Highresolution Computed Tomography Technique

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Coining of the term ''HRCT'' is credited to Todo et al. [2], who described the potential use of this technique in the Japanese literature in 1982. The first reports of HRCT in English date to 1985 [3-5], and since that time, HRCT techniques have undergone dramatic development.

Compared with conventional CT, HRCT requires use of the thinnest collimation possible (1-1.5 mm), image reconstruction with a high-spatial frequency (''bone'') algorithm, increased kVp (120-140) or mA (140-240; mAs 240-400), and use of the largest matrix size available (512 X 512). A range of recommended window settings are available, reflecting differences in personal preference. What is important is that at least one consistent window setting be used. Window mean values ranging from -600 to -700 HU and widow width values ranging from 1000 to 1500 HU are appropriate [6].

With thicker collimation, volume averaging reduces the ability of CT to resolve small structures, such as branches of small airways or vessels, and slight increases or decreases in lung attenuation. Use of a high-spatial frequency algorithm reduces image smoothing and increases spatial resolution, making structures appear sharper. One drawback to this is increased visibility of noise, which can be offset somewhat by increasing the number of photons or scan time (milliamperes-seconds). Because increased scan times can result in increased motion artifacts, it is desirable to limit scan time to 1 -2 sec. Increased kilovolts or milliamperes is desirable in large patients in whom noise is a bigger problem, always keeping in mind that increasing scan technique also increases the radiation dose to the patient. This is usually of little clinical concern since with HRCT, radiation is limited to a few thin scan levels. HRCT scanning at 10- 20-mm intervals results in 12 and 6%, respectively, of the radiation dose associated with conventional CT [7].

The ability of HRCT to resolve fine lung structures depends on their orientation relative to the scan plane [8]. Structures measuring 0.1 to 0.2 mm in thickness can be seen if they are largely oriented perpendicular to the scan plane and extend through the thickness of the scan plane, whereas similarly sized structures that are oriented horizontally within the scan plane will not be visible because of volume averaging with the air-filled lung, which occupies most of the thickness of the voxel. Normal interlobular septa, measuring 0.1 to 0.2 mm in thickness will occasionally be seen on HRCT. Bronchi or bronchioles measuring less than 2 to 3 mm in diameter and having a wall thickness of approximately 0.3 mm are usually invisible in the peripheral lung because they have courses that lie roughly in the plane of the scan.

Routine HRCT is obtained during suspended full inspiration with the patient supine. There is no consensus as to whether scans should be obtained at 1-, 2-, or 4-cm intervals, at three preselected levels or at one or two levels through the lower lungs. HRCT provides a sampling of lung anatomy and is therefore most useful in evaluation of diffuse lung disease, especially when performed in lieu of a conventional CT exam. When patients may have limited disease that manifests as small structures scattered throughout the lungs, such as with low profusion silicosis, HRCT may completely miss the disease. In these cases, HRCT should be performed in conjunction with conventional CT. In patients suspected of having interstitial disease that may be limited to the lung bases, such as asbestosis, HRCT should be performed with the patient in both supine and prone positions when supine images show dependent opacities (Fig. 1).

When patients are suspected of having airways disease, such as oblitera-tive bronchiolitis or asthma, scans obtained during expiration should be obtained to detect air trapping. In normal patients, in most lung regions, lung parenchyma increases uniformly in attenuation during expiration, but in the presence of air trapping lung parenchyma remains lucent on expiration and shows little change in volume [9]. Expiratory HRCT can show air trapping in the absence of abnormalities on inspiratory images.

Figure 1 Supine and prone HRCT. (A) Supine HRCT of a 78-year-old man with congestive heart failure and emphysema shows layers of small ''cysts'' in the dependent portions of the lungs, suggestive of honeycombing and pulmonary fibrosis. (B) Prone HRCT of the same patient in A 1 day later shows no evidence of honeycombing. There are scattered lucent areas (arrows) representing emphysema and scattered areas of linear atelectasis or scarring. There is decreased ground-glass opacification compared with A as a result of interval diuresis and decrease in pulmonary edema.

