emphysema in both lung fields.
Fig. 163: Bulla: HRCT demonstrates a huge thin-walled air space in the right lung field representing a bulla. Also noted are the bronchiectatic changes in the superior segments of both lower lobes.
Clinical features include breathlessness, sometimes accompanied by a wheeze. A stridor is often observed when the obstruction is subglottic or if it involves the main trachea. This condition is often mistaken for asthma because of the presence of a wheeze. Even if the wheeze is present, as for example in a patient with obstruction to the right or left bronchus, it is monophonic in nature and not polyphonic as seen in patients with asthma. Flow volume loop confirms the diagnosis. Initially there is flattening of the inspiratory loop but later a flattening of both inspiratory and expiratory loops of the flow volume curve is observed.
Fig. 164: Pulmonary Langerhans’ cell histiocytosis: HRCT reveals a right-sided pneumothorax with multiple bizarre-shaped cysts in both lung fields. The bizarre shape of the cysts as well as history of exposure to cigarette smoke helps to differentiate from the thin-walled smooth cysts seen predominantly in females in lymphangioleiomyomatosis.
Bronchiectasis: Bronchiectasis is defined as localized irreversible dilatation of the bronchial tree. There are a wide variety of causes. It is usually as a result of acute, chronic or recurrent infection. Bronchiectasis is classified on the basis of its severity as cylindrical (the walls of the bronchi are dilated but parallel), varicose (there is dilatation of the bronchi with focal constrictions, thereby giving a varicose appearance), and cystic, where the bronchi are ballooned (Figs. 167 to 170).
On HRCT, the dilated bronchi are visualized depending on the plane they are traversing in. If perpendicular to the plane of CT, i.e. running vertically down, they are visualized in cross-section. This appearance has been likened to a signet ring appearance—the dilated bronchus as the ring and the accompanying pulmonary artery as the jewel on the ring. If the bronchi are running parallel to the scan plane, i.e. horizontal they are visualized as tram tracks or parallel lines. There may be associated atelectasis resulting in the bronchi being bunched up, this gives an appearance of multiple cysts. Bronchial wall thickening may also be seen as well as air-fluid levels, especially in cystic bronchiectasis.69
Figs. 165A and B: (A) HRCT demonstrates subtle inhomogenous areas of attenuation in both lung fields on inspiratory scan. On expiratory scans (B) there is accentuation of the inhomogenous areas of altered attenuation. Focal areas are seen to be darker and focal areas are brighter. The vessels within the areas which are darker are sparse in distribution and thinner in caliber, representing air-trapping. Mosaic attenuation was due to constrictive bronchiolitis.
Figs. 166A and B: (A) Coronal CT section shows tracheal stenosis at two sites—an upper and a lower one, just above the carina. This patient was a young 23-year-old lady diagnosed as having asthma because of difficulty in breathing and a wheeze on auscultation. Clinical examination revealed noisy breathing, often amounting to a stridor. Auscultation revealed a monophonic wheeze; (B) The flow volume loop demonstrated a marked flattening of the inspiratory and expiratory curve. Surgical correction of this disorder was successfully done. The etiology of this tracheal stenosis was uncertain. It was probably related to Wegener's granulomatosis.
Small Airway Diseases: Bronchiolar Diseases
HRCT has revolutionized our ability to diagnose small airway disease. The HRCT findings can be divided into two groups based on the imaging findings:
- Constrictive bronchiolitis
- Exudative bronchiolitis.
1. Constrictive bronchiolitis: Constrictive bronchiolitis is concentric fibrosis involving the submucosal and peribronchial tissues of the terminal bronchioles resulting in bronchial narrowing and obliteration (Figs. 171A and B).70
Fig. 168: Bronchiectasis: HRCT demonstrates dilated bronchi (blue arrows) in both lung bases. Note marked difference in the diameter of the bronchus and accompanying artery. A few dilated bronchi in the left lower lobe demonstrate soft-tissue within their lumen representing mucoid impaction (red arrows).
The HRCT findings reflect the pathophysiology that causes airflow limitation. There is both hypoventilation of the involved segments of the lung and air-trapping. This is seen as areas of mosaic attenuation. The affected segments are dark and demonstrate air-trapping on expiratory scans. Hypoventilation of the involved areas of the lung results in reflex hypoperfusion so that vessels in the involved segments appear attenuated and sparse. The airways in these segments may also demonstrate abnormalities in the form of focal bronchial dilatation and wall thickening.
Fig. 169: Bronchiectasis: HRCT demonstrates dilated bronchi in both lung fields, note dextrocardia in a case of Kartagener's syndrome.
Fig. 170: Bronchiectasis: Coronal HRCT demonstrates dilated bronchi in the right upper lobe. There is a linear well-defined tubular opacity extending to the subpleural region representing mucoid impaction in dilated bronchus.
2. Exudative bronchiolitis: There is mucoid impaction in the terminal bronchioles. On chest X-ray these are seen as numerous small (5 mm) ill-defined nodules (Figs. 172 and 173). On HRCT the areas of mucoid impaction are seen as tubular branching structures in the peripheral lung parenchyma resembling toy jacks also termed as tree-in-bud appearance. When seen in cross-section they appear as centrilobular nodules.71
Figs. 171A and B: Constrictive bronchiolitis: (A) Inspiratory CT chest: areas of inhomogenous attenuation with areas of increased and decreased attenuation; (B) Expiratory scans reveal air-trapping as the areas of decreased attenuation retain their attenuation whereas the areas of increased attenuation become brighter: the air-trapping indicates small-airway disease.
Fig. 172: Exudative bronchiolitis: HRCT demonstrates multiple small conglomerated nodular lesions representing mucoid impaction in terminal bronchioles as a result of exudative bronchiolitis.
Swyer-James Syndrome (Fig. 174)
This condition is usually caused by a viral infection to the immature lung, before it has completed development (below eight years of age). There is obliterative bronchiolitis involving the distal airways. Usually, an entire lung is involved, occasionally segments are spared. There is hypoplasia of the lung together with hypoplasia of the pulmonary artery to the involved lung.
