Infeccion del lobulo inferiores by Eric Maldonado

Residents’ Section • Pat tern of the Month Nemec et al. Lower Lobe–Predominant Diseases of the Lung

Residents’ Section Pattern of the Month

Residents

inRadiology Stefan F. Nemec1 Alexander A. Bankier Ronald L. Eisenberg Nemec SF, Bankier AA, Eisenberg RL

Keywords: lung, lower lobe–predominant diseases, pulmonary diseases DOI:10.2214/AJR.12.9253 Received May 11, 2012; accepted without revision May 22, 2012. 1

All authors: Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, Boston, MA 02115. Address correspondence to R. L. Eisenberg (rleisenb@bidmc.harvard.edu).

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he lung is a heterogeneous organ because of regional differences in perfusionventilation ratios and in lymphatic, metabolic, and mechanical properties, which are primarily influenced by gravity. In the erect individual, these differences result in relative overventilation of the lung apices and overperfusion of the lung bases. The relative apical overventilation and decreased apical lymphatic flow cause certain pulmonary diseases to have an upper lung predominance [1]. The combination of gravity and relative overperfusion of the lung bases leads other disorders to predominantly involve the lower lung (Table 1). The effect of gravity is responsible for the lower lung predominance in aspiration and hydrostatic pulmonary edema. In addition to the perfusion gradient between the apical and basilar portions of the lung, there also are differences in perfusion between the central and peripheral areas. The longer distance and slower flow in the lung periphery result in a greater transit time for immune complexes or malignant cells to flow through the pulmonary circulation. This prolonged transit time increases the interaction between substances transported in the blood and the peripheral lung and makes it more likely for toxic substances to deposit in the pulmonary vascular bed. The relative overperfusion and prolonged transit time may explain the lower lung predominance in idiopathic interstitial pneumonias and in interstitial pneumonias secondary to autoimmune disorders and drug-induced toxicity, all of which are associated with circulating agents such as immune complexes. Specific gravity, which refers to the gravity of circulating particles relative to that of blood, also affects the distribution of these particles. Those of greater specific gravity are “heavier” and therefore are distributed preferentially to the lower lung when the patient is in the upright position. The combined mechanisms of perfusion and specific gravity are responsible for the lower lung predominance of hematogenous spread of metastases and septic emboli. In asbestos-related disease, the underlying mechanism for the obvious lower lung predominance remains unclear, especially considering that the inhaled particulates preferentially accumulate in the relatively overventilated upper zones in the other pneumoconioses. The paradoxical distribution of asbestos fibers might be explained by their needle shape and other indeterminate biochemical factors. There is also uncertainty about the distribution of panlobular emphysema associated with α1-antitrypsin deficiency. Some authors describe a lower lobe predominance, whereas others state that the findings are more diffuse with only a mild preferential involvement of the lower lung. Because of this controversy, we have not included a detailed discussion of panlobular emphysema in this article.

Aspiration Aspiration refers to the involuntary intake of solid or liquid material into the airways and lungs. Aspiration most commonly affects the right middle and lower lobes, primarily because of the larger caliber and more vertical course of the right main bronchus compared with the left. In contrast, the upper lobes may be preferentially involved in patients who aspirate while in the prone position. In children, aspiration is commonly accidental. In adults, aspiration may be associated with swallowing disorders, pharyngeal abnormalities, esophageal dysmotility, and alcoholism. Clinically, aspiration may be asymptomatic or may produce a range of symptoms including a life-threatening condition, with the major complication being secondary pulmonary infection.

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Lower Lobe–Predominant Diseases of the Lung TABLE 1: Pulmonary Diseases With Lower Lung Predominance Aspiration

Foreign body aspiration Aspiration of liquid materials Lipoid pneumonia Increased hydrostatic pressure edema Interstitial pneumonias UIP Idiopathic UIP Secondary UIP (systemic sclerosis, rheumatoid arthritis, Sjögren syndrome, drug toxicity) NSIP Idiopathic NSIP Secondary NSIP (systemic sclerosis, rheumatoid arthritis, Sjögren syndrome, drug toxicity) OP Idiopathic OP Secondary OP (Sjögren syndrome, infectious agents, drug toxicity) AIP Idiopathic AIP Secondary AIP (chemical agents, infectious pathogens, sepsis, trauma, drug toxicity) Hematogenous spread Hematogenous metastasis Septic embolism Asbestos-related disease Benign pleural disease Pleural effusion Pleural plaques Diffuse pleural thickening Round atelectasis Asbestosis Mesothelioma Note—UIP = usual interstitial pneumonia, NSIP = nonspecific interstitial pneumonia, OP = organizing pneumonia, AIP = acute interstitial pneumonia.

