Diffuse Pulmonary Nodules

Residents’ Section • Pat tern of the Month Boitsios et al. Diffuse Pulmonary Nodules

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Residents’ Section Pattern of the Month

Residents

inRadiology Grammatina Boitsios1 Alexander A. Bankier Ronald L. Eisenberg Boitsios G, Bankier AA, Eisenberg RL

Diffuse Pulmonary Nodules

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diffuse pattern of pulmonary nodules, ranging from a few millimeters to 1 cm in diameter, may indicate interstitial or airspace disease (Algorithm 1). The predominant location of the nodules may provide a clue to the underlying condition. For example, fissural or pleural surfaces are frequently involved in sarcoidosis. Upper lobe predominance suggests silicosis or coal workers’ pneumoconiosis; whereas lower lobe preponderance is more likely in asbestosis or hematogenous metastases, and bronchocentric predominance suggests sarcoidosis or Kaposi sarcoma. The nodules may have a miliary distribution (tuberculosis, silicosis, sarcoidosis, metastases), cavitate (septic emboli, metastases, infection) (Fig. 1), or calcify (tuberculosis, silicosis, metastases). Multiple lung nodules may have a random or centrilobular pattern. Random nodules can have variable density and are most often uniformly distributed (Fig. 2). The nodules are typically of hematogenous origin and thus are situated close to small vessels. They may also occur near the pleural surfaces. In silicosis, the random nodules predominate in the middle and upper lung zones, whereas metastases are most prevalent in the lung bases. Centrilobular nodules are not adjacent to the pleural surfaces and the interlobular septa, often separated from them by a lucent rim. Centrilobular nodules are usually caused by diseases in which the original lesion develops near bronchioles. Nodules may presents with a ground-glass appearance when there is involvement of the adjacent peribronchiolar airspaces (Fig. 3). The tree-in-bud pattern is a manifestation of inflammatory, usually infectious, disease affecting the smallest bronchi and their adjacent alveoli. The “trees” represent dilated bronchioles filled with mucus, pus, or fluid; the “buds” are due to clusters of filled alveoli that have poorly defined margins and are seen in a centrilobular location.

Diffuse pulmonary nodules

Fissural/pleural surfaces

Keywords: diffuse pattern, pulmonary nodules Yes

No

Perihilar versus Random

Centrilobular

Clustered?

Tree-in-bud?

DOI:10.2214/AJR.10.4345 Received January 22, 2010; accepted after revision February 16, 2010. 1

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

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WEB This is a Web exclusive article. AJR 2010; 194:W354–W366

Sarcoidosis Silicosis

Malignant entities

Infection

Small airway disease

Hypersensitivity pneumonitis

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Algorithm 1—Flow chart shows algorithm for treatment of multinodular disease.

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Fig. 1—Cavitation in septic emboli. A and B, CT images at level of carina (A) and lung bases (B) show emboli as primarily peripheral nodules (white arrows), one of which is cavitated (black arrow).

Sarcoidosis Sarcoidosis is a systemic inflammatory disease that predominantly involves the lungs but also may affect the joints, eyes, kidneys, and skin. The disease most commonly develops between the ages of 25 and 40 years. Although the exact cause of sarcoidosis is unknown, it may reflect a disproportional immunologic reaction against a bacterial or environmental antigen. The diagnosis of sarcoidosis is often made when characteristic findings are detected incidentally on a Fig. 2—Random nodules in metastatic melanoma. chest radiograph obtained for unrelated CT image at level of lung bases shows metastases symptoms. Patients may have persistent of varying sizes and shapes throughout lung cough or such systemic manifestations as parenchyma (arrows). erythema nodosum, uveitis, arthralgia, arthritis, and hypercalcemia. The most common complication of sarcoidosis is respiratory failure due to pulmonary fibrosis. Cardiac involvement can result in myocardial infarction, arrhythmias, or even sudden death.

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Fig. 3—Centrilobular nodules in aspiration pneumonia. CT at level of right lower lobe in patient with history of chronic aspiration. A and B, CT image obtained at level of right lower lobe vein (A) shows scattered ground-glass nodules (arrows). At slightly more caudal level (B), these nodules coalesce into larger areas of ground-glass opacities (arrows).