Fig. 173: Exudative bronchiolitis: HRCT demonstrates multiple small conglomerated nodular lesions representing mucoid impaction in terminal bronchioles with associated ground-glass densities as a result of exudative bronchiolitis with peribronchiolar inflammation.
On the chest X-ray there is unilateral transradiancy, the opposite lung appears to be plethoric. The ipsilateral hilum may be small chiefly because of a hypoplastic pulmonary artery supplying the involved lung.
IMPORTANT CONGENITAL MALFORMATIONS AND ANOMALIES
Pulmonary Arteriovenous Malformations
Nearly 70% of cases with pulmonary arteriovenous malformations (PAVM) are associated with hereditary 72hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber disease). This is an autosomal dominant disorder characterized by the triad of telangiectasia, recurrent epistaxis and a family history of the disease. There is a wide spectrum of presentations. Patients may be asymptomatic, lesions being detected incidentally on a chest X-ray. If the AVM is large enough to cause a marked right to left shunt, the patient may present with cyanosis, dyspnea, clubbing, hemoptysis, and cardiac failure. Usually, in these cases a distinct bruit is heard over the hemithorax. Patients may also present with cerebral abscesses and cerebral infarction due to paradoxical embolism. An important clinical finding in PAVMs is orthodeoxia—there is a drop in oxygen saturation from the supine to erect position. This is because PAVMs are mainly in the lower zones; this results in an increased right to left shunting of blood within the lungs in the erect position (Figs. 175 and 176).
Fig. 174: Swyer-James syndrome: Chest X-ray demonstrates unilateral transradiancy on the left side due to infantile bronchiolitis resulting in a Swyer-James syndrome.
Figs. 175A and B: Pulmonary arteriovenous malformation: (A) Maximum intensity projection (MIP) and (B) Volume rendering technique (VRT) images of CT angiography demonstrate an arteriovenous malformation in the right upper zone with feeding arteries and draining veins.
On chest radiographs AVMs are seen as well-defined nodules ranging in size from 1 cm to more than 1 cm. Peripheral AVMs usually demonstrate feeding arteries and draining veins as curvilinear structures. The more central AVMs are more difficult to detect as they may be overlapped by the hilum; the feeding draining vessels may not be visualized as they traverse a short distance.
CT is extremely sensitive and specific in demonstrating pulmonary AVMs. It is able to demonstrate feeding as well as draining vessels. There is intense enhancement of these lesions; CT scans are also able to detect the presence of multiple lesions. Remy Jardin and colleagues in fact found CT more sensitive than pulmonary angiograms, which have been considered the gold standard for the diagnosis of AVMs. CT detected AVMs in 98% of cases compared to pulmonary angiograms, which detected AVMs in 60%.73
CT additionally assists in deciding further management of these lesions. Using 2D and 3D reconstructions the feeding arteries can be demonstrated. Feeding arteries greater than 3 mm in diameter are embolized interventionally using coils, detachable balloons, to decrease the right to left shunting. Contrast echocardiography can be used to demonstrate complex angioarchitecture as well as provide a road map of the extent of the right to left shunt. MRI is useful in demonstrating larger PAVMs but smaller PAVMs may not be as well detected as in a CT.
Fig. 176: Pulmonary arteriovenous malformation: Sagittal multiplanar reconstruction (MPR) demonstrates feeding arteries and draining vein of pulmonary arteriovenous malformation.
Congenital Diaphragmatic Hernia
The classical congenital diaphragmatic hernia results from failure of the pleuroperitoneal cavity to close with resultant herniation of abdominal contents into the thorax. The incidence is 1:2,400 births, and is most commonly left-sided (90%). In the neonatal period these present as respiratory distress, as the herniated abdominal contents cause compressive effects on the lung and mediastinum. The diagnosis is fairly easy on the chest X-ray as there is evidence of soft tissue and air-filled bowel loops in the left hemithorax. When the stomach is included in the hernial sac, the nasogastric tube rather than descending in the abdomen is seen to take a turn upwards into the thorax from the gastroesophageal junction (Figs. 177 and 178).
Hernias on the right side may be difficult to detect as there is usually herniation of liver; the chest radiograph demonstrates a soft tissue opacity in the lower right hemithorax.
Bochdalek Hernia
These result from herniation through a posterior diaphragmatic defect close to the crura. They tend to manifest later in life and may be bilateral and symmetric. The liver prevents herniation on the right side. Occasionally, kidney and/or stomach may herniate on the left side.
Figs. 177A to C: Diaphragmatic hernia: (A) AP and (B) oblique views demonstrate soft-tissue opacity and bowel loops in the left hemithorax with shift of the mediastinum to the right; (C) Barium study confirms bowel loops in the hemithorax.
Morgagni's Hernia
These are due to herniation between sternal and costal attachments usually developing in the right anterior cardiophrenic sulcus. On the left herniation is impeded by the heart. Visual contents of the hernia are liver and omentum, occasionally transverse colon. On chest X-ray herniation of liver and omentum is visualized as a paracardiac mass with a D/D of pericardial cyst, paracardiac fat pad or a pleural/pulmonary mass (Figs. 179A and B). When there is herniation of colon, the presence of a gas-filled viscus makes the diagnosis easy. A lateral view of the chest helps to localize the hernia anteriorly. CT is diagnostic as CT demonstrates the herniation of liver/omentum and bowel (Figs. 180 and 181).
Fig. 178: Diaphragmatic hernia: Chest X-ray in a neonate reveals ill-defined opacities in the left hemithorax with multiple air-filled loops representing a diaphragmatic hernia. There is consequently a shift of the mediastinum to the right.
ABSENCE OF LUNG OR LOBES OF LUNGS
Unilateral agenesis is a rare congenital anomaly presenting with minimal clinical problems. It is frequently associated with other congenital anomalies particularly tracheoesophageal fistula and the VACTERL association (non-random association of birth defects). When the bronchus is absent, it is termed as “agenesis”.