Figure 1 Supine and prone HRCT. (A) Supine HRCT of a 78-year-old man with congestive heart failure and emphysema shows layers of small ''cysts'' in the dependent portions of the lungs, suggestive of honeycombing and pulmonary fibrosis. (B) Prone HRCT of the same patient in A 1 day later shows no evidence of honeycombing. There are scattered lucent areas (arrows) representing emphysema and scattered areas of linear atelectasis or scarring. There is decreased ground-glass opacification compared with A as a result of interval diuresis and decrease in pulmonary edema.

Table 1 Indications for the Use of HRCT

1. Unexplained dyspnea in a patient with suspected chronic diffuse infiltrative lung disease

2. Symptomatic patients with known exposures to inorganic dusts such as silica and asbestos, organic antigens, or drugs

3. Immunosuppressed patients with unexplained dyspnea or fever

4. Patients with unexplained hemoptysis

5. Patients with dyspnea or other respiratory symptoms and suspected airways or obstructive lung disease

III. SENSITIVITY AND SPECIFICITY OF HIGH-RESOLUTION COMPUTED TOMOGRAPHY IN THE DIAGNOSIS OF DIFFUSE INFILTRATIVE LUNG DISEASE

Over a hundred different causes of diffuse infiltrative lung diseases have been described, with a yearly incidence of 31.5 and 26.1 per 100,000 men and women respectively [10]. Chest radiographs are relatively inexpensive and easy to obtain and can answer many clinical questions without requiring further diagnostic imaging. However, it is well documented that chest radiographs are limited in both their sensitivity and specificity in patients with diffuse lung disease [11,12].

Up to 50% of patients with proven lung disease on HRCT have normal chest radiographs [13-15]. Both conventional CT and HRCT are more sensitive than chest radiography for detecting both acute and chronic diffuse lung diseases [16-21]. The sensitivity and specificity of HRCT for detecting pulmonary disease are approximately 94 and 96% compared with 80 and 82% for chest radiographs [12,22]. Because of its excellent sensitivity, HRCT can be used to detect lung disease in patients with normal or questionable radiographic abnormalities or who have symptoms or pulmonary function findings suggestive of acute or chronic diffuse lung disease (Table 1), to assess disease activity, and to guide biopsy procedures.

IV. DIAGNOSTIC PATTERNS OF DISEASE ON HIGH-RESOLUTION COMPUTED TOMOGRAPHY

HRCT findings can often be used to limit the differential diagnosis to a few possibilities or, in some cases, can be sufficiently characteristic (in the appro-

Polymyositis Lung Disease
Figure 2 Septic emboli. HRCT of a 32-year-old man with positive blood cultures for Staphylococcus aureus shows characteristic cavitating nodules in a predominantly peripheral location.

priate clinical setting) to allow a specific or presumptive diagnosis in the absence of histologic verification (Figs. 2 and 3). Patchy and centrilobular (involving the center of the secondary pulmonary lobule) ground-glass opacities, in a patient with the appropriate exposure history and serologic tests, suggest the diagnosis of acute or subacute hypersensitivity pneumonitis [23] (Fig. 4). Abnormalities are found predominantly in the middle lung zones, and the lung bases are relatively spared.

Sarcoidosis is characterized by nonnecrotizing granulomas distributed

Figure 3 Posttransplant lymphoproliferative disease. HRCT of a 39-year-old man with a history of three renal transplants and on large doses of immunosuppressive drugs shows patchy areas of consolidation in a characteristic bronchovascular distribution. Note air bronchograms (arrows).