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Fig. 4—Sarcoidosis. A, CT image through lung base shows typical interstitial distribution of small but well-defined nodules (arrow). B, On different image, there is subpleural mass (black arrow). However, interstitial nodules are still clearly visible at periphery (white arrow).

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The classic radiographic appearance of bilaterally symmetric enlargement of hilar and paratracheal nodes develops in up to 90% of patients with sarcoidosis. The outer borders of the enlarged hila are usually lobulated. About 20% of patients have diffuse parenchymal disease, most commonly a reticulonodular pattern that predominantly involves the upper lung zones and may lead to extensive interstitial pulmonary fibrosis. The nodal enlargement typically resolves as the parenchymal disease develops, unlike lymphoma or tuberculosis. The bilateral symmetry differs from tuberculosis, and there is no retrosternal involvement as in lymphoma. On thin-section CT, sarcoidosis typically presents as irregular micronodules (1–5 mm) with interstitial thickening that extends along the bronchovascular bundles from the hilum to the periphery, predominantly in the upper lung zones (Figs. 4 and 5). In late stages, fibrous distortion of lung parenchyma may be seen at CT before it is apparent on chest radiographs. Other manifestations of sarcoidosis at CT include ground-glass opacities, alveolar sarcoidosis (airspace nodules and consolidation with air bronchograms), cysts and cavitation (in necrotizing sarcoidal angiitis), and bronchial wall thickening and airway stenoses.

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Fig. 5—Sarcoidosis. A–C, CT images at various anatomic levels show primarily perihilar interstitial nodules (arrows) in typical distribution.

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Fig. 6—Silicosis. Numerous lung nodules bilaterally with relative sparing of lung periphery. Note subpleural nodules (arrows). Nodules are smoothly marginated and sharply defined. (Reprinted with permission from Webb WR, Muller NL, Naidich DP. High-resolution CT of the lung, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2001)

Silicosis Silicosis is an irreversible occupational lung disease caused by chronic inhalation of dust containing crystalline silica, which causes diffuse inflammation that leads to lung fibrosis and emphysema. Silica exposure most often occurs in people who work in construction, mining, sandblasting, stonecutting, and the manufacture of abrasives as well as those who work with glass, pottery, and on railroads. Most who develop the disease are men under 50 years old. The symptoms of silicosis develop about 20 years after initial exposure. Some affected individuals are asymptomatic, whereas those with more severe disease present with cough, dyspnea, and increased sputum (black sputum in coal workers). On chest radiographs, the earliest and most characteristic findings are small, well-circumscribed round nodules that predominantly involve the posterior portions of the upper lungs and are likely to calcify. Hilar and mediastinal lymphadenopathy are common; characteristic peripheral eggshell calcification of the enlarged nodes (5% of cases) is virtually pathognomonic of silicosis. The parenchymal pulmonary nodules increase in size and number as the disease advances, eventually forming conglomerate masses (> 1 cm) that are usually irregular and ill defined with peripheral stranding. This process is usually symmetric and located in the upper lobes or superior segments of the lower lobes and tends to progressively migrate toward the hilum as the fibrotic process progresses. The volume of the lungs progressively decreases and cavitation can occur. On thin-section CT, silicosis typically appears as fine nodular opacifications (1–10 mm) that are diffusely scattered throughout both lungs in a centrilobular and subpleural location (Fig. 6). In mild disease, they may be seen only in the upper lobes and have a posterior predominance. The nodules calcify in about 3% of cases, and chains of subpleural nodules may produce pseudoplaques. Unlike lymphangitic spread of carcinoma and sarcoidosis, the nodules in silicosis infrequently occur in relation to thickened interlobular septa. The development of progressive massive fibrosis, indicating the presence of complicated disease, is always associated with a background of small nodules visible on thin-section CT. Malignancy Hematogenous Metastases Pulmonary metastases occur in 20–30% of malignancies, usually the result of hematogenous spread of tumor cells. Less commonly, they are secondary to lymphatic spread. Endobronchial spread is unusual but can occur with head and neck malignancies as well as renal and breast carcinomas. On chest radiographs, pulmonary metastases most commonly produce smooth nodules with well-defined margins that predominantly involve the lower lobes. Depending on their mode of growth, they can vary from diffuse micronodular shadows resembling military disease (especially the snowstorm of thyroid carcinoma) to multiple large, well-defined “cannonballs” (primarily with choriocarcinoma and seminoma). Cavitation occurs in about 4% of metastases, most commonly from squamous cell neoplasms (also adenocarcinomas of the large bowel and sarcomas).