When the bronchus is present but rudimentary, it is termed aplasia. The ipsilateral pulmonary artery develops but is usually hypoplastic.
Agenesis of the right lung is often accompanied by esophageal atresia and is twice as common as left lung agenesis (Figs. 182A and B). Left lung agenesis is often accompanied by tracheoesophageal fistula. On imaging there is loss of aeration and volume on the ipsilateral side as evidenced by elevation of the diaphragm, shift of the mediastinum to the ipsilateral side and increase in extrapleural fat to fill the space due to congenital hypoplasia.
Figs. 179A and B: Morgagni's hernia: (A) PA view and (B) topogram of the chest reveals a bowel loop with an air-fluid level in the right hemithorax.
Figs. 180A and B: Morgagni's hernia: CT scans show herniation of colon through an anterior abdominal wall defect into the anterior hemithorax, representing a Morgagni's hernia.
Fig. 181: Hiatus hernia: CT demonstrates a huge hiatus hernia with the stomach extending into the thoracic cavity.
Absence of individual lobes is a form of hypoplastic lung syndrome. When there is absence of a lobe there is compensatory expansion of the rest of the lung, distorting bronchovascular structures. This overexpansion is never adequate to revert the lung to normal size. The size of the ipsilateral lung is always smaller, similar to what is seen in pulmonary hypoplasia. The difference is easily determined on CT as a bronchus is absent, whereas in hypoplasia all segments are present but the tracheobronchial tree is stunted and underdeveloped.
Tracheoesophageal Fistula
Tracheoesophageal fistulas are associated with esophageal atresia and are usually diagnosed in the neonatal period. Rarely, tracheoesophageal fistulas are not diagnosed till later in life as the symptoms may be nonspecific. These fistulas are of the “H” type—a short horizontal communication between the trachea and esophagus—the horizontal communication being represented by the H bar. Symptoms are due to recurrent aspiration, paroxysmal cough, feeding difficulties and recurrent pneumonia. The appearances on chest radiographs are of aspiration, excessive air may also pass from the trachea into the esophagus as well as into the gut. This may be visualized also on an X-ray as air in the esophagus and/or gaseous distension of the bowel. An obvious tracheoesophageal fistula is fairly easy to demonstrate. A small tracheoesophageal fistula, especially the “H” variety is best demonstrated in the prone position using a feeding tube which is slowly withdrawn while a nonionic water soluble contrast is injected to demonstrate the fistulous communication.76
Figs. 182A and B: Agenesis of right lung: (A) CT chest reveals a marked shift of mediastinum to the right with no lung tissue seen in right hemithorax; (B) there is compensatory expansion of left lung. The right pulmonary artery was absent.
The “H” type of tracheoesophageal fistulas is usually associated with other congenital anomalies—these have been designated by acronyms: VATER—vertebral, anal, tracheoesophageal, renal; VACTEL—vertebral, anal, cardiac, tracheoesophageal and limb. Pulmonary hypoplasia, tracheal stenosis and pulmonary sequestration may also be associated.
Bronchial Atresia
There is a short segment of atresia involving a segment or subsegmental bronchus. There is consequently dilatation of the bronchus distal to the atresia, resulting in accumulation of mucus in the dilated bronchus. This mucocele is seen on imaging as a mass-like structure; there may be a branching configuration which helps establish the diagnosis. The surrounding lung in the affected segment is hypertranslucent as the lung beyond the atretic segment is aerated by collateral drift and because there is reflex hypoperfusion of the vessels in the affected segment. The vessels appear thinner and less is number in the affected segment. Most patients are asymptomatic. Bronchial atresia has limited clinical significance; the only issue is that it may be mistaken for a mass. CT very effectively demonstrates the central mucous-filled mass, atresia of the segmental bronchus, and the hypertranslucent lung segment.
Pulmonary Sequestration
Pulmonary sequestration is characterized by the presence of pulmonary tissue which does not communicate with the central airways through a normal bronchial connection and receives its blood supply via an anomalous systemic artery. Pulmonary sequestration is divided into intralobar and extralobar varieties, based on venous drainage. If the venous drainage is to the pulmonary veins, it is termed “intralobar sequestration” (Figs. 183A and B). If the drainage is to the systemic veins, it is termed “extralobar sequestration”.
Extralobar sequestrations are congenital abnormalities usually associated with other congenital abnormalities, such as congenital heart disease, diaphragmatic hernia, or cystic adenomatoid malformation. They are asymptomatic and therefore discovered incidentally on antenatal ultrasound, chest X-ray, sonography, CT, angiography or during surgical repair of a congenital diaphragmatic hernia with which they are commonly associated. An extralobar sequestration has a complete serosal covering; it may have a narrow vascular pedicle as it is separate from the normal lung. Extralobar sequestrations in 90% of cases occur on the left side. Torsion is a complication and this may result in a tension hydrothorax.
Extralobar sequestrations are seen on imaging as mass lesions of homogenous density. They have well-defined margins, in particular the lateral margin which is covered by pleura.77
Figs. 183A and B: Pulmonary sequestration: (A) CT scan demonstrates an ill-defined consolidation; (B) CT angiography demonstrates arterial branch arising from aorta feeding the consolidation representing an intralobar sequestration.
The medial margin may be difficult to discern as it abuts the mediastinum, often giving the appearance of a mediastinal mass. Sequestration may be seen in relation to the pericardium, diaphragm, and the retroperitoneum, occasionally communicating with the esophagus or stomach, which can be demonstrated by barium studies.