Foreign Body Aspiration Aspirated foreign bodies, most of which are located within the right main bronchus, are often food components, as well as broken teeth in adults or small toy parts in children. Affected individuals may present acutely with cough, shortness of breath, hemoptysis, or pneumonia. Chronic aspiration may result in recurrent infection and the development of bronchiectasis. Nonopaque food components are usually invisible on chest radiography. However, they may cause overinflation secondary to partial bronchial obstruction and a resulting checkvalve mechanism. Complete bronchial obstruction results in segmental or complete lobar collapse. CT is useful for directly showing nonopaque foreign bodies and associated complications such as pneumonia, and for guiding foreign body removal at bronchoscopy.

Aspiration of Liquid Materials In liquid aspiration, the volume and pH of the liquid determine the severity of the lung injury. Vomiting with aspiration of gastric acid may cause reactions ranging from bronchiolitis to acute respiratory distress. The majority of aspiration pneumonias are caused by organisms arising from the oropharynx and gastrointestinal tract. Aspiration of barium is an iatrogenic complication of gastrointestinal imaging (Fig. 1).

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Fig. 1—Aspiration related to swallowing disorder. A and B, Posteroanterior (A) and lateral (B) chest radiographs obtained after fluoroscopic procedure show right middle lobe opacity (white arrows) and residual contrast material (black arrows) in distal esophagus.

Fig. 2—Aspiration in gastroesophageal reflux disease. Transverse CT image of chest shows bilateral airspace opacities (open arrows) predominantly in posterior and lower lung. Note rightsided kinking of dilated esophagus (solid arrow).

Fig. 3—Bronchiolitis in chronic aspiration. Transverse CT image of chest shows bilateral basilar tree-in-bud pattern (arrows), more prominent on left than right.

On radiography and CT, aspiration of liquid materials typically manifests as parenchymal opacity representing pneumonia. Scattered heterogeneous opacities are more common than lobar airspace consolidation (Fig. 2). In recumbent patients, the posterior upper lobes and the apical lower lobes are most often involved; in erect patients, the posterobasilar lungs are more frequently involved. Although chest radiography is the most commonly used imaging modality to evaluate aspiration pneumonia, CT may be helpful in cases of mild aspiration bronchiolitis because it can show tree-in-bud opacities that remain undetected on chest radiography (Fig. 3). CT also may show complications of aspiration pneumonia such as abscess, empyema, and peripheral fibrosis. Fig. 4—Lipoid pneumonia after laxative aspiration. Transverse CT image of chest shows ovoid opacity with virtually pathognomonic central fat density (arrow) in medial segment of middle lobe.

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Lipoid Pneumonia Lipoid pneumonia is a subtype of liquid aspiration related to fat-containing milk, mineral

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Lower Lobe–Predominant Diseases of the Lung oil for constipation treatment, or oily nose drops used for rhinitis therapy. Radiographic findings include nonspecific bilateral opacities predominantly in the lower lobes. The CT visualization of areas of fat attenuation (as low as −30 HU) within the opacities is virtually diagnostic of lipoid pneumonia (Fig. 4). An additional nonspecific finding is “crazy paving,” which consists of ground-glass opacities with interlobular septal thickening. However, this appearance also may be observed in bronchioloalveolar carcinoma, alveolar proteinosis, infection, and pulmonary hemorrhage. Recurrent aspiration may lead to the development of pulmonary fibrosis. Pneumatocele formation may be a complication of the aspiration of petroleum-based products in fire-eaters.

Increased Hydrostatic Pressure Edema

Fig. 5—Redistribution of pulmonary blood flow. Posteroanterior chest radiograph shows apical vascular redistribution, indicated by finding that diameters of upper lobe vessels (solid arrows) are equal to those of lower lobe vessels (open arrows). Note moderate enlargement of heart.