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Boitsios et al. On CT, hematogenous metastases typically appear as small discrete nodules that have a peripheral and basal predominance when limited in number but a uniform distribution when there are innumerable lesions (Figs. 7 and 8). Some nodules may appear to be related to small branches of pulmonary vessels. Lymphangitic metastases, which are thought to be most often of hematogenous origin with secondary growth into the lymphatic system, produce smooth or nodular thickening of the peribronchovascular interstitium and interlobular septa with preservation of normal lung architecture at the lobular level (Fig. 9). Hilar lymphadenopathy occurs in approximately 50% of cases.

Fig. 7—Metastases from prostate cancer. Two relatively uniform metastases are seen in right and left lung (arrows).

Lymphoma Lymphoma most commonly presents as painless cervical or supraclavicular lymphadenopathy. Cough or chest pain may reflect mediastinal involvement, and splenomegaly is often evident. Today, about 90% of patients with lymphoma are cured of the disease. One manifestation of secondary lymphoma is multiple nodules, which often have fuzzy outlines and are most numerous in the lower lobes. This appearance is usually associated with mediastinal and hilar lymph node enlargement. Cystlike lesions may simulate central cavitation. Bronchioloalveolar Carcinoma Bronchioloalveolar carcinoma (BAC) is a subtype of adenocarcinoma of the lung that is distinguished by its peripheral location, well-differentiated cytology, growth along intact alveolar septa (lepidic growth pattern), and tendency for both bronchial and lymphatic spread. BAC is divided histologically into mucinous, nonmucinous, and mixed subtypes. Distinguishing mucinous from nonmucinous subtypes has significant therapeutic and prognostic implications. BAC is three to four times more likely to develop in smokers, especially heavy smokers with long-term exposure. Nevertheless, about one third of cases occur in individuals who have never smoked and a similar number are former or intermittent smokers. Other postulated risk factors for BAC include fibrotic scarring in the lung, occupational exposure, and viral infection. Multiple discrete small nodules, either randomly distributed or primarily centrilobular, in BAC may mimic hematogenous metastases (Fig. 10). A more common appearance of this condition is diffuse, patchy, or multifocal areas of consolidation that are peribronchovascular and contain air bronchograms or air-filled cystic spaces. Because fluid and mucus produced by the tumor are of low attenuation, a characteristic appearance in BAC is the “CT angiogram sign,” in which contrast-enhanced pulmonary vessels appear denser than surrounding opacified lung.

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Fig. 8—Metastases from renal cell cancer. A, CT image obtained at level of carina shows nodules in both central and peripheral lung parenchyma (arrows). B, CT image obtained at lower lobe base shows tiny metastases in very peripheral location (arrows).

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Diffuse Pulmonary Nodules In addition to these manifestations of BAC, it should not be forgotten that early adenocarcinoma may also present as small pulmonary nodules (Fig. 11). Downloaded from www.ajronline.org by 54.210.20.124 on 11/04/15 from IP address 54.210.20.124. Copyright ARRS. For personal use only; all rights reserved

Kaposi Sarcoma Kaposi sarcoma, the most common AIDSrelated multicentric neoplasm, has a propensity to involve the skin, lymph nodes, gastrointestinal tract, and lungs. Kaposi sarcoma develops in about 15–20% of patients with AIDS, almost all homosexual or bisexual men, and pulmonary involvement occurs in about 20% of them. The most common signs and symptoms are dyspnea and cough; hemoptysis may develop in advanced stages. Irregular (flamed-shaped) and ill-defined peribronchovascular nodules combined with peribronchovascular and interlobular septal thickening, pleural effusions, and lymphadenopathy may develop in patients with Kaposi sarcoma. In most cases, the presence of typical nodules on CT and a parahilar distribution of abnormalities allow Kaposi sarcoma to be distinguished from other thoracic complications of AIDS.