As compared to extralobar sequestration which is a congenital abnormality, intralobar sequestration is being considered to be more likely an acquired lesion rather than a congenital abnormality. Chronic bronchial obstruction due to foreign body, carcinoid tumor and postobstructive pneumonia are considered to be causes of intralobar sequestration. The chronic inflammatory process “parasites” its blood supply from the systemic circulation, often a branch from the descending aorta or branches from the inferior pulmonary ligament. Therefore, 98% of all sequestrations occur in the lower lobes. As compared to extralobar sequestrations which are asymptomatic, intralobar sequestrations present as an infective lesion or sequelae of an infective lesion. On imaging they appear as round, oval, lobulated mass lesions simulating an intrapulmonary mass lesion. Air and air-fluid levels may be seen within these masses due to communication with bronchi secondary to episodes of infection. CT appearances are similar to those of a chest X-ray; however, CT more frequently detects air, air-fluid levels, and the presence of emphysema adjacent to the sequestration. The emphysema occurs due to impaired ventilation secondary to chronic obstruction with consequent collateral air drift and air-trapping. Occasionally, a pure cystic form of sequestration is detected with air-trapping, focal emphysema and bulla formation. The key in differentiating from other cystic masses is the demonstration of a systemic arterial supply. CT angiography on MDCT scanner has replaced the need for invasive angiography to demonstrate systemic arterial supply, the key to the diagnosis of sequestration. The differential diagnosis of sequestration encompasses infective lesions, pulmonary masses, mediastinal and pleural masses. The clue to the correct diagnosis is location, arterial supply, venous drainage, and a history of repeated infections.
Congenital Lobar Overinflation
Previously known as congenital lobar emphysema, it is now termed as congenital lobar overinflation (CLO). The pathophysiology of this condition is characterized by overinflation of normal alveoli most likely due to central airway obstruction, presumably due to aplasia, hypoplasia or dysplasia of the bronchial support structures. A clinically similar condition is polyalveolar lobe—the lobe contains four to five times the number of alveoli normally present, resulting in a large lobe having all the compressive effects seen in CLO. CLO manifests in the neonatal period with respiratory distress. On chest X-ray there is hyperexpansion of a lobe of the lung, usually upper or middle lobe. Involvement of more than one lobe or the lower lobe is extremely rare. The hyperexpanded 78lobe causes mass effect on the adjacent structures, heart, mediastinum and diaphragm (Fig. 184). The main differential diagnosis is obstruction to the bronchus by a foreign body, mucous plug, endobronchial mass, extrinsic compression of the airway or a localized pneumothorax. CT is useful to confirm the diagnosis of hyperinflation of a lobe. CT angiography differentiates CLO from other forms of pulmonary hypoplasia.
Pulmonary Hypoplasia
Primary unilateral pulmonary hypoplasia is usually associated with the scimitar syndrome or with other vascular malformations. Patients present with repeated episodes of wheezing and pneumonia. The affected lung is small in size, the mediastinum is displaced toward the ipsilateral hemithorax and the pulmonary vasculature is reduced in size. On the lateral chest X-ray, a sharply marginated opacity is seen behind and parallel to the sternum. This is due to the displacement of the heart and mediastinum into the ipsilateral thorax. Primary bilateral pulmonary hypoplasia is very rare. Chest X-ray reveals bilateral small lungs with a normal-sized abdominal cavity, presenting a bell-shaped appearance of the chest and abdomen.
Unilateral Absence of Pulmonary Artery
This is a rare anomaly characterized by the absence of a short segment or atresia of the proximal left or right pulmonary artery; the more distal segments are usually present. Chest radiographs demonstrate reduction in lung volume, shift of mediastinum, small-sized or absent pulmonary hilum; peripheral pulmonary perfusion is reduced. There may be reticular opacities in the affected lung due to pulmonary-systemic collaterals. The normal lung may be plethoric as the entire cardiac output is shunted through the lung. CT will demonstrate the absence of the pulmonary artery and the presence of systemic pulmonary collaterals.
Fig. 184: Congenital lobar overinflation (CLO). Chest X-ray demonstrates marked overinflation of the left upper lobe causing a shift of the mediastinum to the right and collapse of the left lower lobe. Collapsed left lower lobe is seen along the left cardiac border.
Scimitar Syndrome
This is a condition involving essentially the right lung which is hypoplastic, with underdevelopment of the airways as well as vasculature. The characteristic finding which in turn contributes to its name is anomalous pulmonary drainage. A large anomalous pulmonary vein descends vertically inferiorly to open into the inferior vena cava above or below the diaphragm. The vein broadens as it curves medially to enter into the vena cava, thereby simulating the appearance of a Turkish sword—scimitar. The anomalous vein may also drain into the coronary sinus, right atrium, or rarely into hepatic veins. The scimitar syndrome may be associated with other congenital anomalies such as septal defects, eventration, Bochdalek hernia, bronchiectasis and tracheal diverticuli. On a chest radiograph, the key feature is the presence of the anomalous draining vein. Additional features are a small-sized right lung, shift of the mediastinum to the right and a small ipsilateral pulmonary artery (Fig. 185). CT is useful to confirm the diagnosis, demonstrating the anomalous draining vessel and its termination, tracheobronchial anomalies, small ipsilateral pulmonary artery, as well as associated abnormalities such as tracheal diverticuli and bronchiectasis.
Imaging of Pleura
Pleural Effusions
Free pleural effusions tend to gravitate to the most dependent portions of the pleural cavity. On erect chest X-rays these are seen as homogenous densities in the lower zone with a typical concave or upward-sloping contour (Figs. 186 and 187), the lateral margin being higher than the medial margin. Fluid collects in the subpulmonic space (Fig. 188) then spills into the posterior and finally lateral costophrenic sulcus. The posterior costophrenic (CP) sulcus is the deepest portion of the pleura. This is the site where the fluid tends to first accumulate. Radiologically, this is seen as blunting of the costophrenic angle on the lateral view.79
Fig. 185: Scimitar syndrome: AP view demonstrates typical curvilinear vascular opacity in right paracardiac region.
Fig. 186: Pleural effusion: Chest X-ray reveals a large homogenous opacity in left hemithorax and there is mediastinal shift to the right. This is diagnostic of a pleural effusion.