Hydrostatic edema refers to the presence of excess extravascular fluid in the lung due to hemodynamic dysfunction. Left heart failure and fluid overload are the two main causes of hydrostatic edema, which may show an interstitial or alveolar pattern. The lower lung predominance of hydrostatic edema is determined by gravitational forces on edema fluid and by the relative overperfusion of the lower lobes. Clinically, patients may exhibit dyspnea and peripheral leg swelling. Imaging findings of edema usually lag behind the clinical course because of the slow movement of water through the capillary endothelial cell junctions. An increase in pulmonary capillary pressure results in edema accumulation within 12 hours, with resolution within hours or days after the start of medical treatment. The radiographic distribution of increased hydrostatic pressure edema varies with patient position. In an erect patient, the radiographic precursor of interstitial edema is apical vascular redistribution, in which the diameter of upper lobe vessels is equal to or greater than those in the lower lobes (Fig. 5). Interstitial edema results in loss of definition of subsegmental and segmental vessels, thickening of interlobular septa (Kerley B lines peripherally in the lower

Fig. 6—Interstitial edema in chronic cardiac insufficiency. A, Posteroanterior chest radiograph shows bilateral lower lung predominance of interstitial opacities as well as enlarged central vascular structures and cardiac enlargement. B, Magnified view of A shows poor definition of vessels, thickening of interlobular septa (Kerley B lines) (black arrow), and peribronchial cuffing (white arrows).

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Fig. 7—Iatrogenic fluid overload after trauma in patient without cardiac disease. Anteroposterior chest radiograph shows distinct widening of azygos vein (arrow) without significant cardiac enlargement.

Fig. 8—Alveolar hydrostatic edema in acute myocardial infarction. Anteroposterior chest radiograph shows bilateral interstitial and coalescent alveolar opacities with perihilar and lower lung predominance. Hazy opacity of lower zones indicates associated layering pleural effusion.

lobes), and peribronchial cuffing (Fig. 6). Thickening of the interlobar fissures and subpleural effusions also may occur. Widening of the azygos vein and superior vena cava, combined with a normal heart size, may indicate that hydrostatic edema is caused by fluid overload rather than left heart insufficiency (Fig. 7). Further increase in capillary pressure leads to alveolar edema, which results in coalescent alveolar opacities associated with cardiomegaly and pleural effusions (Fig. 8). Although the combined assessment of clinical presentation and radiographs is usually sufficient for the diagnosis of hydrostatic edema, CT may be useful in patients with severe coexisting pulmonary conditions. On CT, interstitial edema appears as smooth thickening of interlobular septa and bronchovascular bundles, whereas alveolar edema manifests as gravity-dependent, ground-glass or airspace opacities (Fig. 9). In more chronic disease, enlarged mediastinal lymph nodes, resulting from concurrent lymphatic fluid overload, also may be seen. As opposed to the lower lung predominance of hydrostatic edema, batwing edema refers to a central nongravitational alveolar edema that occurs with acute cardiac or renal failure. The mechanism behind the development of this phenomenon is not fully understood. The differential diagnosis of hydrostatic edema includes pneumonia and noncardiogenic edema, such as that due to vascular hyperpermeability. In addition to the clinical findings, the combination of bilateral gravity-dependent opacities with mild cardiomegaly, vascular enlargement, and pleural effusions is indicative of hydrostatic edema.

Idiopathic and Secondary Interstitial Pneumonias

Fig. 9—Hydrostatic pulmonary edema. Transverse CT image of chest shows moderate ground-glass attenuation, thickening of interlobular septa and bronchovascular bundles (black arrow), and pleural effusion (white arrow).

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Among the heterogeneous group of interstitial pneumonias, five show lower lung predominant findings—usual interstitial pneumonia (UIP), nonspecific interstitial pneumonia (NSIP), cryptogenic organizing pneumonia (COP), acute interstitial pneumonia (AIP), and lymphoid interstitial pneumonia (LIP). The peripheral lower lung predominance may be driven by the relative basilar overperfusion and the prolonged peripheral transit time of circulating cellular agents, which cause various degrees of inflammation and fibrosis.

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Lower Lobe–Predominant Diseases of the Lung Although rare in their idiopathic forms, the morphologic patterns of interstitial pneumonias may occur secondary to various conditions (Table 1).

Usual Interstitial Pneumonia UIP is the morphologic pattern of idiopathic pulmonary fibrosis, with the key histologic feature of scattered fibroblastic foci. Although an idiopathic disease, the pattern of UIP may be also encountered secondary to systemic sclerosis, rheumatoid arthritis, Sjögren syndrome, and drug toxicity. Patients are 50 years old or older and present with progressive dyspnea and cough. Unfortunately, there is no effective treatment. Consequently, the idiopathic form of

Fig. 10—Idiopathic usual interstitial pneumonia (UIP). A, Posteroanterior chest radiograph shows bilateral reticular opacities that increase from upper (white arrows) to lower (black arrows) zones. B–E, Transverse (cephalad to caudad) (B–D) and sagittal (E) CT images of chest show obvious apicobasilar gradient of subpleural findings (open arrows) including reticular opacities, moderate ground-glass opacities, traction bronchiectasis, and especially basilar honeycombing. Abnormal mediastinal air collections (solid arrow, B) indicating pneumomediastinum (B) represent complication of UIP.