Fig. 9—Pulmonary lymphangitic carcinomatosis. CT image shows nodular thickening of interlobular septa (curved arrows) and interlobar fissure (straight arrows). (Reprinted with permission from Webb WR, Müller NL, Naidich DP. High-resolution CT of the lung, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2001)

Respiratory Bronchiolitis Respiratory bronchiolitis (RB) is characterized by distortion of the respiratory bronchioles, with irregular projections of epithelium and smooth muscle into the lumen. A distinct interstitial lung disease, known as respiratory bronchiolitis–associated interstitial lung disease (RB–ILB), has been described in smokers or former smokers and is a histologic reaction to dusty envi-

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Fig. 10—Bronchioloalveolar carcinoma. (Reprinted with permission from Webb WR, Müller NL, Naidich DP. High-resolution CT of the lung, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2001) A, CT image shows areas of consolidation in right lower lobes, ill-defined nodules (some of which appear to be centrilobular), and multiple small, well-defined nodules. B, Targeted CT image of left lung shows numerous small nodules, at least some of which show random distribution similar to hematogenous metastases. Note presence of subpleural nodules.

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Fig. 11—Adenocarcinoma. CT image obtained at level of right lower lobe shows two parenchyma nodules, both histologically proven to be adenocarcinoma. One nodule is of soft-tissue density and well defined (white arrow). Second nodule is ill-defined and has heterogeneous texture and less density (black arrow).

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ronments. Histologically, there is an accumulation of pigmented macrophages within the respiratory bronchioles and the surrounding airspaces, with minimal associated mural inflammation. Patients may appear subacutely with cough and dyspnea in their 30s or 40s; less often, they present with pneumothorax, hemoptysis, or acute respiratory failure. Chest radiographs are normal in individuals with noncomplicated RB and about half of those with RB–ILD. The remainder of patients with RB–ILD have normal lung volumes but some thickening of the bronchial walls and a fine reticulonodular pattern. On thin-section CT, RB–ILD typically produces faint micronodular nodules (3–5 mm) and patchy ground-glass opacities that may be widespread but predominantly tend to involve the upper lobes (Fig. 12). Infection Numerous infectious diseases can present the pattern of multiple pulmonary nodules. In septic emboli, which is most commonly

Fig. 12—Respiratory bronchiolitis. A–C, CT images obtained at various levels of right upper lobe show centrilobular emphysema (white arrows). Emphysematous lesions are surrounded by subtle, ill-defined airspace nodules, typical of disease (black arrows).

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caused by endocarditis or an infected central catheter, the nodules are diffusely distributed and frequently cavitate. A characteristic appearance is feeding vessels in association with the peripheral nodules. In reactivation tuberculosis, innumerable tiny, discrete, relatively well-defined nodules may be diffusely distributed throughout both lungs, producing a miliary pattern that reflects endobronchial spread of infection (Fig. 13). Thin-section CT may detect the presence of diffuse lung involvement when corresponding chest radiographs are normal or show only minimal or limited disease. Multiple small and larger nodules also may be a feature of atypical (nontuberculous) mycobacterial infection (Figs. 14 and 15). The presence of Fig. 13—Tuberculosis (endobronchial spread in small nodules in areas of lung distal to a dom- reactivation disease). CT image shows typical appearance of numerous, diffuse, poorly defined inant consolidative focus of infection probably nodules, some of which are perivascular and results from endobronchial spread. centrilobular. (Reprinted with permission from Webb A pattern of miliary or larger pulmonary WR, Muller NL, Naidich DP. High-resolution CT of the 3rd ed. Philadelphia, PA: Lippincott Williams & nodules may be a manifestation of fungal in- lung, Wilkins, 2001) fection. The most common cause is histoplasmosis, in which the generally round or oval nodules are well circumscribed and often calcify. Other fungal disorders that can produce multiple pulmonary nodules include coccidioidomycosis, blastomycosis, and candidiasis. More irregular and poorly defined masses may be seen in Pseudomonas infection, and