Fig. 187: Pleural effusion: PA view of chest reveals a left-sided pleural effusion. There is also an underlying spiculated mass which on biopsy was proven to be an adenocarcinoma of lung.
Fig. 188: Subpulmonic pleural effusion: PA view of the chest demonstrates a homogenous opacity in the right lower zone, appearing as an elevated flattened dome of the diaphragm. This appearance is suggestive of a subpulmonic pleural effusion. Sonography confirmed the presence of a pleural effusion.
At least 200 mL of fluid is required to cause obliteration of the CP angle on a PA view of the chest, though in some cases there is no blunting of the angle even when 500 mL of fluid is present. The lateral decubitus view is the most sensitive X-ray to demonstrate free fluid. Fluid is seen layering the dependent part of the chest wall as a thin uniform opacity. This view however may be technically difficult to obtain in a patient who is critically ill. In patients who are too critically ill to sit erect, a diagnosis of pleural effusion has to be made on a supine X-ray chest. 80The findings in moderate-sized or large effusions are a homogenous opacity of the affected hemithorax with absence of the vascular markings. This is because the fluid is layering posteriorly along the chest wall. Fluid also tends to accumulate along the apex, like an apical pleural cap, and in the base, as these are the most dependent areas on a supine film. Small pleural effusions can be easily missed on a supine radiograph. In fact only 67% sensitivity and 70% specificity have been reported for the detection of a pleural effusion on supine chest X-ray as opposed to a lateral decubitus view.
In critically ill patients who cannot be positioned for a lateral decubitus view, or if a supine radiograph shows equivocal or negative findings, sonography is an excellent means for demonstrating pleural fluid. This imaging modality is portable and can be easily performed at the bedside. Pleural fluid is seen as an anechoic area separating the echogenic line of the diaphragm and the echogenic inferior margin of the lung (Figs. 189 and 190). Sonography is also useful in differentiating a pleural effusion from atelectasis/consolidation which may simulate an effusion on the chest X-ray. Further, it is an excellent guide for thoracocentesis, markedly reducing the incidence of iatrogenic pneumothorax.
Occasionally, free pleural fluid may accumulate in a subpulmonic location between the lung and diaphragm, with the lung floating on the fluid. The upper margin of the fluid may then take the appearance of the diaphragm. There is however a subtle difference from the normal appearance of the diaphragm in a subpulmonic effusion (see Fig. 188). The peak of the diaphragm is more lateral, the medial aspect has a more gradual slope and the lateral aspect a steeper slope. On a lateral X-ray the posterior costophrenic sulcus is obliterated. Left-sided subpulmonic effusions may be detected by noting the wide distance between the stomach air bubble and diaphragm. On the right side differentiation from an enlarged liver pushing the diaphragm upwards may be difficult. In these cases either a lateral decubitus view or sonography is useful to clinch the diagnosis. A loculated effusion may occur when there are adhesions between the visceral and parietal pleura, as a result of which the fluid does not shift with change of the patient's position (Figs. 191A and B). Empyema and hemothorax may appear as loculated effusions. Sonography will demonstrate the fluid is echogenic rather than anechoic in empyemas/hemothorax.
Fig. 189: Pleural effusion: Sonography demonstrates a hypoechoic appearance of pleural fluid layering above diaphragm.
CT is extremely sensitive in detecting even small pleural fluid collections (Fig. 192). With the patient supine, free fluid accumulates posteriorly as a hypodense layer conforming to the contour of the chest wall. The presence of septae in the pleural fluid (denoting a likely exudate) is however brought out by a sonographic study rather than by a CT scan. Acute hemorrhage in the pleural space can be well-identified by the hyperdensity of blood (Fig. 193). CT is also useful in the assessment of the site, extent and wall thickening of loculated effusions (Fig. 194), and for loculated interlobar effusions. These may simulate a mass lesion on plain X-ray but can easily be differentiated on CT. CT with intravenous contrast medium is very useful in differentiating parenchymal from pleural lesions, especially when a plain radiograph has not been helpful.
Fig. 190: Pleural effusion: Sonography demonstrates pleural effusion as an echoic fluid collection. There are multiple linear bands within this fluid collection; these represent septae. Presence of septae is highly suggestive of the effusion being an exudate.
Figs. 191A and B: Interlobar effusion: (A) PA view demonstrates a well-defined opacity in the right mid-zone (B) Lateral view demonstrates the homogenous opacity seen on the PA view, represents loculated fluid in the major interlobar fissure. The inferior part of the fissure as well as the minor fissure is mildly thickened. The homogenous appearance on the PA view of an opacity in the location of the fissure would suggest the need for a lateral view to localize the lesion.
Fig. 192: Pleural effusion: CT is extremely sensitive in detecting small pleural and pericardial effusion.
Fig. 193: Hemorrhagic pleural effusion: CT chest without IV contrast reveals a thin pleural effusion on the right side and a moderate-sized pleural fluid collection on the left. The pleural fluid collection on the left is hyperdense indicating hemorrhage and the right side hypodense indicating fluid. CT is useful in differentiating pleural effusion from a hemothorax.
Empyema
On a chest radiograph an empyema is usually seen as a loculated fluid collection. It tends to be lenticular in shape as compared to a lung abscess which is rounded (Figs. 195 and 196A). Further, an empyema usually forms an obtuse angle with the chest wall while a lung abscess forms an acute angle. CT is very useful in the diagnosis and management of empyema. On CT an empyema appears as a well-defined fluid collection with enhancing parietal and visceral pleura (Fig. 196B). This sign of separation of the pleura is known as the split pleura sign.
Traditionally, empyemas have been treated with insertion of chest tubes. The success rate with chest tube drainage is 35–71%. However, 35% of all patients treated with conventional chest tubes are found to subsequently require either open chest tube drainage or decortication. Several studies have estimated the success rate of fluoroscopy, sonography and CT in image-guided percutaneous insertion of chest tubes to be between 70% and 90%. Under imaging guidance, the chest tube can be placed accurately in the fluid collection. In fact image-guided percutaneous drainage of empyemas is advocated as the primary method of treating empyemas. Patients who show inadequate drainage or progressive persistent pleural thickening may finally require decortication.