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Nemec et al. UIP, with a median survival time of 2–4 years, is associated with a substantially poorer prognosis than other interstitial diseases. In early UIP, chest radiographs may be normal, whereas in advanced disease there are decreased lung volumes and subpleural reticular opacities that increase from the lung apices to the bases (Fig. 10). CT is superior to radiography for delineating the typical findings of UIP, which include subpleural reticular opacities with prominent honeycombing, traction bronchiectasis, and architectural distortion, all of which have an apicobasilar gradient (Figs. 10 and 11). Additional ground-glass opacities may show rapid progression to honeycombing (Fig. 12). In view of the heterogeneous involvement in UIP, with fibrosis alternating with normal parenchyma, CT is useful in determining the most appropriate site for biopsy to confirm the diagnosis (Fig. 10). There is substantial overlap of the CT patterns and even of the histologic findings of UIP and fibrotic NSIP. The CT features that favor the diagnosis of UIP are summarized in Table 2. Patients with chronic hypersensitivity pneumonitis or end-stage sarcoidosis, which both show an upper lung predominance, may uncommonly develop fibrosis similar to that of UIP. The presence of pleural plaques or pleural thickening helps differentiate asbestosis from UIP.

Nonspecific Interstitial Pneumonia

Fig. 11—Usual interstitial pneumonia secondary to systemic sclerosis. Transverse CT image of chest shows basilar ground-glass opacities with especially prominent honeycombing (arrows) that is not seen in nonspecific interstitial pneumonia.

NSIP is as a subtype of idiopathic interstitial pneumonia with histologic findings that are different from those of other interstitial pneumonias. Two distinct subtypes can be differentiated—cellular NSIP dominated by inflammation and fibrosing NSIP. The pattern of NSIP frequently occurs in association with

Fig. 12—Rapid progression of idiopathic usual interstitial pneumonia. A, Transverse CT image of chest at initial examination shows subpleural reticular opacities (arrows), traction bronchiectasis, and minor ground-glass attenuation. B, Transverse CT image of chest 3 months after A shows progression of reticular opacities (arrows) with advancing destruction of lung.

TABLE 2: Predominant Imaging Features of Usual Interstitial Pneumonia (UIP) and Nonspecific Interstitial Pneumonia (NSIP) Patterns UIP

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NSIP

Honeycombing

Reticular opacities

Traction bronchiectasis

Ground-glass opacities

Architectural distortion

Micronodules

Spatial and temporal heterogeneity

No particular heterogeneity

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Fig. 13—Nonspecific interstitial pneumonia (early stage). A and B, Coronal (A) and transverse (B) CT images of chest show lower lung–predominant ground-glass attenuation and fine subpleural reticular opacities (arrows) without consolidation or honeycombing.

Fig. 14—Nonspecific interstitial pneumonia (advanced stage). A–C, Transverse (A and B) and sagittal (C) CT images of chest show subpleural reticular opacities with slight honeycombing (arrows) in lower lung but no apicobasilar gradient of findings.

connective tissue diseases (systemic sclerosis, rheumatoid arthritis, Sjögren syndrome) or drug exposure (bleomycin; methotrexate). Patients with NSIP are typically between 40 and 50 years old and present with worsening dyspnea, fatigue, and weight loss, which are usually milder than in UIP. In contrast to UIP, NSIP may stabilize after patients undergo combined therapy of corticosteroids and cytotoxic drugs. In early NSIP, chest radiographs are usually normal; in advanced disease, bilateral nonspecific opacities are most frequently seen. CT typically reveals a subpleural and symmetric distribution of ground-glass opacities combined with fine reticular opacities and micronodules (Fig. 13). The lower lung zones are more affected than the upper zones, but there is a less pronounced apicobasilar gradient of abnormalities, which are more homogeneous than in UIP. Findings in advanced or fibrotic NSIP may occasionally include moderate honeycombing with

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Nemec et al. traction bronchiectasis and with consolidation, which also is less pronounced than in UIP (Fig. 14). The key imaging features that favor the diagnosis of NSIP over UIP are summarized in Table 2. Unlike systemic sclerosis or rheumatoid arthritis (Fig. 15), both of which may be associated with NSIP, systemic lupus erythematosus tends to produce pneumonitis and alveolar hemorrhage. On CT, lupus pneumonitis appears as bilateral basilar ground-glass opacities, whereas alveolar hemorrhage shows extensive bilateral consolidation, interstitial opacities, and pleural effusions.

