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- 发布日期：2025-01-04 10:50 点击次数：106
- case98HRCT in a 45-year-old man with a history of cigarette smoking, chronic cough, and recent hemoptysis (Figure 1, Figure 2, Figure 3).HRCT shows numerous, thick and thin-walled lung cysts (Figure 2) appearing in clusters, with intervening lung appearing normal. Note that the lung bases are spared (Figure 3). A scan through the right upper lobe shows ground-glass opacity (Figure 1) in association with some interlobular septal thicknening.Could this be: LAMNo. This is a man! Also, the cysts predominate in the upper lobes. pneumocystis pneumonia with pneumatocelesPossibly. However, the patient is not immunosuppressed, and the ground-glass opacity is unilateral, a very unusual appearance for PCP. histiocystosis with pulmonary hemorrhageThis is the best diagnosis. The patient is a smoker, the cysts are upper lobe in distribution, and the ground-glass opacity could represent hemorrhage, leading to his hemoptysis.Diagnosis: Langerhans histiocytosis with pulmonary hemorrhage, presenting with lung cystsDISCUSSIONCommon presenting complaints in patients with histiocytosis are cough and dyspnea, but hemoptysis occurs in more than 5% of cases. （缩略图，点击图片链接看原图）case99HRCT in a 27-year-old man with AIDS, a low CD4 count, marked dyspnea, and fever (Figure 1).HRCT shows patchy ground glass opacity in the upper lobes, more pronounced on the left than the right. The ground-glass opacity is accompanied by mild interstitial thickening, manifested as a faintly nodular appearance and septal thickening. Two thin-walled lung cysts are visible.The presence of ground-glass opacity in an AIDS patients with a low CD4 count is highly predictive of pneumocystis pneumonia.Diagnosis: Pneumocystis carinii pneumonia with pneumatocelesDISCUSSIONIt has been estimated that 10-35% of patients with PCP demonstrate either air-filled cysts or pneumatoceles, typically involving the upper lobes. Also, up to 35% of patients with cysts develop a pneumothorax.Initially, cysts appears as small lucencies in areas of parenchymal consolidation. With time, these coalesce to form bizarre shaped, thick-walled cysts that often appear septated. Following therapy these lesions eventually regress, resulting either in complete disappearance, or residual nodules or scars. screen.width-333)this.width=screen.width-333" width=420 height=223 title="Click to view full case99.jpg (420 X 223)" border=0 align=absmiddle>case100HRCT in a 35-year-old man with AIDS, a low CD4 count, and a history of previous pneumocystis pneumonia (Figure 1, Figure 2, Figure 3).HRCT shows numerous thin walled cysts in both lungs, and a right sided pneumothorax. Note that one cyst projects from the pleural surface. The rupture of such a cyst is the likely cause of the pneumothorax. Some focal and patchy areas of ground-glass opacity are also present; this could reflect ongoing pneumocystis infection or the result of prior infections.Diagnosis: Pneumocystis carinii pneumonia (previous) with pneumatoceles and pneumothorax.DISCUSSIONIt has been estimated that 10-35% of patients with PCP demonstrate either air-filled cysts or pneumatoceles, typically involving the upper lobes. Also, up to 35% of patients with cysts develop a pneumothorax. （缩略图，点击图片链接看原图）case101HRCT in a 22-year-old woman with a known history of laryngeal papillomas for which she has had multiple laryngoscopic resections (Figure 1, Figure 2, Figure 3, Figure 4, Figure 5, Figure 6).HRCT shows numerous thin-walled cysts (Figure 2) in both lungs. Some are quite irregular in shape or appear fused. In several locations, small nodules are visible, as isolated abnormalities or in relation to or within the cysts.Diagnosis: Bronchopulmonary papillomatosis with lung cystsDISCUSSIONSquamous papillomas occur most commonly as laryngeal tumors in children, and are caused by human papilloma virus. In most cases, they resolve spontaneously, but in patients requiring resection, they may recur and progress. In 1-2% of cases, distal spread occurs with involvement of the trachea (most common) or bronchi (least common).With involvement of small airways, papillomas may be seen as nodular opacities, and cavitation is common. Progression to form cystic lesions lined by papillomatous epithelium is typical. The presence of nodules within the cysts is often seen, as in this case.When papillomas involve small bronchi and lung, this condition tends to be progressive. Although there may be some response to antiviral agents, the prognosis is poor. Malignant degeneration may occur.Other tumors may be associated with thin walled, cystic lung metastases, including squamous cell carcinoma, adenocarcinoma, and sarcomas. （缩略图，点击图片链接看原图）case102HRCT in a 81-year-old man with a smoking history, a clinical diagnosis of COPD, and increasing shortness of breath (Figure 1, Figure 2, Figure 3, Figure 4, Figure 5).HRCT shows numerous areas of lucency, as compared to the background of normal lung. The lucencies do not have visible walls. They appear to be evenly spaced throughout the lung, when viewed in cross section. Some of the lucencies can be seen to be centrilobular or surround the centrilobular artery.Although these lucencies are diffuse, when a scan at the lung apices (Figure 1) is compared to one at the bases (Figure 5), it is clear that the lucencies have an upper lobe predominance in both size and number.This appearance is diagnostic of centrilobular emphysema. Centrilobular emphysema results in focal lucencies without walls, has a spotty or centrilobular distribution in cross section, and an upper lobe predominance.Diagnosis: Centrilobular emphysemaDISCUSSIONEmphysema is defined as a permanent, abnormal enlargement of airspaces distal to the terminal bronchiole, accompanied by the destruction of the walls of the involved airspaces. Emphysema is accurately diagnosed using HRCT, and results in focal areas of very low attenuation which can be easily contrasted with surrounding, higher attenuation, normal lung parenchyma if sufficiently low window means (-600 HU to -800 HU) are used. Although some types of emphysema can have walls visible on HRCT, these are usually inconspicuous. In many patients it is possible to classify the type of emphysema based on its HRCT appearance.Centrilobular emphysema predominantly affects the respiratory bronchioles in the central portions of acini, and therefore involves the central portion of the lobule. Centrilobular emphysema usually results from cigarette smoking, and is most common in clinical practice. It mainly involves the upper lung zones.Centrilobular emphysema of mild to moderate degree is characterized on HRCT by the presence of multiple small, round areas of abnormally low attenuation, several millimeters in diameter, distributed throughout the lung, but usually having an upper lobe predominance. Areas of lucency often appear to be grouped near the centers of secondary pulmonary lobules, surrounding the centrilobular artery branches. Although the centrilobular location of lucencies cannot always be recognized on HRCT, the presence of multiple, small, areas of emphysema, scattered throughout the lung, is diagnostic of centrilobular emphysema. In most cases, the areas of low attenuation lack visible walls, although very thin and relatively inconspicuous walls are occasionally seen on HRCT, probably related to surrounding fibrosis. （缩略图，点击图片链接看原图）case103HRCT in a 46-year-old male nonsmoker with a left lung transplant for emphysema (Figure 1, Figure 2, Figure 3, Figure 4).In this patient, the normal transplanted left lung to be compared to the abnormal right lung (Figure 3). Note that the right lung is more lucent, larger, and contains much smaller vessels than the normal left lung. The abnormality is diffuse, and the upper and lower lobes are involved to the same degree.These findings are typical of panlobular emphysema. The lung is diffusely abnormal, being too lucent and contains to few vessels. Focal lucencies, as would be seen with centrilobular or bullous emphysema, are not visible.Diagnosis: Panlobular emphysema associated with alpha-1-antitrypsin deficiency.DISCUSSIONPanlobular emphysema involves all the components of the lobule. Panlobular emphysema is classically associated with alpha-1-protease inhibitor (alpha-1-antitrypsin) deficiency, although it may also be seen without protease deficiency in smokers, in the elderly, and distal to bronchial and bronchiolar obliteration.Panlobular emphysema is characterized by uniform destruction of the pulmonary lobule, leading to widespread areas of abnormally low attenuation. Pulmonary vessels in the affected lung appear fewer and smaller than normal. Panlobular emphysema appears diffuse or most severe in the lower lobes.While it may lead to extensive destruction of the lung parenchyma, focal lucencies less than 1 cm in diameter, which are characteristically present in mild and moderate centrilobular emphysema, are not seen in panlobular emphysema. In severe panlobular emphysema, the characteristic appearance of extensive lung destruction and the associated paucity of vascular markings are easily distinguished from normal lung parenchyma. On the other hand, mild and even moderately severe panlobular emphysema can be very subtle and