Fig. 194: Loculated pleural effusion: CT chest demonstrates pleural fluid in the right hemithorax loculated along the right lateral chest wall with multiple loculations.
Pneumothorax
Pneumothorax may be spontaneous, either primary or secondary. A rupture of an apical pleural bleb is the most likely cause for a primary spontaneous pneumothorax.
The radiographic appearances depend upon the patient's position (air is seen in the most nondependent portion of the pleural cavity) as well as the presence or absence of loculations. In an erect patient, air rises in the pleural space to the apicolateral regions, separating lung from chest wall, allowing the visceral pleural line to become visible (Figs. 197 to 199). The visceral pleural line separates the vessel-containing lung from the avascular pneumothorax. This line remains parallel with the chest wall; therefore, in a shallow pneumothorax it may be difficult to separate the visceral pleural line from the chest wall, especially if covered by ribs. To demonstrate these questionable or subtle pneumothoraxes an expiratory film is very useful (Figs. 200A and B). This increases the volume of the pneumothorax as well as changes the orientation of the ribs.
There are a number of mimics of a pneumothorax on a chest X-ray. Any curvilinear shadow projected over the lung, especially the apex, may mimic a visceral pleural line. Skin folds, tubes, vascular lines, clothing, scapulae, walls of bulla/cavities all may mimic a visceral pleural line. One of the most helpful differentiators is to follow the so-called visceral pleural line beyond the margins of the chest wall. Other helpful differentiators are when the orientation of the line is not in the orientation of the collapsed lung, or vessels are seen beyond the line. The above circumstances negate the diagnosis of a pneumothorax.
Fig. 195: Empyema: PA view of the chest demonstrates a homogenous lenticular fluid collection along right lateral chest wall with an air-fluid level. Sonography confirmed the homogenous opacity was fluid with internal echoes. An aspiration revealed an empyema.
Figs. 196A and B: Empyema: Chest X-ray and CT chest demonstrate a loculated fluid collection in the left hemithorax. There are multiple specks of air in the fluid collection. The presence of air in a pleural collection is highly suggestive of infection in the pleural fluid. Air may also be present in pleural fluid if it has been inadvertently introduced during aspiration of the fluid.
Fig. 197: Pneumothorax: PA view of chest demonstrates a right sided pneumothorax with underlying partial collapse of right upper lobe.
Fig. 198: Pneumothorax: AP portable erect X-ray reveals a large pneumothorax on the right side with partial collapse of right lung. A central line is seen in situ on the right side. The pneumothorax occurred following placement of the central line.
Figs. 199A and B: Hydropneumothorax: (A) Chest X-ray demonstrates a right upper zone pneumothorax with an air-fluid level representing a hydropneumothorax. Intercostal drainage (ICD) was placed to drain the hydropneumothorax; (B) Chest X-ray demonstrates total evacuation of hydropneumothorax.
Figs. 200A and B: Pneumothorax: (A) Chest X-ray inspiratory PA view demonstrates a suspicious thin visceral pleural line at the left apex. (B) Expiratory PA view demonstrates a large pneumothorax with a well-defined visceral pleural line. Expiratory chest X-rays are very useful to demonstrate a suspicious pneumothorax as well as the extent of the pneumothorax.
The outer margin is transradiant due to air trapped between skin fold and skin (Fig. 201). The scapula edge is a common mimic and must be looked out for. Extrapleural dissection of air from a pneumomediastinum may also be mistaken for a pneumothorax, the linear abnormality is confined to the lung apex and does not progress in size. The most difficult to differentiate are bullae as they appear translucent/avascular, and have thin well-defined margins. One differentiating feature is that the inner margin of a bulla is concave as compared to a pneumothorax, which would be convex, in line with the chest wall. CT is very helpful in excluding these mimics of a pneumothorax (Figs. 202 and 203).
As the pneumothorax increases in size and the lung collapses, the density of the underlying lung increases, till finally in total collapse it appears like a fist-like opacity overlying the hilum.85
Fig. 201: PA view of the chest revealed a well-defined line in the left hemithorax simulating a pneumothorax. This, however, is a skin fold resembling a pneumothorax as the line is seen to extend beyond the confines of the thorax into the abdomen.
Fig. 202: Pneumothorax: CT lung window demonstrates a left pneumothorax with a large thin-walled bulla in the left lingula.
As the density of the collapsing lung increases it becomes easier to detect etiological causes for the pneumothorax. For this reason, apical pleural blebs, the most common cause of a primary spontaneous pneumothorax are visible only on 15% of chest X-rays at the time of the pneumothorax. These blebs are best seen on a CT scan, being detected in 85% of cases. On both X-rays and CT scans other causes such as cysts/bullae/bronchiectasis, etc. should also be looked for. It is also important from a management perspective to estimate the size of a pneumothorax. A simple method is to measure hemithorax distance, interpleural distance.
For example, if the hemithorax distance is 10 cm and the interpleural distance is 2 cm, the size of the pneumothorax is 50%, an indication that the pneumothorax is much larger than what might be apparent on an X-ray chest.
Pneumothorax in a Supine Patient
In a number of patients in a critical care setting X-rays can only be done in a supine position. It is important to recognize the signs of a pneumothorax in a supine patient. Air collects in the highest portion of the pleural cavity which in the supine position is anterior or anteriomedially at the base. The displaced visceral pleural line is difficult to demonstrate on a supine X-ray. In the absence of this specific sign, other signs to demonstrate the collection of air are important. As air collects in the anterior costophrenic sulcus there is transradiancy in the hypochondrial region overlying the diaphragm. There is increased sharpness of the adjacent mediastinal margin and diaphragm. The costophrenic sulcus becomes deep with a well-defined margin. The inferior edge of collapsed lung becomes visible. The ipsilateral hemidiaphragm is depressed. Cardiac margins become sharp and pericardial fat pads become well-outlined.