Organizing Pneumonia Organizing pneumonia is a nonspecific response to lung injury that is characterized histologically by granulation tissue in the alveolar ducts and alveoli. This entity may be idiopathic/ cryptogenic (COP) or secondary to collagen vascular disease (Sjögren syndrome), infection, or drugs (bleomycin; amiodarone). Patients with COP have a mean age of 55 years. They typically present with a several weeks’ history of mild dyspnea, cough, and fever, which may completely resolve after corticosteroid therapy. Chest radiographs of patients with COP usually show unilateral or bilateral patchy consolidations that resemble pneumonia. The CT appearance varies from consolidations that may

Fig. 15—Nonspecific interstitial pneumonia secondary to rheumatoid arthritis. A and B, Transverse CT images of chest show bilateral subpleural findings (arrows) of fine reticular changes and accompanying ground-glass opacities without parenchymal distortion or honeycombing.

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Fig. 16—Cryptogenic organizing pneumonia. A and B, Transverse (A) and coronal (B) CT images of chest show bilateral bizarre-shaped consolidations (arrows) with air bronchograms in posterior lower lobes. C, Transverse CT image of different patient shows bilateral peripheral consolidations (arrows) with partial subpleural sparing, more prominent on left.

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Fig. 17—“Atoll” sign in cryptogenic organizing pneumonia. Transverse CT image of chest shows several round areas of ground-glass attenuation surrounded by denser opacity (arrows).

Fig. 18—Acute interstitial pneumonia due to nitric acid inhalation. Anteroposterior chest radiograph shows extensive bilateral airspace opacities with sparing of medial and lateral costophrenic angles.

have air bronchograms to a ground-glass pattern with a surrounding dense, ring-shaped opacity (“atoll” sign or “reversed halo” sign) (Figs. 16 and 17). These lower lung–predominant opacities may range from a few centimeters to involvement of an entire lobe. On CT, findings have a characteristic peripheral or peribronchial distribution that may spare the outermost subpleural area (Fig. 16). These abnormalities may increase over several weeks despite antibiotic therapy, or they may change location and size even without treatment. Atypical CT patterns of COP include irregular linear opacities, solitary masslike lesions that resemble lung cancer, and multiple nodules that may cavitate. In amiodarone-induced organizing pneumonia, the pulmonary opacities and lesions in the liver and spleen may show high attenuation because this medication contains iodine. Based on its variable appearance, COP should always be confirmed by biopsy to establish the diagnosis.

Acute Interstitial Pneumonia AIP is characterized by permeability edema with diffuse alveolar damage that consists of partially overlapping stages (exudative, proliferative, fibrotic). The pattern of AIP may be encountered in an idiopathic or secondary form. Secondary AIP is the morphologic basis of acute respiratory distress syndrome (ARDS). ARDS may be caused by exposure to chemical agents or infectious pathogens or by systemic processes such as sepsis or trauma. AIP affects a wide age range, with a mean age of 50 years, and shows no sex predilection. Patients with AIP rapidly develop respiratory failure requiring mechanical ventilatory assistance, and the mortality rate is at least 50%. Because mechanical ventilation can augment or cause pulmonary damage, therapy also aims to protect the lung from this iatrogenic injury. Chest radiographs initially are normal but subsequently show bilateral coalescent airspace opacities that characteristically spare the costophrenic angles (Fig. 18). As the disease progresses, the lungs tend to become diffusely consolidated—in particular, the lower lung zones. These extensive opacities are often termed “white lungs.” CT is more sensitive than radiography in showing the overlapping stages of disease. In the early exudative phase, the dominant CT pattern is symmetric, bilateral ground-glass opacities with sparing of the costophrenic angles. As the disease progresses, consolidation resulting from alveolar collapse (atelectasis) primarily affects the dependent lung (Fig. 19). In the late phase, consolidation tends to be replaced by ground-glass opacities and is often associated with cysts and traction bronchiectasis. In patients who survive, CT may show progression of changes to end-stage fibrosis with honeycombing and architectural distortion especially in the nondependent lung. This appearance may be explained as a “protective” effect of atelectasis on the dependent lung during the acute phase, which attenuates injury caused by mechanical ventilation. The differential diagnosis of AIP includes widespread infection and hydrostatic edema. Because AIP does not result from cardiac insufficiency, signs of hydrostatic edema such as cardiomegaly, vessel enlargement, and pleural effusions are typically absent.

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Fig. 19—Acute interstitial pneumonia in sepsis. Transverse CT image of chest shows distinct bilateral ground-glass opacities and consolidations, primarily located in dependent lung.