difficult to detect. （缩略图，点击图片链接看原图）case104HRCT in a 58-year-old man with a smoking history and shortness of breath (Figure 1, Figure 2).HRCT shows spotty areas of lucency without visible walls typical of centrilobular emphysema.In addition, a row of discrete subpleural lucencies, 1-2 cm in size, appear to be marginated by interlobular septa. These represent paraseptal emphysema.Diagnosis: Paraseptal emphysema associated with centrilobular emphysema.DISCUSSIONParaseptal emphysema predominantly involves the alveolar ducts and sacs, with areas of destruction often marginated by interlobular septa. Paraseptal emphysema can be an isolated phenomenon in young adults, often associated with spontaneous pneumothorax, or can be seen in older patients with centrilobular emphysema.Paraseptal emphysema is most striking in a subpleural location. Areas of subpleural paraseptal emphysema often have visible walls, but these walls are very thin; they often correspond to interlobular septa.When larger than 1 cm in diameter, areas of paraseptal emphysema are most appropriately termed bullae. Subpleural bullae are frequently considered to be a manifestation of paraseptal emphysema although they may be seen in all types of emphysema and as an isolated phenomenon; regardless of the cause of the subpleural bullae, they usually have thin walls which are visible on HRCT.This type of emphysema is seen on CT in the majority of non-smoking patients with spontaneous pneumothorax. （缩略图，点击图片链接看原图）case105HRCT in a 34-year-old man with a smoking history and marked, progressive, shortness of breath (Figure 1, Figure 2).HRCT shows numerous large and small areas of lucency (Figure 1), as compared to the background density of normal lung. Note that some spotty lucencies without visible walls can be seen. These are typical of centrilobular emphysema.In addition, a row of discrete subpleural lucencies, 1-2 cm in size, appear to be marginated by interlobular septa. These represent paraseptal emphysema.In some regions, areas of paraseptal emphysema are associated with air trapping, and have markedly increased in size. These cystic regions of emphysema, often marginated by a thin wall, are termed bullae.Diagnosis: Bullous emphysema.DISCUSSION"Bullous emphysema" does not represent a specific pathologic entity, but refers to the refers to the presence of emphysema associated with large bullae; it is generally seen in patients with centrilobular emphysema and/or paraseptal emphysema. A syndrome of bullous emphysema, or "giant bullous emphysema," has been described on the basis of clinical and radiologic features, and is also known as "vanishing lung syndrome." Giant bullous emphysema is often seen in young men, and is characterized by the presence of large, progressive, upper lobe bullae, which occupy a significant volume of a hemithorax, and are often asymmetric. Most patients with giant bullous emphysema are cigarette smokers, but this entity may also occur in non-smokers.CT has been reported to be of value in the preoperative assessment of patients with bullous emphysema. Surgery is generally impossible if bullae are associated with extensive emphysema. Bullectomy is most effective when localized giant bullae are associated with localized paraseptal emphysema. screen.width-333)this.width=screen.width-333" width=420 height=616 title="Click to view full case105.jpg (420 X 616)" border=0 align=absmiddle>case106HRCT in a 59-year-old woman with a smoking history and increasing shortness of breath (Figure 1, Figure 2, Figure 3, Figure 4, Figure 5).HRCT shows numerous focal areas of lucency (Figure 2), as compared to the background of normal lung. The lucencies do not have visible walls, and have a spotty distribution. Although the lucencies are large and confluent in the upper lobes, small centrilobular lucencies can still be seen in some less abnormal regions (Figure 4).Although the abnormality is diffuse, when a scan at the lung apices (Figure 1) is compared to one at the bases (Figure 5), it is clear that the lucencies have an upper lobe predominance in both size and number.In addition to findings of emphysema, an irregular lung nodule is visible in the right upper lobe.Diagnosis: Centrilobular emphysema associated with adenocarcinomaDISCUSSIONCentrilobular emphysema usually results from cigarette smoking. It predominantly involves the upper lung zones. Although in cases of mild to moderate centrilobular emphysema, HRCT is characterized by the presence of multiple small, round areas of lucency, several millimeters in diameter, with more severe centrilobular emphysema, areas of destruction can become confluent. When this occurs, the centrilobular distribution of abnormalities is no longer recognizable on HRCT (or pathologically); the term confluent centrilobular emphysema is sometimes used to describe this occurrence. This appearance can closely mimic the appearance of panlobular emphysema, and a distinction between these is of little clinical significance.Because of the common association of both emphysema and lung cancer with smoking, it is not uncommon to incidentally detect a neoplasm in patients being studied with CT for assessment of emphysema. Incidental cancer has been detected in as many as 5% of such cases. （缩略图，点击图片链接看原图）case107HRCT in a 43-year-old nonsmoker with a right lung transplant (Figure 1).What type of emphysema is shown in this patient's native left lung? Centrilobular PanlobularCorrect. HRCT shows a diffuse decrease in attenuation in the left lung with a decrease in the size of vessels, typical of panlobular emphysema. Incidentally noted is a linear scar or area of atelectasis.Subpleural lucencies are absent.The lung is diffusely decreased in density. Focal air-containing cysts with visible walls are absent.Diagnosis: Panlobular emphysema with lung transplanation.DISCUSSIONPanlobular emphysema is not usually associated with paraseptal emphysema or bullae. screen.width-333)this.width=screen.width-333" width=420 height=310 title="Click to view full case107.jpg (420 X 310)" border=0 align=absmiddle>case108HRCT in a 56-year-old man with a smoking history and increasing shortness of breath (Figure 1, Figure 2, Figure 3).HRCT shows numerous focal and spotty areas of emphysema (Figure 1) typical of centrilobular emphysema. In this patient, there is also some prominence of interlobular septa. This can be seen in some patients with centrilobular emphysema, probably due to mild associated fibrosis.Although the emphysema is confluent in some regions, the diffuse lucency seen with panlobular emphysema is not visible.Typical subpleural lucencies are visible in several locations. Large bullae with visible walls are present.Diagnosis: Centrilobular emphysema with paraseptal emphysema and bullae.DISCUSSIONIn patients with a smoking history, all of these 3 types of emphysema may be seen in conjunction. （缩略图，点击图片链接看原图）case109HRCT in a 28-year-old man with AIDS, a low CD4 count, a history of prior pneumonias, and a history of smoking (Figure 1, Figure 2).HRCT shows patchy areas of lucency (Figure 1), most without visible walls, having an aymmetrical distribution. Bullae (Figure 2) are also present.What is the most likely diagnosis? Pneumocystis carinii pneumonia with pneumatoceles EmphysemaThis is a diffficult case. Although ground-glass opacity typical of pneumocystis pneumonia is present, it is not a prominent feature. Prior infection cannot be ruled out. The appearance of these areas of lucency are most typical of centrilobular emphysema, being spotty and centrilobular in location. The presence of bullae also suggest emphysema. The asymmetry seen in this patient is atypical for emphysema, but may reflect prior infection.Diagnosis: Emphysema in an AIDS patient.DISCUSSIONIn addition to development of cysts and pneumatoceles, AIDS patients may also develop premature emphysema and bullous disease. Bullae are visible in as many as 40% of patients. In 70% of these cases, emphysema was preceded by one or more documented episodes of infection. Although this appearance can mimic the presence of cystic lung disease occurring in a patient with PCP, well-defined cysts randomly distributed throughout the lungs are more characteristic in patients with PCP and pneumatoceles. In this case, a combination of emphysema and lung cysts may be present. screen.width-333)this.width=screen.width-333" width=420 height=487 title="Click to view full case109.jpg (420 X 487)" border=0 align=absmiddle>case110HRCT in a 60-year-old man with a history of recent treated pneumonia with persistent cough and fever (Figure 1, Figure 2, Figure 3, Figure 4).HRCT shows numerous focal lucencies (Figure 2), without visible walls, in the right upper lobe, occurring in association with focal ground-glass opacity and consolidation. Some of the lucencies are seen in adjacent normal appearing lung.What is the most likely diagnosis? Pneumonia with pneumatocelesCorrect. Although the appearance of these lucencies (Figure 3) is similar to that of centrilobular emphysema, the abnormality is focal and unilateral, occurring in association with ground-glass opacity and consolidation. The cysts do not appear to have a centrilobular distribution.Diagnosis: Pneumatoceles in a patient with BOOPDISCUSSIONPneumatoceles may be seen in association