A pneumothorax suspected on a supine film can be confirmed on a cross-table lateral view or lateral decubitus with suspect side uppermost. If there is any doubt a CT will be very useful, as it would be confirmatory (Figs. 204 and 205).
Tension pneumothorax is an absolute emergency and if untreated results in death. A tension pneumothorax occurs when air enters during inspiration but cannot exit during expiration due to a check valve mechanism (Figs. 206 and 207). On a chest X-ray, the entire hemithorax is hypertranslucent, the mediastinum is shifted to the opposite side and the ipsilateral lung is compressed. In addition the diaphragm on the affected side may be deeply inverted.86
Figs. 203A and B: Pneumothorax: (A) CT lung window and (B) minimum intensity projection demonstrate a loculated pneumothorax with adhesions along the left anterior lateral parietal pleura.
Fig. 204: Pneumothorax: Supine AP view in a patient who was hemodynamically unstable; an erect view was not possible. The costophrenic and cardiophrenic recess on the right side are deep and well-outlined. The right dome of the diaphragm is well-outlined as compared to the left. These are all features of a pneumothorax in a supine patient.
Fig. 205: Pneumothorax: Supine AP view reveals bilateral pneumothorax as evidenced by a sharp diaphragmatic contour and sharp deep bilateral costophrenic sulci. There is extensive surgical emphysema.
Management of Pneumothorax
Not every pneumothorax requires drainage. An asymptomatic pneumothorax with interpleural distance less than 2.0 cm may be successfully managed by observation with or without oxygen therapy. Larger symptomatic pneumothoraces may resolve if the air is totally aspirated and the two pleural surfaces appose each other.87
Figs. 206A and B: Tension pneumothorax: (A) Chest PA view reveals a translucency in left hemithorax due to a large pneumothorax. There is a mediastinal shift to right. These are features of a tension pneumothorax; (B) After intercostal drainage (ICD) tube insertion there is expansion of lung with return of mediastinal structures to their normal position.
Figs. 207A and B: Tension pneumothorax: (A) Axial and (B) coronal CT demonstrate a large pneumothorax on the right side. The pneumothorax is under tension as evidenced by inversion of the right dome of the diaphragm and displacement of the mediastinum. Extensive centrilobular emphysema is seen in both lung fields.
Bronchopleural Fistula
A bronchopleural fistula may be central when the communication is between the bronchus and pleura. A peripheral BPF exists when the communication is between lung parenchyma or a peripheral bronchus and the pleura. The chest radiography signs of a bronchopleural fistula are an increase in air in a pneumonectomy space, with a loss of normal mediastinal shift toward the operated side. Occasionally, the only sign is a persistence of air following pneumonectomy. CT is useful to demonstrate the bronchopleural fistula, but may do so in only 30–50% of cases (Figs. 208 to 210).
Pleural Thickening
Pleural thickening is seen as a veil-like opacity along the inner margins of the chest wall, sharply marginated along its inner aspect and fading into the chest wall along its lateral aspect. Pleural thickening involving the costophrenic angle is seen as an angular opacity differentiating it from pleural fluid which is seen as a smooth curvilinear margin (Figs. 211A and B). In cases of difficulty, a lateral decubitus or ultrasound would help in differentiation. CT is very sensitive in the detection of pleural thickening. Extrapleural fat can mimic pleural thickening; this is also well-differentiated on CT.88
Fig. 208: Bronchopleural fistula: PA view of the chest reveals well-defined walled rounded air-space in the left mid zone with an associated another small more lucent air-space along its lateral aspect.
Fig. 209: Bronchopleural fistula: CT chest with multiplanar reconstruction demonstrates a dilated bronchus communicating with a loculated pneumothorax. The thin-walled large air-space seen on the X-ray represents the located pneumothorax seen on the CT scan. The well-defined smaller lucent air-space along the lateral aspect represents a dilated bronchus communicating with the loculated pneumothorax. These are seen end on the X-ray.
Fig. 210: Bronchopleural fistula: In a case of pneumothorax, air bronchograms are seen to communicate with the left pleural cavity indicating a peripheral bronchopleural fistula.
Pleural Calcification
Pleural calcification is visualized as a sheet of calcification. When visualized en face, it appears as a veil-like opacity; when visualized in profile it is seen as a linear dense band parallel to the inner chest wall (Fig. 212). Following resolution of an empyema, calcification may be seen as a double layer due to calcification of visceral and parietal pleura. This is well-appreciated on CT.
Mesothelioma
On imaging, there are plaques/nodules on visceral/parietal pleura forming a lobular sheet of tumor up to several centimeters thick encasing the lung and growing into the interlobar fissure. Invasion of the mediastinum, diaphragm, lung may occur, though late. An important sign is the loss of lung volume on the ipsilateral side, because the mesothelioma grows as a sheet entrapping the lung (Figs. 213 and 214). These appearances are very well demonstrated on a CT, which is useful for detection, as also for demonstration of chest wall and or mediastinal invasion. Occasionally, the only finding may be pleural thickening with a small-sized ipsilateral hemithorax. The pleural masses are seen to creep along the pleural surfaces. MRI is also useful for demonstrating chest wall and mediastinal involvement.89
Figs. 211A and B: Pleural thickening: (A) PA and (B) lateral views demonstrate thickening of the minor fissure following resolution of an interlobar effusion.
Fig. 212: Pleural calcification: AP view of chest reveals veil-like calcification in the left hemithorax.
Fig. 213: Pleural mesothelioma: CT chest shows presence of multiple lobulated enhancing lesions along the entire right pleural surface.