Fig. 20—Lymphocytic interstitial pneumonia secondary to Sjögren syndrome. Transverse CT image of chest shows diffuse ground-glass opacities and multiple small perivascular cysts (arrows) with lower lung predominance.

Lymphoid Interstitial Pneumonia LIP represents lymphocytic infiltration of the alveolar interstitium and airspaces. Idiopathic LIP is extremely rare. Secondary LIP may occur in various immunodeficiency diseases, such as HIV infection, and is particularly common in Sjögren syndrome. LIP is more common in women, between the ages of 40 and 50 years, and usually presents with slowly progressive dyspnea and cough. There is also an increased incidence of lymphoma in LIP. Chest radiographs of patients with LIP reveal nonspecific bilateral reticular, reticulonodular, or alveolar opacities. The typical CT features are ground-glass opacities in combination with thin-walled perivascular cysts, both of which have a lower lung predominance (Fig. 20). Centrilobular nodules and septal thickening are occasionally seen. Unlike the subpleural cysts in patients with UIP and NSIP, the cysts in those with LIP usually occur diffusely within the lung parenchyma.

Hematogenous Spread Hematogenous spread is the seeding of blood-borne agents to the lungs. The lower lung predominance of metastases and bacteremic septic emboli may be explained by the relative overperfusion of the lung bases, the delayed peripheral blood transit time, and the higher specific gravity of these malignant and infectious agents relative to the circulating blood.

Hematogenous Metastasis

Fig. 21—Multiple pulmonary metastases in renal cell carcinoma. Posteroanterior chest radiograph shows multiple nodules (arrows) of varying size in right lower and mid lung.

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Hematogenous metastases frequently involve the lungs because of their rich vasculature. The peripheral distribution, in the outer 2–3 cm of lung including along the fissures, and lower lung predominance may relate to the prolonged transit time in the peripheral lung and the relative basilar overperfusion. The most common primary tumors that cause lung metastases are cancers of the breast, kidney, colon, and thyroid and melanoma. The detection of pulmonary metastases has a crucial influence on cancer staging and thus on treatment options and prognosis. Chest radiography is usually the first imaging examination to detect pulmonary metastases. Pulmonary metastases typically appear as round nodules of variable size that are scattered throughout both lungs and predominantly involve the lower lung (Fig. 21).

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Fig. 22—Solitary pulmonary metastasis in melanoma. A and B, Posteroanterior (A) and lateral (B) chest radiographs show single nodular lesion (arrows) in paravertebral location at left base. C and D, Transverse contrast-enhanced CT images confirm presence of enhancing mass in left lower lobe (arrows) without evidence of other suspicious lesions.

CT is the imaging modality of choice for detecting pulmonary metastasis as well as for guiding biopsy, planning treatment, and following up after therapy. CT is more sensitive than radiography in showing pulmonary nodules smaller than 10 mm, and a solitary metastasis detected on radiography is often associated with additional lesions on CT. This modality is of particular value for identifying radiographically occult nodules in the lung apices and bases or lesions adjacent to the heart, mediastinum, and pleura. Pulmonary metastases typically have soft-tissue attenuation and more often occur in the periphery of the lower lung (Figs. 22 and 23). They usually are multiple and vary in size from 2–3 mm to 15 cm or larger (Fig. 23). Nodules smaller than 2 cm are often round with smooth margins, whereas larger nodules may have irregular margins and become confluent with adjacent masses (Fig. 23). Furthermore, CT may show a prominent pulmonary vessel heading into a metastasis, which is called the “feeding vessel” sign. It is important to consider atypical patterns of metastatic disease and their differential diagnoses. Innumerable small metastases may occur in thyroid cancer and produce an appearance similar to miliary tuberculosis, whereas a solitary metastasis may occur in colorectal carcinoma. Even in patients with a known malignancy, biopsy may be necessary to differentiate a

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Fig. 23—Multiple pulmonary metastases in colon carcinoma. A–C, Transverse (A and B) and coronal (C) contrastenhanced CT images of chest show multiple contrastenhancing metastases (arrows) that predominantly involve peripheral lower lung. Some masses have irregular margins and are confluent with adjacent lesions.

solitary pulmonary metastasis from a primary lung carcinoma. Hemorrhagic metastases of choriocarcinoma, angiosarcoma, or renal cell carcinoma may show a ground-glass halo on CT. Cavitation in squamous cell pulmonary metastases may mimic granulomatosis with polyangiitis (Fig. 24). Calcification in pulmonary metastases from osteogenic sarcoma or chondrosarcoma may be difficult to distinguish from granulomas, although growth of the lesion on follow-up scans indicates metastatic disease. Necrobiotic pulmonary nodules (diameter of 0.5–5.0 cm) mimicking metastases may rarely occur in rheumatoid arthritis. Finally, some metastases may show complete fibrosis and necrosis after chemotherapy.