with a variety of pneumonias, probably representing focal areas of lung destruction associated with air trapping.Bronchiolitis obliterans organizing pneumonia (BOOP) is most often idiopathic, but BOOP may also be seen in patients with pulmonary infection. Patients with BOOP typically present with a several-month history of nonproductive cough. They often have a low-grade fever, malaise, and shortness of breath. The characteristic HRCT features of BOOP consist of patchy, nonsegmental, unilateral or bilateral areas of air-space consolidation. Focal opacities as seen in this case may be seen following focal pneumonia. （缩略图，点击图片链接看原图）case111HRCT in a 23-year-old man with chronic purulent sputum production and shortness of breath (Figure 1, Figure 2, Figure 3, Figure 4, Figure 5).There is thickening and dilatation of bronchi throughout the lung, diagnostic of bronchiectasis. The tubular shape of the dilated bronchi allows them to be differentiated from lung cysts. Nodular opacities at the lung base represent mucous or pus filling peripheral bronchi, and are commonly seen in patients with infected bronchiectasis.Diagnosis: Cystic fibrosis with bronchiectasisDISCUSSIONBronchiectasis is defined as localized, irreversible bronchial dilatation. While bronchiectasis usually results from chronic infection, airway obstruction by tumor, stricture, impacted material, or inherited abnormalities can also play a significant role.Bronchiectasis results in characteristic abnormalities identifiable on HRCT. These include bronchial dilatation, bronchial wall thickening, lack of normal bronchial tapering with visibility of airways in the peripheral lung, gross irregularities in airway contour, and mucus or fluid retention in the bronchial lumen. Also, bronchiectasis is often associated with atelectasis in affected lung regions or sometimes air trapping. A diagnosis of bronchiectasis is usually based on a combination of these findings.In most patients with bronchiectasis, HRCT findings are similar regardless of the mechanism or cause of disease.A key finding in diagnosing bronchiectasis is the "signet ring sign" shown in a different patient. This finding is said to be present if the internal diameter of a bronchus appears larger than its accompanying artery, giving the appearance of a signet ring. （缩略图，点击图片链接看原图）case112HRCT in a 35-year-old woman with chronic cough (Figure 1).The internal diameter of the bronchus is larger than the diameter of the adjacent artery, i.e. "signet-ring sign," although bronchial dilatation is mild.Is bronchiectasis present in the left lower lobe?Although the "signet-ring sign" appears to be present, the bronchus appears larger than the adjacent artery because the artery has divided while the bronchus has not. The divided artery branches will normally appear smaller than the bronchus. This is a common normal appearance.What appears to represent bronchiectasis with "tram tracks" is a "doubling artifact" due to cardiac pulsation.Diagnosis: Focal bronchiectasis (mild) in the right lower lobe.DISCUSSIONA signet-ring sign is said to be present if the internal diameter of a bronchus is larger than the diameter of the accompanying artery, although this can sometimes be seen in normals.Several potential pitfalls in the diagnosis of bronchiectasis should be avoided. First, a bronchus may normally appear larger than the adjacent artery is the CT slice is at a level where the artery has divided while the bronchus has not. Secondly, transmitted cardiac motion may cause linear structures to show ghosting or doubling artifacts that can closely mimic the appearance of tram-tracks. These are common adjacent to the heart. （缩略图，点击图片链接看原图）case113HRCT in a 38-year-old woman with cough and recent hemoptysis (Figure 1, Figure 2, Figure 3).Focal areas of bronchial wall thickening and dilatation are visible in the posterior right upper lobe and right middle lobe. Bronchiectasis in the middle lobe is associated with atelectasis of surrounding lung, mimicking the appearance of focal honeycombing.Because of the focal nature of the abnormality, prior infection is most likely.Diagnosis: Cylindrical bronchiectasis, focalDISCUSSIONThe most common cause of bronchiectasis is prior infection, usually viral, at an early age. A multifocal distribution is most common in such patients. Recurrent infection, cough, purulent sputum, and hemoptysis, as in this case, are common symptoms.Bronchiectasis has been classified into 3 types, depending on the morphology of the abnormal bronchi, although these distinctions are of little clinical value. These three types are cylindrical, varicose, and cystic or saccular. This patient shows cylindrical bronchiectasis.Cylindrical bronchiectasis, mildest and most common, is characterized on HRCT by the presence of thick walled bronchi, which extend into the lung periphery and fail to show normal tapering (Figure 2). On HRCT, bronchi are not normally visible in the peripheral 1-2 cm of lung, but in patients with bronchiectasis, bronchial wall thickening, peribronchial fibrosis, and dilatation of the bronchial lumen, allow them to be seen in the lung periphery (Figure 3). Depending on their orientation relative to the scan plane they can simulate "tram tracks" or can show the "signet-ring sign," in which the dilated, thick-walled bronchus and its accompanying pulmonary artery branch are seen adjacent to each other. Ectatic bronchi containing fluid or mucus appear as tubular opacities. （缩略图，点击图片链接看原图）case114HRCT in a 19-year-old man with chronic purulent sputum production and shortness of breath (Figure 1, Figure 2, Figure 3, Figure 4).Findings of bronchiectasis in this patient include:the signet ring signbronchial wall thickeningtram tracksbronchi visible in the lung peripherymucous or pus-filling bronchivolume lossBecause of the patients young age, symptoms, and the severity and diffuse nature of the abnormalities, cystic fibrosis is most likely. Another finding suggestive of this disease is an increase in lung volumes (Figure 4). Notice that some of the bronchi appear quite irregular in contour. This is appearance is termed varicose bronchiectasis.Diagnosis: Cystic fibrosis with varicose bronchiectasis.DISCUSSIONVaricose bronchiectasis is similar in appearance to cylindrical bronchiectasis; however, with varicose bronchiectasis the bronchial walls are more irregular, and can assume a beaded appearance. The term "string of pearls" has been used to describe varicose bronchiectasis. （缩略图，点击图片链接看原图）case115HRCT in a 45-year-old woman with respiratory difficulties since childhood, who had progressive respiratory insufficiency leading to left lung transplantation (Figure 1, Figure 2, Figure 3, Figure 4).Although this appearance mimics both cystic lung disease and bullous emphysema, the presence of the "signet-ring sign" indicates that bronchiectasis is present. The cystic appearance of the dilated bronchi is typical of cystic bronchiectasis. Note the abnormal bronchi appear central in location. Lung appears lucent because of air trapping. The left lung, resected at surgery, showed a deficiency of bronchial cartillage involving medium sized bronchi resulting in bronchiectasis.Diagnosis: Williams-Campbell syndrome with cystic bronchiectasis.DISCUSSIONCystic bronchiectasis most often appears as a group or cluster of air-filled cysts, but cysts can also be fluid-filled, giving the appearance of a "cluster of grapes". Cystic bronchiectasis is often patchy in distribution, allowing it to be distinguished from a cystic lung disease such as LAM. Also, air-fluid levels, which may be present in the dependent portions of the cystic dilated bronchi, are a very specific sign of bronchiectasis, and are not usually seen in patients with lung cysts.Williams-Campbell syndrome is a rare type of cystic bronchiectasis due to defective cartilage in the fourth-to sixth-order bronchi. CT can show areas of central cystic bronchiectasis with distal regions of abnormal lucency, probably related to air trapping. These findings are useful in differentiating Williams-Campbell syndrome from other causes of cystic bronchiectasis. Ballooning of central bronchi on inspiration and collapse on expiration has also been reported. （缩略图，点击图片链接看原图）case116HRCT in a 48-year-old woman with symptoms of asthma and bronchial wall thickening seen on chest radiographs (Figure 1).HRCT shows several areas of bronchiectasis involving the mid lung regions. The bronchi appear thick walled, irregular, and fail to show normal tapering. What is the most likely diagnosis in this patient? uncomplicated asthma cystic fibrosis allergic bronchopulmonary aspergillosisCorrect. In a patient with symptoms of asthma, the presence of bronchiectasis, particularly involving central bronchi, is typical of allergic bronchopulmonary aspergillosis.Diagnosis: Allergic bronchopulmonary aspergillosis with bronchiectasisDISCUSSIONAllergic bronchopulmonary aspergillosis (ABPA) is characteristically associated with eosinophilia, symptoms of asthma such as wheezing, and findings of "central" or "proximal" bronchiectasis, mucoid impaction, atelectasis, and sometimes consolidation similar to that seen in patients with eosinophilic pneumonia.CT may be valuable in the early identification of lung damage in patients with ABPA and thus help