MEDIASTINUM
The chest radiograph is usually the first investigation performed for a suspected mediastinal/hilar mass lesion. Mediastinal masses may also be detected incidentally on X-rays done for other reasons. If a mediastinal pathology is suspected and the chest X-ray reveals no abnormality, a cross-sectional imaging technique, ideally a CT scan is required. Mediastinal pathology may be obscured by mediastinal vasculature on an X-ray. A CT scan is very useful to characterize the mass lesion; it also serves as a guide for biopsy of a mediastinal mass. Mediastinal masses appear on chest X-rays as projections from the mediastinal silhouette. Hilar masses are visualized as prominence and or enlargement of the hilum. The first step in the differential diagnosis is to determine if the lesion arises from the mediastinum or lung. A spiculated mass lesion will nearly always be of pulmonary origin. Homogenous masses which project beyond the confines of the mediastinum, have a broad base and form obtuse angles with the mediastinum, arise from the mediastinum or mediastinal pleura. The differential diagnosis of mediastinal masses is based on their location and internal morphology.90
LOCATION
Prevascular Masses
Prevascular masses are located anterior to the ascending aorta and its branches. These are most commonly thymic masses, thyroid masses, germ cell tumors or lymphadenopathy. Thyroid masses are easy to diagnose as they are seen in the superior mediastinum contiguous with the thyroid in the neck. On unenhanced scans they are of a higher attenuation than adjacent skeletal muscle in view of their iodine content. Internally, thyroid masses are heterogeneous with calcific densities and cysts. Thyroid masses are the most common lesions to cause deviation of the trachea. Thymic and germ cell tumors appear similar on imaging; their differentiation is based on clinical and laboratory features. Thymomas may be clinically associated with myasthenia gravis, red cell aplasia, and hypogammaglobulinemia. An elevated HCG or alpha fetoprotein levels are indicative of a germ cell tumor. Thymoma, germ cell tumors may demonstrate calcification. Presence of fat, cartilaginous calcification, teeth or a fat-fluid level are indicative of a mature teratoma.
Fig. 214: Mesothelioma: CT chest reveals plaque-like thickening of pleural surface with nodularity of surface in left apical region. Biopsy revealed a mesothelioma. Note vascular encasement of the great vessels by the mesothelioma.
Unusual causes of prevascular masses are parathyroid adenoma (usually evidence of hyperparathyroidism). Lymphangioma (cystic with multiple internal septations). Cystic hygroma should be considered when a cystic mass is seen extending from the neck into the mediastinum.
Paracardiac Masses
Chiefly include pericardial cyst, diaphragmatic hernia and lymphadenopathy.
Pericardial cysts are easily diagnosed as they are homogenous, of water attenuation, with thin walls. Diaphragmatic hernias (Morgagni's hernia) are due to a defect in the diaphragm with herniation of a pad of fat and or bowel loops into the thorax. Occasionally, germ cell tumors and thymomas may be visualized in a paracardiac location.
Paratracheal, Subcarinal and Paraesophageal Masses
These are considered together as they are contained in one fascial sheath. The group includes lymphadenopathy (Figs. 215 to 219), foregut malformations, esophageal tumors, thyroid mass lesions, hiatus hernia, aneurysms, vascular anomalies and pancreatic pseudocyst. The most common of these is lymphadenopathy. Esophageal carcinoma presents early as dysphagia and generally results in a small mass lesion. Vascular anomalies and aneurysms are visualized as homogenous enhancing structures. Foregut malformations are fluid-filled well-defined lesions in relation to the vertebrae, esophagus or tracheobronchial tree.
Figs. 215A to C: Mediastinal adeuopathy: Chest X-ray (A) reveals a large right paratracheal mass lesion. Note it is homogenous with a wide mediastinal base and obtuse angles with the lung indicating a mediastinal mass lesion. Lateral view (B) demonstrates the mass lesion to be anterior mediastinum. CT chest (C) confirms that the mass lesion is a large necrotic adenopathy. CT-guided aspiration confirmed the adenopathy to be of tubercular origin.
Figs. 216A to C: Mediastinal adenopathy: (A) Chest X-ray reveals right paratracheal and left hilar adenopathy (B and C) CT chest confirms adenopathy as well as demonstrates small left prevascular adenopathy and large subcarinal adenopathy, not detected on the X-ray as these were covered by the mediastinum.
Figs. 217A to C: Mediastinal adenopathy: (A) Chest X-ray demonstrates large right paratracheal and hilar adenopathy; (B) CT chest; (C) confirms adenopathy, which are necrotic, indicating tuberculosis.
Fig. 218: Mediastinal adenopathy: Chest X-ray demonstrates large hilar and right paratracheal mass lesions representing adenopathy.
Prevertebral Masses
These are most commonly neurogenic tumors, or lymph gland masses. Other pathologies include mesenchymal tumors, lesions arising from the pharynx, or vertebra. A paraspinal abscess and an aneurysm of the descending aorta are also observed in the prevertebral location.
Imaging studies of prevascular masses, of paracardiac masses, of paratracheal, subcarinal, paraesophageal masses and of prevertebral masses have been amply illustrated in the chapter on Diseases of the Mediastinum and therefore do not bear repetition.92
Figs. 219A to E: Metastatic mediastinal adenopathy: (A) Chest X-ray reveals an opacity in the left para-aortic region, however, not silhouetting the aorta; (B) Coronal CT demonstrates a spiculated mass lesion in the left apex; (C) axial CT demonstrates spiculated apical mass lesion very well. CT-guided fine-needle aspiration cytology (FNAC) revealed mass to be squamous cell carcinoma; (D) axial post-contrast CT reveals large anterior mediastinal mass lesion representing metastatic adenopathy; (E) coronal reconstruction demonstrates large anterior mediastinal adenopathy.
SUGGESTED READING
- David MH, Peter A, David L, et al. Imaging of the Diseases of the Chest, 4th edition. Philadelphia: Elsevier Mosby; 2005.
- Grenier PA. Imaging of airway diseases. Radiol Clin North Am. 2009;47.
- Sanjiv B. Thoracic MDCT comes of age. Radiol Clin North Am. 2010;48.