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Fig. 14—Mycobacterium avium intracellulare infection. A–D, CT images obtained at various lung levels. Arrows show ill-defined, subtle ground-glass nodules (A); larger partly calcified nodules (B); small peripheral peribronchial nodules (C); and small, dense subpleural nodules (D).

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Fig. 15—Mycobacterium avium intracellulare infection. A, CT scan in right upper lobe shows small, dense nodules in peribronchial location. B, More caudal CT image better depicts peripheral location of nodules.

well-circumscribed cystic masses with the predilection of the periphery of the lower lobes are a characteristic appearance of Paragonimus westermani. In varicella pneumonia (adults more than children), there is often a miliary pattern of pulmonary nodules that heal with diffuse calcifications (as in histoplasmosis). Parasitic diseases that may produce military nodules include schistosomiasis and filariasis. A common finding on thin-section CT in infectious lung disease is the tree-in-bud pattern, in which centrilobular bronchial dilatation and filling by mucus, pus, or fluid resembles a budding tree The pattern of patchy clusters of small nodules and branching soft-tissue opacities is generally most pronounced in the lung periphery (within 3–5 mm of the pleural surface) and associated with abnormalities of the larger airways. Aspergillosis is a fungal infection that often occurs in preexisting cavities caused by tuberculosis, fungal disease, or sarcoidosis. The disease develops in immune-compromised patients and typically presents with cough, fever, chills, dyspnea, and chest pain. A halo or ground-glass opacity surrounding focal dense parenchymal nodules is a characteristic CT appearance of invasive pulmonary aspergillosis (Fig. 16). The halo and central nodule are reported to reflect, respectively, a rim of coagulation necrosis or hemorrhage surrounding a central fungal nodule or infarct. Small Airway Disease Small airway disease (SAD) refers to a spectrum of disorders in which inflammation of the smallest bronchi and bronchioles with minimal emphysema leads to distortion and obliteration of small airways. Diseases affecting the small airways are difficult to detect by traditional diagnostic tests. There must be widespread involvement before the appearance of symptoms and abnormalities on pulmonary function testing or chest radiography. However, on thin-section CT, changes associated with SAD are accurately detected. One manifestation of SAD is multiple small nodules, which are often found abundantly along the bronchovascular bundles and histologically prove to be centered about abnormal bronchioles (Fig. 17). Individual abnormal regions generally can be separated from other involved areas by normal or near-normal lung parenchyma. However, if the nodules coalesce, larger consolidations or airspace opacities may occur. Hypersensitivity Pneumonitis Also known as extrinsic allergic alveolitis, hypersensitivity pneumonitis refers to a group of allergic lung diseases that are caused by chronic inhalation of a variety of organic and chemical antigens that leads to an immunologic response of the lung tissues. The most common forms are farmer’s lung and bird fancier’s lung.

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Fig. 16—Invasive pulmonary aspergillosis. CT image shows multiple pulmonary nodules associated with halo sign. (Reprinted with permission from Webb WR, Müller NL, Naidich DP. High-resolution CT of the lung, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2001)

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Fig. 17—Chronic aspiration. A, CT image at level of left lower lobe shows moderate bronchiectasis and bronchial wall thickening (arrow), indicative of chronic airways disease. B, CT image obtained at basis of left lower lobe shows peribronchial ground-glass nodules (arrow) indicating presence of concomitant parenchymal disease.