in planning treatment. HRCT is more sensitive than are plain radiographs in detecting of abnormalities associated with ABPA. HRCT findings in patients with ABPA include bronchiectasis involving central bronchi and small airways abnormalities, including dilatation and "tree-in-bud." Uncomplicated asthma does not result in bronchiectasis, as seen in this case. （缩略图，点击图片链接看原图）case117HRCT in a 63-year-old man with chronic cough and sputum production (Figure 1, Figure 2, Figure 3, Figure 4).What diagnosis would you consider? post-infectious bronchiectasis chronic immune deficiency immotile cilia syndrome infection with mycobacterium avium complex (MAC)In fact, any of these diagnoses is possible. HRCT shows multifocal bronchiectasis associated with the finding of "tree-in-bud" at the lung bases. "Tree-in-bud" is indicative of chronic airway infection with impaction of bronchioles, and would be expected in any of these. In this man, there was no evidence of immune deficiency or immotile cilia syndrome, and culture yielded bacteria rather than MAC.Diagnosis: Bronchiectasis (post infectious) associated with chronic bacterial infection and tree-in-bud.DISCUSSIONBronchiectasis is most commonly the result of prior infection, but may be associated with a number of abnormalities. In an elderly patient showing the combination of bronchiectasis and tree-in-bud, chronic infection with bacterial organisms or MAC should be considered most likely.80% of patients with MAC infection have bronchiectasis in combination with small nodules (70%) or an appearance of "tree-in-bud". （缩略图，点击图片链接看原图）case11835-year-old college student with dry cough, mild shortness of breath and an abnormal chest radiograph (Figure 1, Figure 2, Figure 3).This is a difficult diagnosis. The air containing cystic structures appear too thick walled and numerous to represent bullae, and there is no other evidence of emphysema. The upper lobe distribution would be very unusual for honeycombing. This appearance is consistent with histiocytosis, but the presence of branching tubular structures is most in keeping with bronchiectasis. Bronchiectasis is more easily diagnosed at other levels.These findings are typical of end-stage sarcoidosis, with cystic bronchiectasis related to fibrosis. Traction bronchiectasis and cysts are common, and an upper lobe and posterior distribution is typical. Also note note thickening and nodularity of the major fissures, a common finding in sarcoidosis.Diagnosis: End-stage sarcoidosis with cystic bronchiectasisDISCUSSIONIn 20-25% of patients with sarcoidosis, fibrosis results from healing of granulomas. Progressive fibrosis leads to abnormal central conglomeration of parahilar bronchi and vessels, associated with bronchiectasis, typically most marked in the upper lobes. Posterior displacement of the main and upper lobe bronchi indicating volume loss in the posterior segments of the upper lobes is commonly present. （缩略图，点击图片链接看原图）case119HRCT in a 21-year-old man with chronic purulent sputum production and shortness of breath (Figure 1, Figure 2, Figure 3, Figure 4, Figure 5).Because of the patient's young age, symptoms, and the severity and diffuse nature of the abnormalities, cystic fibrosis is most likely.Diagnosis: Cystic fibrosis with bronchiectasis.DISCUSSIONCystic fibrosis (CF) is the most common cause of pulmonary insufficiency in the first 3 decades of life. It results from an autosomal recessive genetic defect in the structure of the "cystic fibrosis transmembrane regulator protein," which leads to abnormal chloride transport across epithelial membranes. The mechanisms by which this leads to lung disease are not entirely understood, but an abnormally low water content of airway mucus is at least partially responsible, resulting in decreased mucus clearance, mucus plugging of airways, and an increased incidence of bacterial airway infection. Bronchial wall inflammation progressing to secondary bronchiectasis are universal in patients with long-standing disease, and is commonly visible on chest radiographs.HRCT findings largely reflect the airway abnormalities typical of this disease. Bronchiectasis is present in all patients with advanced cystic fibrosis who are studied using HRCT. Proximal or parahilar bronchi are always involved when bronchiectasis is present, and bronchiectasis is limited to these central bronchi in about a third of cases, a finding which is referred to as "central bronchiectasis". Both the central and peripheral bronchi are abnormal in about two-thirds of patients. All lobes are typically involved, although in patients early disease, abnormalities are often predominantly upper lobe in distribution, and a right upper lobe predominance may be present in some patients. Cylindrical bronchiectasis is most frequent pattern seen. Atelectasis may be associated.Bronchial wall and/or peribronchial interstitial thickening is also commonly present in patients with cystic fibrosis. It is generally more evident than bronchial dilatation in patients who have early disease, and may be seen independent of bronchiectasis. Mucus plugging is also common. Collapse or consolidation can also be seen.Branching or nodular centrilobular opacities, which reflect the presence of bronchial or bronchiolar dilatation with associated mucus impaction, infection, or peribronchiolar inflammation, can be an early sign of disease. Focal areas of decreased lung opacity, occurred in a geographic fashion with sharply defined margins, reflect air trapping with deceased lung perfusion (i.e., "mosaic perfusion"). Areas of decreased lung opacity sometimes appear to surround mucus-plugged bronchi.Cystic or bullous lung lesions can also be visible, and typically predominate in the subpleural regions of the upper lobes. Hilar or mediastinal lymph node enlargement, and pleural abnormalities can also be seen, largely reflecting chronic infection. Pulmonary artery dilatation resulting from pulmonary hypertension can also be seen in patients with longstanding disease. （缩略图，点击图片链接看原图）case120HRCT in a 22-year-old man with a known history of cystic fibrosis Figure 1, Figure 2, Figure 3, Figure 4, Figure 5).In addition to extensive bronchiectasis, HRCT shows inhomogeneous lung attenuation (Figure 1), with some regions appearing lucent, and other appearing relatively dense. This inhomogeneous appearance is due to "mosaic perfusion", a very important finding in patients with airway obstruction. Note that lung vessels appear larger in areas of denser lung; this is a key finding in recognizing the presence of mosaic perfusion as a cause of inhomogeneous lung attenuation, and distinguishing it from ground-glass opacity.Diagnosis: Cystic fibrosis with bronchiectasis and mosiac perfusionLung density and attenuation are partially determined by the amount of blood present in lung tissue. On HRCT, inhomogeneous lung opacity can represent ground-glass opacity. It may also result from regional differences in lung perfusion in patients with airways disease or pulmonary vascular disease.Because this phenomenon is often patchy or mosaic in distribution, with adjacent areas of lung having relatively decreased and increased opacity, it has been termed "mosaic perfusion". Areas of relatively decreased lung opacity seen on HRCT can be of varying sizes, and sometimes appear to correspond to lobules, segments, lobes, or an entire lung.Mosaic perfusion has also been reported in association with pulmonary vascular obstruction such as that caused by pulmonary embolism.Regardless of its cause, when mosaic perfusion is present, pulmonary vessels in the areas of decreased opacity often appear smaller than vessels in relative dense areas of lung (Figure 5). This difference reflects differences in regional blood flow, and can be quite helpful in distinguishing mosaic perfusion from "ground-glass" opacity, which can otherwise have a similar patchy appearance. In patients with ground-glass opacity, vessels usually appear of equal in size throughout the lung.Furthermore, in patients with mosaic perfusion due to bronchiolitis obliterans, cystic fibrosis, or other airways diseases, gross abnormalities of large bronchi (i.e. bronchiectasis) can often be seen in the relatively lucent areas of lung (Figure 5). In patients with mosaic perfusion occurring in association with chronic pulmonary embolism, enlargement of the main pulmonary arteries may be visible, because of pulmonary hypertension. （缩略图，点击图片链接看原图）case121HRCT in a 46-year-old woman with progressive shortness of breath following a bone marrow transplant (Figure 1, Figure 2).This appearance is typical of bronchiolitis obliterans occurring as a complication of bone marrow transplantation. Note that there is bronchiectasis present, a common finding in this disease. This findings suggests that mosaic perfusion is present, due to airway obstruction. Also note that vessels appear larger in the dense lung regions.Diagnosis: Bronchiolitis obliterans with mosiac perfusionDISCUSSIONBronchiolitis obliterans (BO), also referred to as constrictive bronchiolitis, is characterized by small airway inflammation and fibrosis, and results in airflow obstruction.Bronchiolitis obliterans (constrictive bronchiolitis) represents a nonspecific reaction and may be caused by a variety of insults, including