Septic Embolism Septic embolism occurs from infected embolic material in the blood that is typically bacterial (Staphylococcus aureus) but may also be caused by fungi or parasites. Predisposing factors include tricuspid valve endocarditis, drug addiction, alcoholism, skin infection, immunologic deficiencies, and infected indwelling catheters or pacemaker wires. Chest radiographs may show rapidly evolving bilateral peripheral, nodular, or wedge-shaped opacities that vary in size (1–3 cm diameter), may show cavitation, and usually occur in the lower lung zones. CT findings of septic embolism include nodules with varying degrees of cavitation and subpleural wedge-shaped opacities with rimlike peripheral enhancement, all of which predominantly involve the lower lobes (Fig. 25). Another common CT finding is feeding vessels leading directly to the nodules. CT may also show an empyema developing as a complication of septic embolism. The differential diagnosis of septic emboli includes noninfectious pulmonary embolism, which may show wedge-shaped, pleura-based opacities and accompanying filling defects in Fig. 24—Cavitating metastases in bronchogenic pulmonary arteries. Fat emboli, which are a carcinoma. Transverse CT image of chest shows complication of long bone trauma, burns, pandiffuse, bilateral, ill-defined opacities with cavitation.

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Lower Lobe–Predominant Diseases of the Lung creatitis, or liposuction, may appear as widespread areas of increased opacities that often result in acute respiratory distress. Finally, metastases and nodules in granulomatosis with polyangiitis also may cavitate, but these lesions do not evolve as rapidly as septic emboli.

Asbestos-Related Disease Asbestos comprises a group of silicate minerals used in many commercial settings, such as shipyards, and for fire proofing and as insulation in domestic settings. The biohazard arises from inhalation of asbestos fibers through exposure in mining and processing. Asbestosrelated diseases may have a long latency period of 10–50 years. Patients usually present with Fig. 25—Septic emboli due to infected central venous access device. Transverse CT image of chest progressive dyspnea and cough, with men af- shows mainly subpleural nodular cavitating opacities fected more often than women. Different phys- (arrows) in basilar portion of right lung. iochemical properties of asbestos fibers, such as their length-width ratio, are believed to determine the fiber distribution and disease severity. Asbestos exposure may cause pleural effusion, pleural plaques, diffuse pleural thickening, round atelectasis, asbestosis, and mesothelioma. It also favors the development of bronchogenic carcinoma.

Fig. 26—Pleural plaques in asbestos-related disease. A and B, Posteroanterior (A) and lateral (B) chest radiographs show multiple calcifications (arrows) of ventral, lateral, and diaphragmatic pleural surfaces. C and D, Coronal (C) and transverse (D) CT images of chest show bilateral calcified pleural plaques (arrows). (Fig. 26 continues on next page)

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Asbestos-Related Pleural Disease

E Fig. 26 (continued)—Pleural plaques in asbestosrelated disease. E, Transverse CT image of different patient shows bilateral plaques associated with interstitial lines (arrows) radiating from plaques (“hairy plaques”) in adjacent lung.

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Pleural effusion is the earliest imaging finding of asbestos-related pleural disease, and pleural plaques, which may calcify, are the most common manifestation of pleural disease (Fig. 26). On radiographs, plaques may involve the lateral chest wall between the sixth and tenth ribs, the diaphragmatic domes, and the mediastinal pleura (Fig. 26). Diffuse pleural thickening may be observed as a smooth continuous sheet of pleural opacity. CT precisely shows anterior and paravertebral plaques that are not well seen on radiography (Fig. 26). On CT, there may be fine interstitial lines radiating from the plaque (“hairy plaque”) in the adjacent lung (Fig. 26). CT is also of value for differentiating diffuse pleural thickening from adipose tissue, organizing effusion, infection, metastases, rib fractures, and mesothelioma.

Fig. 27—Round atelectasis in asbestos-related disease. A, Transverse CT image of chest shows mass (black arrow) in left lung that abuts pleura and has “comet tail” of bronchovascular structures (white arrow) extending into mass. B and C, Transverse contrast-enhanced CT images of different patient shows enhancing mass (arrow, B) in right lower lobe with pleural adhesion. Bronchovascular structures (white arrow, C) extend into mass (black arrow, C).