The radiographic findings vary with the stage of the disease. In the acute phase, chest radiographs are normal in 90% of cases. There may be a fine nodular or reticulonodular pattern or airspace consolidation (primarily in the lower lobes) that is often misdiagnosed as pneumonia. In the subacute stage, 90% of chest radiographs are abnormal, showing poorly defined small nodules or lung opacifications with obscuration of vascular margins. In chronic disease, the major findings are fibrosis with architectural distortion and volume loss. On thin-section CT, hypersensitivity pneumonitis appears acutely as small, ill-defined centrilobular nodules and bilateral airspace consolidation (Fig. 18). In the subacute stage, there are patchy ground-glass opacities with ill-defined centrilobular nodules. Characteristic mosaic perfusion generally affects the middle and lower lung. In the chronic stage of hypersensitivity pneumonitis, lung fibrosis produces honeycombing, traction bronchiectasis, and architectural distortion. There also may be reticular opacities randomly distributed in the peri-

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Fig. 18—Hypersensitivity pneumonitis. A and B, Transverse (A) and coronal (B) CT images show subtle increase of lung density in upper lobes. In addition, transverse image shows partly confluent and partly individual small and subtle nodules in lung parenchyma (arrows).

bronchial and subpleural regions. A combination of these findings can also be seen in early stages of nonspecific interstitial pneumonia, in which parenchymal nodules and early architectural distortion are key features (Fig. 19). Miscellaneous Conditions Many disorders are extremely rare but have been included for the sake of completeness. Alveolar Microlithiasis Alveolar microlithiasis is a rare disorder of unknown cause characterized by diffuse bilateral deposition of intraalveolar microliths. Most prevalent in Turkey, which accounts for 33% of the world’s cases, in half of patients there is a genetic anomaly that is familial autosomal recessive. Despite radiographic abnormalities, about 70% of patients with alveolar microlithiasis are asymptomatic when the diagnosis is made. These patients later may develop cough and dyspnea, and slow progression of the disease may eventually result in respiratory or cardiac failure.

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Fig. 19—Nonspecific interstitial pneumonia. A and B, CT images show nodular component of disease (arrow). C, CT image shows ground-glass opacities resulting from coalescent nodules with early architectural distortion (arrow).

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Diffuse Pulmonary Nodules Alveolar microlithiasis produces diffuse, very fine micronodules of calcific density. A characteristic appearance on chest radiographs is the black pleura sign due to contrast between the extreme density of the lung parenchyma on one side of the pleura and the ribs on the other side. Downloaded from www.ajronline.org by 54.210.20.124 on 11/04/15 from IP address 54.210.20.124. Copyright ARRS. For personal use only; all rights reserved

Amyloidosis Amyloidosis represents a heterogeneous group of disorders characterized by abnormal extracellular accumulation of insoluble fibrillar proteins. Vascular deposition of these substances leads to fragility and bleeding. Patients may be asymptomatic or present with cough, respiratory insufficiency, hemoptysis, recurrent pneumonia, and involvement of other organs or tissue (heart, kidney, tongue, gastrointestinal tract, skin, and muscle). Discrete masses of amyloid may develop in the rare parenchymal form of the disease. Multiple nodules may cavitate and show calcification or ossification. The nodular parenchymal form of the disease has a better prognosis than the tracheobronchial (obstructive) or diffuse interstitial type. Papillomatosis of the Lung Papillomatosis is a human papillomavirus infection that involves the larynx in 95% of cases. Airway dissemination seeding the lung occurs in < 1% of cases, most frequently in children or young adults, and surgical manipulation of a laryngeal papilloma increases the likelihood of this complication. Papillomas of the lung typically obstruct the airways, resulting in peripheral atelectasis and obstructive pneumonia. A rare manifestation is round, sharply circumscribed nodules that frequently cavitate (often resembling advanced cystic bronchiectasis). Polyarteritis Poorly defined nodules, often associated with patchy consolidations, are a rare manifestation of polyarteritis. The pulmonary appearance in this condition typically shows progression and regression of lesions on serial studies, reflecting the appearance of new lesions and the healing of old ones. The CT angiography visualization of multiple arterial aneurysms in one or more abdominal organs is considered virtually diagnostic of this disease. Pulmonary Arteriovenous Fistulas Pulmonary arteriovenous fistula is an abnormal direct communication between pulmonary arteries and pulmonary veins, which may be acquired or congenital and produce high blood flow through the right-to-left shunt. About one third are multiple, and about 50% have hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease). A definitive diagnosis requires identification of the feeding artery and the draining vein. Pulmonary arteriovenous fistulas appear as sharply defined, round or oval, often slightly lobulated nodules that predominantly involve the lower lobes. The lesions may change in size between the Valsalva and the Müller maneuver. Pulmonary Hemosiderosis Pulmonary hemosiderosis most commonly affects young individuals and is characterized by recurrent episodes of diffuse pulmonary hemorrhage without an identifiable cause. A fine miliary pattern of densely calcified or ossified nodules diffusely scattered throughout the lungs may develop in patients with long-standing mitral stenosis (or other causes of elevated left atrial pressure) who have had multiple episodes of hemoptysis. Pulmonary Varices Pulmonary varices are characterized by rare congenital or acquired tortuosity and dilatation of the pulmonary veins just before their entrance into the left atrium. The varicosities change shape and size with the Valsalva and Müller maneuvers (similar to arteriovenous fistulas). On imaging, pulmonary varices appear as multiple round, well-defined opacities. On chest radiographs, they most commonly are seen on lateral images projecting posterior and inferior to the hilar structures. Anatomically, varices are most often solitary and preferentially involve the right lower lobe pulmonary vein.