infection (the Swyer-James syndrome), toxic-fume inahaltion, connective tissue disease, drug therapy, and lung or bone-marrow transplantation. It is rarely idiopathic.Chest radiographs are often normal. In some patients mild hyperinflation or subtle peripheral attenuation of the vascular markings may be seen.The HRCT appearance of bronchiolitis obliterans includes focal, often sharply defined, areas of decreased lung attenuation associated with vessels of decreased caliber. These changes represent a combination of air-trapping and oligemia, typically occurring in the absence of parenchymal consolidation, and termed "mosaic perfusion". Bronchiectasis, both central and peripheral, may be present as well.Air trapping is commonly visible on expiratory HRCT in patients with BO, occurring in the areas of relative lucency seen on the inspiratory scans. In some patients, air trapping may be seen in the presence of normal inspiratory scans.Bronchiolitis obliterans may occur in patients following allogeneic bone marrow transplants, presumably the result of chronic graft-versus host disease (GVHD). Histologically, BO (constrictive bronchiolitis) is the predominant abnormality. Typically, these patients also have evidence of GVHD involving the skin, liver, and gastrointestinal tract. However, bronchiolitis has also been identified in patients following autologous bone marrow transplants, leaving the true etiology of bronchiolitis unexplained. （缩略图，点击图片链接看原图）case122HRCT in a 48-year-old woman with progressive shortness of breath following bilateral lung transplantation (Figure 1).This appearance is typical of bronchiolitis obliterans occurring as a complication of lung transplantation. The lungs are inhomogeneous in attenuation. Also note that vessels appear larger in the dense lung regions.This diagnosis may be confirmed by using post-expiratory HRCT scans (Figure 2). On the post-expiratory scan, note that lung inhomogeneity increases. The inspiratory and expiratory scan can be compared using Figure 3. The lung regions appearing denser on the inspiratory scans increase in attenuation on expiration, as is normal. The areas appearing more lucent on the inspiratory scans remain lucent on the expiratory scan due to air trapping.Diagnosis: Bronchiolitis obliterans with mosiac perfusionDISCUSSIONAlthough a discrepancy in vascular size can be helpful in making the diagnosis of mosaic perfusion, in some cases, it can be very difficult to distinguish mosaic perfusion from patchy ground-glass opacity on inspiratory scans HRCT.Obtaining post expiratory HRCT can be very helpful in differentiating patients with mosaic perfusion related to airways obstruction from patients with ground-glass opacity. Differences in lung attenuation resulting from airways obstruction and mosaic perfusion are accentuated on expiratory HRCT scans; this is not the case with ground-glass opacity.In normal subjects, lung attenuation increases in a homogeneous fashion on expiratory scans, although small areas of air trapping can sometimes be seen. Figure 4 and Figure 5 show inspiratory and expiratory scans in a normal subject.Air-trapping is commonly visible on expiratory HRCT in patients with BO, occurring in the areas of relative lucency seen on inspiratory scans. In some patients, air trapping may be seen in the presence of normal inspiratory scans. （缩略图，点击图片链接看原图）case123Inspiratory (Figure 1) and expiratory (Figure 2) HRCT in a 15-year-old boy with hemoptysis.Inhomogeneous lung opacity is visible on the HRCT (Figure 1). Note that both the dense and less dense regions increase in attenuation on the expiratory view. This is typical of ground-glass opacity. There is no evidence of air trapping.Diagnosis: Pulmonary hemorrhage due to Goodpasture's syndrome, presenting with ground-glass opacityDISCUSSIONIn patients with ground-glass opacity, both normal and abnormal regions increase in attenuation on the expiratory scans. No air trapping is seen. screen.width-333)this.width=screen.width-333" width=420 height=582 title="Click to view full case123.jpg (420 X 582)" border=0 align=absmiddle>case124HRCT in a 45-year-old woman with progressive shortness of breath following an upper respiratory infection. Inspiratory (Figure 1) and expiratory (Figure 2) scans were obtained.Although the inspiratory scan is normal, the post-expiratory scan shows significant patchy air trapping. The differential diagnosis of this combination includes bronchiolitis obliterans, asthma, and hypersensitivity pneumonitis as the most common causes. These diseases can produce small airway obstruction as the only recognizable abnormality.Diagnosis: Bronchiolitis obliterans (post-infectious) with air trapping screen.width-333)this.width=screen.width-333" width=420 height=613 title="Click to view full case124.jpg (420 X 613)" border=0 align=absmiddle>case125HRCT in a 53-year-old woman with cough and asthma. Inspiratory (Figure 1, Figure 2) and expiratory (Figure 3, Figure 4) scans were obtained.Although the inspiratory scan is normal, the post-expiratory scan shows significant patchy air trapping. The differential diagnosis of this combination includes bronchiolitis obliterans, asthma, and hypersensitivity pneumonitis as the most common causes. These diseases can produce small airway obstruction as the only recognizable abnormality.Diagnosis: Asthma with air trapping （缩略图，点击图片链接看原图）case12647-year-old woman with an aviary in her house, progressive shortness of breath, low-grade fever, and nonproductive cough. Inspiratory (Figure 1, Figure 2) and expiratory (Figure 3, Figure 4) scans were obtained.HRCT on inspiration shows ill defined patchy areas of ground-glass opacity. Focal areas of lucency, due to air trapping or mosaic perfusion are also visible. This appearance, with mixed ground-glass opacity and mosaic perfusion, the "head-cheese sign", suggests hypersensitivity pneumonitis as most likely. Expiratory scans show air trapping in the lucent lung regions.Diagnosis: Hypersensitivity pneumonitis presenting with ground-glass opacity and air trapping.DISCUSSIONThe combination of patchy ground-glass opacity and patchy lucency due to air trapping is highly suggestive of hypersensitivity pneumonitis. This combination reflects lung infiltration (ground-glass opacity), and bronchiolitis (patchy lucency due to air trapping). This variegated appearance is similar to that of a sausage, so-called "head cheese." The "head cheese sign", indicating the presence of ground-glass opacity in association with normal lung attenuation, and areas of low attenuation due to air trapping, is strongly suggestive of hypersensitivity pneumonitis. The differential diagnosis of this finding includes atypical infections such as mycoplasma, and occasionally sarcoidosis. （缩略图，点击图片链接看原图）case12740-year-old woman with exposure to birds, progressive shortness of breath, and nonproductive cough. Inspiratory (Figure 1, Figure 2, Figure 3) and expiratory (Figure 4) scans were obtained.HRCT on inspiration shows ill defined ground-glass opacity Figure 1). Multiple lobular areas of lucency, due to air trapping and mosaic perfusion are also visible (Figure 3). Expiratory scans show lobular air trapping (Figure 4).Diagnosis: Hypersensitivity pneumonitis, presenting with centrilobular nodules and air trapping.DISCUSSIONCentrilobular nodules of ground-glass opacity and patchy lucency due to air trapping is highly suggestive of hypersensitivity pneumonitis. In a patient with a known exposure history, the HRCT findings are sufficiently diagnostic to allow appropriate treatment—steroids or removal of the offending antigen.Congratulations! You have reached the final case in the Learning Pathway. （缩略图，点击图片链接看原图）病名索引Allergic bronchopulmonary aspergillosis (Case 116)Alveolar microlithiasis (Case 92)Alveolar proteinosis (Case 89)Amyloidosis (Case 94)Asbestos exposure, possible fibrosis (Case 26)Asbestosis (Case 22)Asbestosis-related pleural disease (Case 23)Asbestos-related pleural disease (Case 24)Asbestos-related pleural disease (Case 25)Aspergilloma (Case 28)Aspergillosis (Case 116)Aspergillosis, invasive (Case 62)Aspergillosis, invasive (Case 63)Asthma (Case 125)Bronchiectasis, bacterial bronchitis and bronchiolitis (Case 57)Bronchiectasis, cylindrical (Case 113)Bronchiectasis, cystic (Case 115)Bronchiectasis, focal (Case 112)Bronchiectasis, post-infectious (Case 117)Bronchiolitis obliterans (Case 121)Bronchiolitis obliterans (Case 122)Bronchiolitis obliterans organizing pneumonia (BOOP) (Case 67)Bronchiolitis obliterans organizing pneumonia (BOOP) (Case 68)Bronchiolitis obliterans organizing pneumonia (BOOP) (Case 69)Bronchiolitis obliterans organizing pneumonia (BOOP), pneumatoceles (Case 110)Bronchiolitis obliterans, post-infectious (Case 124)Bronchiolitis, infectious (Case 50)Bronchiolitis, infectious, and bronchopneumonia (Case 51)Bronchioloalveolar carcinoma (Case 54)Bronchopneumonia (Case 51)Bronchopneumonia, bacterial (Case 52)Bronchopneumonia, bacterial (Case 55)Bronchopneumonia, bacterial (Case 56)Bronchopulmonary papillomatosis (Case 101)Bullous emphysema (Case 105)Centrilobular emphysema (Case 102)Centrilobular emphysema (Case 108)Centrilobular emphysema associated with adenocarcinoma (Case 106)Chronic eosinophilic pneumonia (Case 0)Chronic eosinophilic pneumonia (Case 