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Fig. 28—Asbestosis. A and B, Transverse CT images of chest show bilateral ground-glass opacities and subpleural fibrotic changes (arrows) that show basilar predominance.

Round Atelectasis Round atelectasis is a peripheral form of atelectasis that is thought to be caused by an inflammatory pleural reaction associated with pleural effusion and that is frequently related to asbestos exposure. The radiographic appearance is a rounded peripheral mass associated with pleural thickening. Contrast-enhanced CT typically shows an enhancing round mass that abuts the pleura and thickens the adjacent pleural surface. It is typically associated with a characteristic “comet tail” of bronchovascular structures extending into the mass (Fig. 27).

Fig. 29—Mesothelioma. A, Posteroanterior chest radiograph shows irregular pleural opacities (black arrows) that encircle right lower lung and also show fissural extension (white arrow). B and C, Transverse contrast-enhanced CT images of chest show diffuse, ill-defined, enhancing soft-tissue masses (arrows) extending along pleura of chest wall, fissure, mediastinum, and diaphragm.

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Asbestosis Asbestosis, which refers to the lung fibrosis caused by asbestos fibers, predominantly affects the subpleural portions of the lower lung. Radiography may show interstitial and nodular opacities, but CT is the more sensitive modality for depicting asbestosis. An early CT feature of asbestosis is subpleural curvilinear fibrotic opacities that extend parallel to the pleura. CT may also show fibrous band-shaped opacities that project in from the pleura along bronchovascular structures or interlobular septa. In advanced disease, CT may show ground-glass opacities, subpleural nodular opacities, and honeycombing (Fig. 28). Most patients with asbestosis have coexistent pleural disease apparent on CT.

Asbestos-Related Malignancies Asbestos-related bronchogenic carcinoma, which may be located anywhere in the lungs, occurs more frequently than mesothelioma, especially among asbestos-exposed workers who smoke. Mesothelioma is the most common primary neoplasm of the pleura and has a strong association with asbestos exposure. Lobulated pleural thickening and pleural effusion may be seen on radiographs (Fig. 29). The most common CT finding is contrast-enhancing lobular pleural thickening accompanied by pleural effusion. CT may also show tumor extension along the fissures and invasion of the chest wall, mediastinum, and diaphragm (Fig. 29). PET/ CT may assist in differentiating mesothelioma from benign pleural thickening. Reference 1. Nemec SF, Bankier AA, Eisenberg RL. Upper lobe–predominant diseases of the lung. AJR 2013; 200:3; [web]w222–w237

Selected Reading 1. American Thoracic Society; European Respiratory Society. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias. This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Executive Committee, June 2001. Am J Respir Crit Care Med 2002; 165:277–304 [Erratum in Am J Respir Crit Care Med 2002; 166:426] 2. Capobianco J, Grimberg A, Thompson BM, Antunes VB, Jasinowodolinski D, Meirelles GS. Thoracic manifestations of collagen vascular diseases. RadioGraphics 2012; 32:33–50 3. Franquet T, Giménez A, Rosón N, Torrubia S, Sabaté JM, Pérez C. Aspiration diseases: findings, pitfalls, and differential diagnosis. RadioGraphics 2000; 20:673–685 4. Gluecker T, Capasso P, Schnyder P, et al. Clinical

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and radiologic features of pulmonary edema. RadioGraphics 1999; 19:1507–1531 5. Gurney JW. Atypical manifestations of pulmonary atelectasis. J Thorac Imaging 1996; 11:165–175 6. Gurney JW. Cross-sectional physiology of the lung. Radiology 1991; 178:1–10 7. Han D, Lee KS, Franquet T, et al. Thrombotic and nonthrombotic pulmonary arterial embolism: spectrum of imaging findings. RadioGraphics 2003; 23:1521–1539 8. Roach HD, Davies GJ, Attanoos R, Crane M, Adams H, Phillips S. Asbestos: when the dust settles—an imaging review of asbestos-related disease. RadioGraphics 2002; 22:167–184 9. Roberton BJ, Hansell DM. Organizing pneumonia: a kaleidoscope of concepts and morphologies. Eur Radiol 2011; 21:2244–2254 10. Silva CI, Müller NL. Drug-induced lung diseases: most common reaction patterns and corresponding high-resolution CT manifestations. Semin Ultrasound CT MR 2006; 27:111–116 11. Seo JB, Im JG, Goo JM, Chung MJ, Kim MY. Atypical pulmonary metastases: spectrum of radiologic findings. RadioGraphics 2001; 21:403–417 12. Wheeler AP, Bernard GR. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet 2007; 369:1553–1564

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