Figure 4 Acute hypersensitivity pneumonitis. HRCT of a 59-year-old woman with fever, chills, dyspnea on exertion, headache, minimal nonproductive cough, fatigue, crackles at the lung bases, and hypoxemia shows multifocal areas of ground-glass opacification in a centrilobular distribution. The patient's symptoms resolved while in the hospital but recurred when she went home, where she was exposed to her pet parakeets. Transbronchial biopsy specimen showed noncaseating granulomas and lymphocytes.

along the lymphatic pathways of the bronchovascular bundles and interlobular septa. The opacities tend to be nodular and predominate in upper and middle lung zones. In later stages, cicatricial changes result in architectural distortion and fibrotic areas of consolidation, with surrounding areas of emphysema, similar to the findings that can be seen in patients with complicated silicosis (Fig. 5). Eliciting an appropriate history of exposure to dusts can be helpful

Figure 5 Complicated silicosis. HRCT of a 48-year-old man with a long history as a foundry worker shows numerous small nodules (small arrows) and bilateral conglomerate masses (large arrows) referred to as ''progressive massive fibrosis.'' The same findings can also be seen in sarcoidosis.

in distinguishing the two diseases. In the appropriate clinical setting, classic findings of peribronchovascular (thickening of the axial interstitium surrounding the parahilar bronchi and vessels) and subpleural nodules, especially when associated with central airway abnormalities, should allow a confident diagnosis of sarcoidosis without needing biopsy in most cases [17,24-26].

HRCT of lymphangitic carcinomatosis is characterized by nodular thickening of the interlobular septa without cicatricial distortion of polygonal architecture. Distribution tends to be basilar and peribronchovascular nodularity is often present [27]. A unilateral distribution suggests primary bronchogenic carcinoma as the underlying tumor, as most other tumors result in bilateral lung involvement (Fig. 6).

Smooth subpleural and peribronchovascular thickening associated with increased thickness and number of visible interlobular septal lines without nodularity are characteristics of the interstitial abnormalities seen in pulmonary edema (Fig. 7). The abnormal opacities usually are predominant in the dependent portions of lung. Various degrees of consolidation and ground-glass opacification may be present when there is air-space edema, along with cardiac enlargement, vascular engorgement, and pleural effusions.

Lymphangioleiomyomatosis and pulmonary involvement in tuberous sclerosis are radiologically and pathologically identical. Both are characterized by proliferation of smooth muscle cells along bronchovascular bundles, lymphatics, and pulmonary veins. Numerous small parenchymal cysts are uniformly distributed throughout the lungs and are a characteristic finding on HRCT (Fig. 8) [28,29]. Additional findings that may not be evident on chest

Diffuse Alveolar Hemorrhage

Figure 6 Lymphangitic carcinomatosis. HRCT of a 53-year-old man with large cell bronchogenic carcinoma and symptoms of cough and wheezing shows nodular thickening of the interlobular septa (large arrows) and bronchovascular bundles (small arrow). Unilateral involvement is characteristic of a primary bronchogenic carcinoma.

Figure 6 Lymphangitic carcinomatosis. HRCT of a 53-year-old man with large cell bronchogenic carcinoma and symptoms of cough and wheezing shows nodular thickening of the interlobular septa (large arrows) and bronchovascular bundles (small arrow). Unilateral involvement is characteristic of a primary bronchogenic carcinoma.

Figure 7 Pulmonary edema. HRCT of a 69-year-old woman shows smooth interlobular septal thickening (Kerley A and B lines, arrows), patchy ground-glass opacification (arrowheads), and a small right pleural effusion (E).

radiographs include pneumothorax, chylous pleural effusion, mediastinal lym-phangiomyomatous adenopathy, and renal or hepatic angiomyolipomata.