65)Chronic eosinophilic pneumonia (Case 66)Coccidioidomycosis, miliary (Case 45)Cystic fibrosis (Case 111)Cystic fibrosis (Case 114)Cystic fibrosis (Case 119)Cystic fibrosis (Case 120)Desquamative interstitial pneumonia (DIP) (Case 86)Drug-related lung injury (Case 13)Emphysema in an AIDS patient (Case 109)Emphysema, bullous (Case 105)Emphysema, centrilobular (Case 102)Emphysema, centrilobular (Case 108)Emphysema, centrilobular, associated with adenocarcinoma (Case 106)Emphysema, panlobular (Case 103)Emphysema, panlobular (Case 107)Emphysema, paraseptal (Case 104)Hemorrhage secondary to leukemia (Case 81)Hemorrhage secondary to lupus vasculitis (Case 83)Hemorrhage, Goodpasture's syndrome (Case 123)Hemorrhage, Goodpasture's syndrome (Case 70)Hypersensitivity pneumonitis (Case 126)Hypersensitivity pneumonitis (Case 127)Hypersensitivity pneumonitis (Case 53)Hypersensitivity pneumonitis (Case 71)Hypersensitivity pneumonitis (Case 72)Hypersensitivity pneumonitis (Case 72)Hypersensitivity pneumonitis (Case 73)Hypersensitivity pneumonitis (Case 73)Hypersensitivity pneumonitis, end stage (Case 18)Hypersensitivity pneumonitis, end stage (Case 29)Idiopathic pulmonary fibrosis (Case 0)Idiopathic pulmonary fibrosis (Case 12)Idiopathic pulmonary fibrosis (Case 15)Idiopathic pulmonary fibrosis (Case 16)Idiopathic pulmonary fibrosis (Case 17)Idiopathic pulmonary fibrosis (Case 84)Idiopathic pulmonary fibrosis (Case 85)Idiopathic pulmonary fibrosis (Case 95)Idiopathic pulmonary fibrosis, complicated by lung cancer (Case 30)Interstitial pneumonia, active, idiopathic pulmonary fibrosis (Case 84)Interstitial pneumonia, active, secondary to systemic lupus erythematosus (Case 82)Kaposi sarcoma in an AIDS patient (Case 40)Langerhans histiocytosis (Case 97)Langerhans histiocytosis, with pulmonary hemorrhage (Case 98)Lipoid pneumonia (Case 90)Lymphangiomyomatosis, in association with tuberous sclerosis (Case 96)Lymphangitic spread of breast carcinoma (Case 38)Lymphangitic spread of breast carcinoma (Case 5)Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma (Case 6)Lymphangitic spread of lymphoma (Case 7)Lymphangitic spread of thyroid carcinoma (Case 39)Lymphocytic interstitial pneumonia (LIP), in assocation with AIDS (Case 41)Lymphoma arising from Mucosa Associated Lymphoid Tissue (MALToma) (Case 42)Metastases, hematogenous from breast cancer (Case 46)Metastases, hematogenous from breast cancer (Case 47)Metastatic calcification (Case 93)Metastatic carcinoma, thyroid (Case 48)Mixed connective tissue disease, pulmonary fibrosis (Case 21)Mycobacterium avium intracellular complex (MAC) infection (Case 60)Mycobacterium avium intracellular complex (MAC) infection (Case 61)Mycoplasma pneumonia (Case 77)Nodules (Case 0)Non-specific interstitial pneumonia (NSIP) (Case 87)Nontuberculosis mycobacterium (BCG), miliary (Case 44)Normal lung (Case 1)Normal lung (Case 2)Normal lung (Case 3)Normal lung (Case 4)Panlobular emphysema (Case 103)Panlobular emphysema (Case 107)Paraseptal emphysema (Case 104)Pneumatoceles with bronchiolitis obliterans organizing pneumonia (BOOP) (Case 110)Pneumocystis carinii pneumonia (PCP) (Case 100)Pneumocystis carinii pneumonia (PCP) (Case 74)Pneumocystis carinii pneumonia (PCP) (Case 75)Pneumocystis carinii pneumonia (PCP) (Case 99)Pulmonary alveolar proteinosis (PAP) (Case 88)Pulmonary edema (Case 79)Pulmonary edema (Case 8)Pulmonary edema (Case 80)Rheumatoid lung disease (Case 11)Rheumatoid lung disease (Case 20)Sarcoidosis (Case 31)Sarcoidosis (Case 32)Sarcoidosis (Case 33)Sarcoidosis (Case 34)Sarcoidosis (Case 36)Sarcoidosis (Case 49)Sarcoidosis (Case 9)Sarcoidosis (Case 91)Sarcoidosis, end stage (Case 10)Sarcoidosis, end stage (Case 118)Sarcoidosis, end stage (Case 27)Sarcoidosis, end stage , complicated by an aspergilloma (Case 28)Sarcoidosis, progressive (Case 35)Scleroderma (Case 14)Silicosis (Case 37)Systemic lupus erythematosus (Case 19)Systemic lupus erythematosus (Case 82)Tuberculosis, active (Case 58)Tuberculosis, active (Case 59)Tuberculosis, miliary (Case 43)Viral pneumonia (Case 78)Viral pneumonia (cytomegalovirus) (Case 76)Wegener's granulomatosis (Case 64)Williams Campbell syndrome (Case 115)征象索引Air bronchograms (Case 71, Hypersensitivity pneumonitis)Air crescent (Case 63, Aspergillosis, invasive)Air trapping (Case 72, Hypersensitivity pneumonitis)Air trapping (Case 73, Hypersensitivity pneumonitis)Air trapping (Case 77, Mycoplasma pneumonia)Air trapping (Case 115, Williams Campbell syndrome)Air trapping (Case 119, Cystic fibrosis)Air trapping (Case 122, Bronchiolitis obliterans)Air trapping (Case 124, Bronchiolitis obliterans, post-infectious)Air trapping (Case 125, Asthma)Air trapping (Case 126, Hypersensitivity pneumonitis)Air trapping (Case 127, Hypersensitivity pneumonitis)Airway obstruction (Case 124, Bronchiolitis obliterans, post-infectious)Airway obstruction (Case 125, Asthma)Areas of lucency (Case 102, Centrilobular emphysema)Artifacts (Case 4, Normal lung)Atelectasis (Case 3, Normal lung)Atelectasis (Case 25, Asbestosis-related pleural disease)Atelectasis (Case 113, Bronchiectasis, cylindrical )Atelectasis (Case 119, Cystic fibrosis)Branching tubular structures (Case 118, Sarcoidosis, end stage )Bronchi visible in the lung periphery (Case 114, Cystic fibrosis)Bronchial dilatation (Case 112, Bronchiectasis, focal)Bronchial wall thickening (Case 57, Bronchiectasis, bacterial bronchitis and bronchiolitis)Bronchial wall thickening (Case 113, Bronchiectasis, cylindrical )Bronchial wall thickening (Case 114, Cystic fibrosis)Bronchiectasis (Case 57, Bronchiectasis, bacterial bronchitis and bronchiolitis)Bronchiectasis (Case 61, Mycobacterium avium intracellular complex (MAC) infection)Bronchiectasis (Case 111, Cystic fibrosis)Bronchiectasis (Case 112, Bronchiectasis, focal)Bronchiectasis (Case 113, Bronchiectasis, cylindrical )Bronchiectasis (Case 115, Williams Campbell syndrome)Bronchiectasis (Case 116, Allergic bronchopulmonary aspergillosis)Bronchiectasis (Case 117, Bronchiectasis, post-infectious)Bronchiectasis (Case 118, Sarcoidosis, end stage )Bronchiectasis (Case 119, Cystic fibrosis)Bronchiectasis (Case 120, Cystic fibrosis)Bronchiectasis (Case 121, Bronchiolitis obliterans)Bullae (Case 105, Bullous emphysema)Bullae (Case 108, Centrilobular emphysema)Bullae (Case 109, Emphysema in an AIDS patient)Bullous lung lesions (Case 119, Cystic fibrosis)Calcification (Case 23, Asbestosis-related pleural disease)Calcification (Case 92, Alveolar microlithiasis)Calcification (Case 93, Metastatic calcification)Calcification (Case 94, Amyloidosis)Cavitation (Case 58, Tuberculosis, active )Cavitation (Case 59, Tuberculosis, active )Cavity (Case 63, Aspergillosis, invasive)Centrilobular (Case 102, Centrilobular emphysema)Centrilobular (Case 106, Centrilobular emphysema associated with adenocarcinoma)Centrilobular location (Case 0, Nodules, an introduction)Centrilobular nodules (Case 50, Bronchiolitis, infectious )Centrilobular nodules (Case 51, Bronchiolitis, infectious, and bronchopneumonia)Centrilobular nodules (Case 53, Hypersensitivity pneumonitis)Centrilobular nodules (Case 54, Bronchioloalveolar carcinoma)Centrilobular nodules (Case 56, Bronchopneumonia, bacterial)Centrilobular nodules (Case 57, Bronchiectasis, bacterial bronchitis and bronchiolitis)Centrilobular nodules (Case 59, Tuberculosis, active )Centrilobular nodules (Case 69, Bronchiolitis obliterans organizing pneumonia (BOOP))Centrilobular nodules (Case 127, Hypersensitivity pneumonitis)Centrilobular opacities (Case 75, Pneumocystis carinii pneumonia (PCP))Centrilobular opacities (Case 79, Pulmonary edema)Centrilobular pattern (Case 55, Bronchopneumonia, bacterial)Confluence (Case 90, Lipoid pneumonia)Conglomeration of parahilar bronchi and vess... (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Consolidation (Case 65, Chronic eosinophilic pneumonia)Consolidation (Case 66, Chronic eosinophilic pneumonia)Consolidation (Case 67, Bronchiolitis obliterans organizing pneumonia (BOOP))Consolidation (Case 68, Bronchiolitis obliterans organizing pneumonia (BOOP))Consolidation (Case 73, Hypersensitivity pneumonitis)Consolidation (Case 75, Pneumocystis carinii pneumonia (PCP))Consolidation (Case 76, Viral pneumonia (cytomegalovirus))Consolidation (Case 77, Mycoplasma pneumonia)Consolidation (Case 110, Pneumatoceles with bronchiolitis obliterans organizing pneumonia (BOOP))Cyst (Case 30, Idiopathic pulmonary fibrosis, complicated by lung cancer)Cystic bronchiectasis (Case 115, Williams Campbell syndrome)Cystic bronchiectasis (Case 118, Sarcoidosis, end stage )Cystic lung lesions (Case 119, Cystic fibrosis)Cysts (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Cysts (Case 95, Idiopathic pulmonary fibrosis)Cysts (Case 96, Lymphangiomyomatosis, in association with tuberous sclerosis)Cysts (Case 97, Langerhans histiocytosis)Cysts (Case 98, Langerhans histiocytosis, with pulmonary hemorrhage)Cysts (Case 99, Pneumocystis carinii pneumonia (PCP))Cysts (Case 100, Pneumocystis carinii pneumonia (PCP))Cysts (Case 101, Bronchopulmonary papillomatosis)Cysts (Case 110, Pneumatoceles with bronchiolitis obliterans organizing pneumonia (BOOP))Cysts or bullae (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Decrease in attenuation (Case 107, Panlobular emphysema)Dependent opacity (Case 3, Normal lung)Diffuse (Case 103, Panlobular emphysema)Diffusely abnormal lung (Case 103, Panlobular emphysema)Dilatation of bronchi (Case 111, Cystic fibrosis)Dilated bronchi (Case 115, Williams Campbell syndrome)Displacement of upper lobe bronchi (Case 27, Sarcoidosis, end stage )Distortion of fissures (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Distortion of lung architecture (Case 27, Sarcoidosis, end stage )Doubling artifact (Case 4, Normal lung)Doubling artifact (Case 112, Bronchiectasis, focal)Emphysema (Case 103, Panilobular emphysema)Emphysema (Case 108, Centrilobular emphysema)Emphysema, paracicatricial (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Emphysema, paraseptal (Case 108, Centrilobular emphysema)Endobronchial spread (Case 58, Tuberculosis, active )Fibrosis (Case 10, Sarcoidosis, end stage )Fibrosis (Case 11, Rheumatoid lung disease)Fibrosis (Case 13, Drug-related lung injury)Fibrosis (Case 14, Scleroderma)Fibrosis (Case 19, Systemic lupus erythematosus)Fibrosis (Case 20, Rheumatoid lung disease)Fibrosis (Case 29, Hypersensitivity pneumonitis, end stage)Fibrosis (Case 95, Idiopathic pulmonary fibrosis)Fibrosis (Case 118, Sarcoidosis, end stage )Fibrous tissue (Case 27, Sarcoidosis, end stage )Fibrous tissue masses (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Ground glass opacity (Case 8, Pulmonary edema)Ground glass opacity (Case 53, Hypersensitivity pneumonitis)Ground glass opacity (Case 62, Aspergillosis, invasive)Ground glass opacity (Case 67, Bronchiolitis obliterans organizing pneumonia (BOOP))Ground glass opacity (Case 69, Bronchiolitis obliterans organizing pneumonia (BOOP))Ground glass opacity (Case 70, Hemorrhage, Goodpasture's syndrome)Ground glass opacity (Case 71, Hypersensitivity pneumonitis)Ground glass opacity (Case 72, Hypersensitivity pneumonitis)Ground glass opacity (Case 73, Hypersensitivity pneumonitis)Ground glass opacity (Case 74, Pneumocystis carinii pneumonia (PCP))Ground glass opacity (Case 75, Pneumocystis carinii pneumonia (PCP))Ground glass opacity (Case 76, Viral pneumonia (cytomegalovirus))Ground glass opacity (Case 77, Mycoplasma pneumonia)Ground glass opacity (Case 78, Viral pneumonia)Ground glass opacity (Case 79, Pulmonary edema)Ground glass opacity (Case 80, Pulmonary edema)Ground glass opacity (Case 81, Hemorrhage secondary to leukemia)Ground glass opacity (Case 82, Interstitial pneumonia, active, secondary to systemic lupus erythematosus)Ground glass opacity (Case 83, Hemorrhage secondary to lupus vasculitis)Ground glass opacity (Case 84, Interstitial pneumonia, active, idiopathic pulmonary fibrosis)Ground glass opacity (Case 85, Idiopathic pulmonary fibrosis)Ground glass opacity (Case 86, Desquamative interstitial pneumonia (DIP))Ground glass opacity (Case 87, Non-specific interstitial pneumonia (NSIP))Ground glass opacity (Case 88, Pulmonary alveolar proteinosis (PAP))Ground glass opacity (Case 89, Alveolar proteinosis)Ground glass opacity (Case 90, Lipoid pneumonia)Ground glass opacity (Case 91, Sarcoidosis)Ground glass opacity (Case 98, Langerhans histiocytosis, with pulmonary hemorrhage)Ground glass opacity (Case 99, Pneumocystis carinii pneumonia (PCP))Ground glass opacity (Case 100, Pneumocystis carinii pneumonia (PCP))Ground glass opacity (Case 110, Pneumatoceles with bronchiolitis obliterans organizing pneumonia (BOOP))Ground glass opacity (Case 123, Hemorrhage, Goodpasture's syndrome)Ground glass opacity (Case 126, Hypersensitivity pneumonitis)Ground glass opacity (Case 127, Hypersensitivity pneumonitis)Halo sign (Case 62, Aspergillosis, invasive)Head cheese sign (Case 72, Hypersensitivity pneumonitis)Head cheese sign (Case 126, Hypersensitivity pneumonitis)Hilar mass (Case 6, Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma)Honeycombing (Case 11, Rheumatoid lung disease)Honeycombing (Case 12, Idiopathic pulmonary fibrosis)Honeycombing (Case 13, Drug-related lung injury)Honeycombing (Case 15, Idiopathic pulmonary fibrosis)Honeycombing (Case 18, Hypersensitivity pneumonitis, end stage)Honeycombing (Case 19, Systemic lupus erythematosus)Honeycombing (Case 27, Sarcoidosis, end stage )Honeycombing (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Honeycombing (Case 29, Hypersensitivity pneumonitis, end stage)Honeycombing (Case 30, Idiopathic pulmonary fibrosis, complicated by lung cancer)Honeycombing (Case 95, Idiopathic pulmonary fibrosis)Infarction (Case 63, Aspergillosis, invasive)Inhomogeneity (Case 122, Bronchiolitis obliterans)Inhomogeneous lung opacity (Case 120, Cystic fibrosis)Inhomogeneous lung opacity (Case 122, Bronchiolitis obliterans)Inhomogeneous lung opacity (Case 123, Hemorrhage, Goodpasture's syndrome)Interlobular septa (Case 0, Nodules, an introduction)Interlobular septal thickening (Case 11, Rheumatoid lung disease)Interlobular septal thickening (Case 14, Scleroderma)Interlobular septal thickening (Case 29, Hypersensitivity pneumonitis, end stage)Interlobular septal thickening (Case 40, Kaposi sarcoma in an AIDS patient)Interlobular septal thickening (Case 48, Metastatic carcinoma, thyroid)Interlobular septal thickening (Case 75, Pneumocystis carinii pneumonia (PCP))Interlobular septal thickening (Case 76, Viral pneumonia (cytomegalovirus))Interlobular septal thickening (Case 78, Viral pneumonia)Interlobular septal thickening (Case 79, Pulmonary edema)Interlobular septal thickening (Case 88, Pulmonary alveolar proteinosis (PAP))Interlobular septal thickening (Case 89, Alveolar proteinosis)Interlobular septal thickening (Case 98, Langerhans histiocytosis, with pulmonary hemorrhage)Interstitial thickening (Case 99, Pneumocystis carinii pneumonia (PCP))Intralobular interstitial thickening (Case 16, Idiopathic pulmonary fibrosis)Intralobular interstitial thickening (Case 17, Idiopathic pulmonary fibrosis)Intralobular interstitial thickening (Case 19, Systemic lupus erythematosus)Intralobular interstitial thickening (Case 20, Rheumatoid lung disease)Intralobular interstitial thickening (Case 21, Mixed connective tissue disease, pulmonary fibrosis)Intralobular interstitial thickening (Case 22, Asbestosis)Intralobular interstitial thickening (Case 29, Hypersensitivity pneumonitis, end stage)Intralobular septal thickening (Case 19, Systemic lupus erythematosus)Irregular fissures (Case 13, Drug-related lung injury)Irregular fissures (Case 14, Scleroderma)Irregular interlobular septal thickening (Case 13, Drug-related lung injury)Irregular interlobular septal thickening (Case 17, Idiopathic pulmonary fibrosis)Irregular interlobular septal thickening (Case 22, Asbestosis)Irregular interlobular septal thickening (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Irregular linear opacities (Case 24, Asbestosis-related pleural disease)Irregular linear opacities (crows feet) (Case 25, Asbestosis-related pleural disease)Irregular opacities (Case 27, Sarcoidosis, end stage )Irregularity and distortion of the fissures (Case 10, Sarcoidosis, end stage )Lobular areas of consolidation (Case 52, Bronchopneumonia, bacterial)Lobular lucency (Case 71, Hypersensitivity pneumonitis)Lobular opacities (Case 75, Pneumocystis carinii pneumonia (PCP))Low attenuation necrosis (Case 62, Aspergillosis, invasive)Lucency (Case 73, Hypersensitivity pneumonitis)Lucency (Case 77, Mycoplasma pneumonia)Lucency (Case 104, Paraseptal emphysema)Lucency (Case 105, Bullous emphysema)Lucency (Case 106, Centrilobular emphysema associated with adenocarcinoma)Lucency (Case 109, Emphysema in an AIDS patient)Lucency (Case 126, Hypersensitivity pneumonitis)Lucency (Case 127, Hypersensitivity pneumonitis)Lucent lung (Case 103, Panlobular emphysema)Lung bases (Case 12, Idiopathic pulmonary fibrosis)Lymph node enlargement (Case 6, Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma)Lymph node enlargement (Case 34, Sarcoidosis)Lymph node enlargement (Case 36, Sarcoidosis)Lymph node enlargement (Case 39, Lymphangitic spread of thyroid carcinoma)Lymph node enlargement (Case 42, Lymphoma arising from Mucosa Associated Lymphoid Tissue (MALToma))Mosaic perfusion (Case 120, Cystic fibrosis)Mosaic perfusion (Case 121, Bronchiolitis obliterans)Mosaic perfusion (Case 122, Bronchiolitis obliterans)Mosaic perfusion (Case 126, Hypersensitivity pneumonitis)Mosaic perfusion (Case 127, Hypersensitivity pneumonitis)Mucous or pus-filling bronchi (Case 114, Cystic fibrosis)Mucous or pus-filling peripheral bronchi (Case 111, Cystic fibrosis)Mycetoma (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Nodular areas of consolidation (Case 68, Bronchiolitis obliterans organizing pneumonia (BOOP))Nodular centrilobular opacities (Case 119, Cystic fibrosis)Nodular opacities (Case 58, Tuberculosis, active )Nodular opacities (Case 59, Tuberculosis, active )Nodular opacities (Case 111, Cystic fibrosis)Nodular septa (Case 9, Sarcoidosis)Nodule (Case 30, Idiopathic pulmonary fibrosis, complicated by lung cancer)Nodule (Case 62, Aspergillosis, invasive)Nodule (Case 63, Aspergillosis, invasive)Nodule, irregular (Case 75, Pneumocystis carinii pneumonia (PCP))Nodule, irregular (Case 106, Centrilobular emphysema associated with adenocarcinoma)Nodules (Case 31, Sarcoidosis)Nodules (Case 32, Sarcoidosis)Nodules (Case 34, Sarcoidosis)Nodules (Case 37, Silicosis)Nodules (Case 38, Lymphangitic spread of breast