The parenchymal disease of Langerhan's cell histiocytosis tends to have an upper lung predominance. Even when diffuse, the disease tends to spare the costophrenic angles. Cystic changes and nodules are the predominant HRCT finding (Fig. 9) [30]. Usually, small thin-walled, air-filled cysts or nodules are present. Nodules may progress to cavitated nodules to cysts to confluent cysts. The cysts seen on HRCT in patients with lymphangioleiomyomatosis can have a similar appearance but are generally not associated with nodular changes or an upper lung distribution. The HRCT cystic findings in Langerhan's cell

Figure 8 Lymphangioleiomyomatosis. HRCT of a 50-year-old woman with increasing shortness of breath and hemoptysis shows characteristic thin-walled cysts (arrows) with surrounding normal pulmonary architecture. Note pneumothorax on right (P).
Hot Tub Lung
Figure 9 Langerhan's cell histiocytosis. HRCT of an adult male cigarette smoker shows characteristic combination of thin-walled cysts (small arrows) and nodules (large arrows). The upper and middle lungs were predominantly involved.

histiocytosis can also resemble bronchiectasis, but examination of serial sections can differentiate tubular from spherical structures. Cysts in lymphangio-leiomyomatosis and Langerhan's cell histiocytosis do not have a peripheral distribution as they do in honeycomb cysts of pulmonary fibrosis.

HRCT findings have been shown to be highly accurate in diagnosing idiopathic pulmonary fibrosis or other causes of usual interstitial pneumonitis (UIP) [31]. UIP is the most common abnormal finding in patients with chronic progressive infiltrating lung disease. It is a histopathological term referring to a pattern of interstitial fibrosis that occurs in patients with various disorders, including idiopathic pulmonary fibrosis, asbestosis, rheumatoid arthritis, mixed connective tissue disease, and scleroderma. The patient's clinical presentation determines the specific diagnosis in these situations. HRCT is often useful in demonstrating the typical features of UIP: patchy reticular, honeycomb, and ground-glass opacities. The abnormalities have a distinctive bibasi-lar and subpleural distribution. HRCT can be used to assess response to steroid therapy. Patients with UIP who are found to have areas of ground-glass opacity in the absence of significant honeycombing or traction bronchiectasis are more likely to have a response to steroid therapy than are those with only honeycombing or linear or nodular opacities [32]. In the majority of patients who present with clinical features of idiopathic pulmonary fibrosis, the presence of predominately subpleural and bibasilar distribution of fibrosis on HRCT can be sufficiently characteristic to obviate biopsy (Fig. 10) [33,34].

HRCT of emphysema is characterized by bullae or small lucent areas (or both) without the well-defined walls one would expect to see with lung

Figure 10 Usual interstitial pneumonitis. HRCT of a 74-year-old man with rheumatoid arthritis shows characteristic rows of small thick-walled cysts in a peripheral, bi-basilar distribution.

cysts or honeycombing. HRCT can show changes of centrilobular, panacinar, paracicatricial, and paraseptal emphysema [35]. In some cases, HRCT may show that apparent diffuse infiltrative lung disease on chest radiographs is due to emphysema.

Less than 50% of patients with chronic eosinophilic pneumonia have the classic pattern of peripheral air-space disease involving the middle and upper lung zones on chest radiography [36]. HRCT, unlimited by superimposition of structures, can better display the peripheral distribution of consolidation and ground-glass opacities. The appearance can be identical to bronchiolitis obliterans organizing pneumonia (BOOP). However, in BOOP, bronchial wall thickening and dilatation are frequently found within the areas of consolidation. BOOP can also infrequently be characterized by a central distribution of disease without subpleural involvement.

Bronchiectasis is defined as irreversible dilatation of bronchi. The etiology is usually infectious and bronchiectasis is commonly associated with underlying airway obstruction as occurs with inspissated secretions in patients with cystic fibrosis. The diagnosis of bronchiectasis can be made on HRCT when airways are larger in diameter than the accompanying pulmonary arteries or when small airways are visualized in the periphery of the lungs or along the mediastinal pleural surface. With increasing grades of severity, bronchiectasis can appear smooth-walled (cylindrical), beaded (varicose), or cystic, with clusters of cysts often associated with air-fluid levels. Certain patterns of bronchiectasis are sufficiently characteristic to suggest a specific diagnosis in the appropriate clinical context. For example, central bronchiectasis is a frequent finding in patients with allergic bronchopulmonary aspergillosis. Bronchiectasis associated with ipsilateral hypoplasia of the lung is characteristic of Swyer-James syndrome.

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