carcinoma)Nodules (Case 39, Lymphangitic spread of thyroid carcinoma)Nodules (Case 40, Kaposi sarcoma in an AIDS patient)Nodules (Case 41, Lymphocytic interstitial pneumonia (LIP), in assocation with AIDS)Nodules (Case 42, Lymphoma arising from Mucosa Associated Lymphoid Tissue (MALToma))Nodules (Case 43, Tuberculosis, miliary)Nodules (Case 44, Nontuberculosis mycobacterium (BCG), miliary )Nodules (Case 45, Coccidioidomycosis, miliary)Nodules (Case 46, Metastases, hematogenous from breast cancer)Nodules (Case 47, Metastases, hematogenous from breast cancer)Nodules (Case 48, Metastatic carcinoma, thyroid)Nodules (Case 49, Sarcoidosis)Nodules (Case 50, Bronchiolitis, infectious )Nodules (Case 51, Bronchiolitis, infectious, and bronchopneumonia)Nodules (Case 52, Bronchopneumonia, bacterial)Nodules (Case 53, Hypersensitivity pneumonitis)Nodules (Case 54, Bronchioloalveolar carcinoma)Nodules (Case 55, Bronchopneumonia, bacterial)Nodules (Case 61, Mycobacterium avium intracellular complex (MAC) infection)Nodules (Case 64, Wegener's granulomatosis)Nodules (Case 93, Metastatic calcification)Nodules (Case 94, Amyloidosis)Nodules, large ill defined (Case 60, Mycobacterium avium intracellular complex (MAC) infection)Nodules, multiple (Case 64, Wegener's granulomatosis)Normal lung (Case 1, Normal lung)Normal lung (Case 2, Normal lung)Parenchymal bands (Case 24, Asbestosis-related pleural disease)Parenchymal bands (Case 25, Asbestosis-related pleural disease)Parietal pleural plaques (Case 23, Asbestosis-related pleural disease)Parietal pleural thickening (Case 23, Asbestosis-related pleural disease)Patchy lung involvement (Case 36, Sarcoidosis)Peribronchial areas of consolidation (Case 52, Bronchopneumonia, bacterial)Peribronchovascular interstitium (Case 0, Nodules, an introduction)Peribronchovascular nodules (Case 32, Sarcoidosis)Peribronchovascular nodules (Case 33, Sarcoidosis)Peribronchovascular nodules (Case 40, Kaposi sarcoma in an AIDS patient)Peribronchovascular nodules (Case 42, Lymphoma arising from Mucosa Associated Lymphoid Tissue (MALToma))Perilymphatic nodules (Case 31, Sarcoidosis)Perilymphatic nodules (Case 32, Sarcoidosis)Perilymphatic nodules (Case 33, Sarcoidosis)Perilymphatic nodules (Case 34, Sarcoidosis)Perilymphatic nodules (Case 35, Sarcoidosis, progressive )Perilymphatic nodules (Case 37, Silicosis)Perilymphatic nodules (Case 38, Lymphangitic spread of breast carcinoma)Perilymphatic nodules (Case 39, Lymphangitic spread of thyroid carcinoma)Perilymphatic nodules (Case 41, Lymphocytic interstitial pneumonia (LIP), in assocation with AIDS)Perilymphatic nodules (Case 41, Lymphocytic interstitial pneumonia (LIP), in assocation with AIDS)Peripheral and subpleural lung regions (Case 12, Idiopathic pulmonary fibrosis)Peripheral nodules (Case 50, Bronchiolitis, infectious )Peripheral nodules (Case 51, Bronchiolitis, infectious, and bronchopneumonia)Peripheral nodules (Case 53, Hypersensitivity pneumonitis)Peripheral nodules (Case 0, Nodules, an introduction)Pleural effusion (Case 6, Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma)Pleural plaque (Case 26, Asbestos exposure, possible fibrosis)Pleural surfaces (Case 0, Nodules, an introduction)Pleural thickening (Case 23, Asbestosis-related pleural disease)Pleural thickening (Case 24, Asbestosis-related pleural disease)Pleural thickening (Case 25, Asbestosis-related pleural disease)Pneumatoceles (Case 99, Pneumocystis carinii pneumonia (PCP))Pneumatoceles (Case 100, Pneumocystis carinii pneumonia (PCP))Pneumatoceles (Case 110, Pneumatoceles with bronchiolitis obliterans organizing pneumonia (BOOP))Pneumothorax (Case 100, Pneumocystis carinii pneumonia (PCP))Random nodules (Case 43, Tuberculosis, miliary)Random nodules (Case 44, Nontuberculosis mycobacterium (BCG), miliary )Random nodules (Case 45, Coccidioidomycosis, miliary)Random nodules (Case 46, Metastases, hematogenous from breast cancer)Random nodules (Case 47, Metastases, hematogenous from breast cancer)Random nodules (Case 48, Metastatic carcinoma, thyroid)Random nodules (Case 49, Sarcoidosis)Reticular opacities (Case 84, Interstitial pneumonia, active, idiopathic pulmonary fibrosis)Reticular opacities (Case 87, Non-specific interstitial pneumonia (NSIP))Reticular pattern (Case 81, Hemorrhage secondary to leukemia)Reticulation (Case 26, Asbestos exposure, possible fibrosis)Reticulation (Case 28, Sarcoidosis, end stage , complicated by an aspergilloma)Septal thickening (Case 10, Sarcoidosis, end stage )Septal thickening (Case 26, Asbestos exposure, possible fibrosis)Septal thickening (Case 84, Interstitial pneumonia, active, idiopathic pulmonary fibrosis)Septal thickening (Case 99, Pneumocystis carinii pneumonia (PCP))Signet ring sign (Case 112, Bronchiectasis, focal)Signet ring sign (Case 114, Cystic fibrosis)Signet ring sign (Case 115, Williams Campbell syndrome)Small lung nodules (Case 101, Bronchopulmonary papillomatosis)Small nodules (Case 91, Sarcoidosis)Smooth septa (Case 6, Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma)Star artifacts (Case 4, Normal lung)Subpleural distribution (Case 15, Idiopathic pulmonary fibrosis)Subpleural honeycombing (Case 14, Scleroderma)Subpleural line (Case 15, Idiopathic pulmonary fibrosis)Subpleural line (Case 20, Rheumatoid lung disease)Subpleural line (Case 22, Asbestosis)Subpleural lucencies (Case 104, Paraseptal emphysema)Subpleural lucencies (Case 105, Bullous emphysema)Subpleural lucencies (Case 108, Centrilobular emphysema)Subpleural nodules (Case 31, Sarcoidosis)Subpleural nodules (Case 32, Sarcoidosis)Subpleural nodules (Case 33, Sarcoidosis)Subpleural nodules (Case 34, Sarcoidosis)Subpleural nodules (Case 35, Sarcoidosis, progressive )Subpleural nodules (Case 36, Sarcoidosis)Subpleural nodules (Case 37, Silicosis)Subpleural nodules (Case 38, Lymphangitic spread of breast carcinoma)Subpleural nodules (Case 39, Lymphangitic spread of thyroid carcinoma)Subpleural nodules (Case 41, Lymphocytic interstitial pneumonia (LIP), in assocation with AIDS)Subpleural nodules (Case 43, Tuberculosis, miliary)Subpleural nodules (Case 44, Nontuberculosis mycobacterium (BCG), miliary )Subpleural nodules (Case 45, Coccidioidomycosis, miliary)Subpleural nodules (Case 46, Metastases, hematogenous from breast cancer)Subpleural nodules (Case 47, Metastases, hematogenous from breast cancer)Subpleural nodules (Case 48, Metastatic carcinoma, thyroid)Subpleural nodules (Case 49, Sarcoidosis)Thickened interlobular septa (Case 5, Lymphangitic spread of breast carcinoma)Thickened interlobular septa (Case 6, Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma)Thickened interlobular septa (Case 7, Lymphangitic spread of lymphoma)Thickened interlobular septa (Case 8, Pulmonary edema)Thickened interlobular septa (Case 9, Sarcoidosis)Thickened interlobular septa (Case 10, Sarcoidosis, end stage )Thickened interlobular septa (Case 38, Lymphangitic spread of breast carcinoma)Thickened interlobular septa (Case 41, Lymphocytic interstitial pneumonia (LIP), in assocation with AIDS)Thickening of bronchi (Case 111, Cystic fibrosis)Thickening of fissures (Case 6, Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma)Thickening of fissures (Case 7, Lymphangitic spread of lymphoma)Thickening of fissures (Case 79, Pulmonary edema)Thickening of peribronchovascular interstitium (Case 5, Lymphangitic spread of breast carcinoma)Thickening of peribronchovascular interstitium (Case 6, Lymphangitic spread of carcinoma, right hilar bronchogenic carcinoma)Thickening of peribronchovascular interstitium (Case 7, Lymphangitic spread of lymphoma)Thickening of peribronchovascular interstitium (Case 8, Pulmonary edema)Thickening of peribronchovascular interstitium (Case 9, Sarcoidosis)Traction bronchiectasis (Case 13, Drug-related lung injury)Traction bronchiectasis (Case 14, Scleroderma)Traction bronchiectasis (Case 16, Idiopathic pulmonary fibrosis)Traction bronchiectasis (Case 17, Idiopathic pulmonary fibrosis)Traction bronchiectasis (Case 19, Systemic lupus erythematosus)Traction bronchiectasis (Case 20, Rheumatoid lung disease)Traction bronchiectasis (Case 21, Mixed connective tissue disease, pulmonary fibrosis)Traction bronchiectasis (Case 22, Asbestosis)Traction bronchiectasis (Case 27, Sarcoidosis, end stage )Traction bronchiectasis (Case 29, Hypersensitivity pneumonitis, end stage)Traction bronchiectasis (Case 85, Idiopathic pulmonary fibrosis)Traction bronchiectasis (Case 95, Idiopathic pulmonary fibrosis)Tram tracks (Case 112, Bronchiectasis, focal)Tram tracks (Case 114, Cystic fibrosis)Tree in bud (Case 55, Bronchopneumonia, bacterial)Tree in bud (Case 56, Bronchopneumonia, bacterial)Tree in bud (Case 57, Bronchiectasis, bacterial bronchitis and bronchiolitis)Tree in bud (Case 58, Tuberculosis, active )Tree in bud (Case 59, Tuberculosis, active )Tree in bud (Case 60, Mycobacterium avium intracellular complex (MAC) infection)Tree in bud (Case 61, Mycobacterium avium intracellular complex (MAC) infection)Tree in bud (Case 117, Bronchiectasis, post-infectious)Varicose bronchiectasis (Case 114, Cystic fibrosis)Volume loss (Case 114, Cystic fibrosis)本来是航母上下的资料，不过好像有些板油错过了，所以尽量把原文贴了上来。没想到折腾了一个下午才算完，昏了头，可能有有些错漏的情况，还请见谅。That is all.protocol应该译为技术参数。支持一下楼主！谢谢楼主的辛苦工作！翻译确实是一件又苦又累的差事。然而成就感也就在大功告成的那一刻！如此经典的论著希望I9708活着能抽空把它译完奉献给大家。再次感谢！