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Boitsios et al. Rheumatoid Necrobiotic Nodules This rare manifestation of rheumatoid lung disease tends to wax and wane in relation to the activity of rheumatoid arthritis and the presence of subcutaneous nodules. Rheumatoid lung nodules may be associated with pneumoconiosis (Caplan syndrome). They generally appear as smooth, well-circumscribed nodules that predominantly occur in peripheral subpleural locations. Cavitation is common, producing thick-walled lesions with smooth inner margins. A miliary pattern of pulmonary nodules may occur in the early subacute stage of the disease before the development of the more characteristic diffuse interstitial pulmonary fibrosis. Wegener Granulomatosis Wegener disease, now often called “antineutrophil cytoplasmic autoantibody (ANCA)-associated granulomatous vasculitis,” is a necrotizing granulomatous vasculitis of small to medium vessels without associated infection. Of unknown cause, the classic triad consists of abnormalities involving the sinuses, lungs, and kidneys. In the chest, Wegener granulomatosis typically produces round, fairly well-circumscribed nodules that may simulate metastases. Cavitation (thick-walled with irregular, shaggy inner margins) develops in approximately half the patients. Rarely, small fine nodules may develop in combination with larger, more ill-defined densities, representing a diffuse granulomatous reaction occurring around vessels. Suggested Reading 1. Colby TV, Swensen SJ. Anatomic distribution and histopathologic patterns in diffuse lung disease: correlation with HRCT. J Thorac Imaging 1996; 11:1–26 2. Gruden JF, Webb WR, Warnock M. Centrilobular opacities on HRCT: diagnosis and differential diagnosis with pathologic correlation. AJR 1994; 162:569–574 3. Hansell DM, Wells AU, Padley SP, et al. Hypersensitivity pneumonitis: correlation of individual CT patterns with functional abnormalities. Radiology 1996; 199:123–128 4. Hartman TE, Primack SL, Lee KS, et al. CT of bronchial and bronchiolar disease. RadioGraphics 1994; 14:991–1003 5. Hirakata K, Nakata H, Haratake J. Appearance of pulmonary metastases on high-resolution CT

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scans: comparison with histopathologic findings from autopsy specimens. AJR 1993; 161:37–43 6. Müller NL, Kullnig P, Miller RR. The CT findings of pulmonary sarcoidosis: analysis of 25 patients. AJR 1989; 152:1179–1182 7. Nishimura K, Itoh H, Kitaichi M, et al. Pulmonary sarcoidosis: correlation of CT and histopathologic findings. Radiology 1993; 189:105–109 8. Raoof S, Amchentsev A, Vlahos I, et al. Pictorial essay: multinodular disease. Chest 2006; 129: 805–815 9. Ryu JH, Myers JH, Swensen SJ. Bronchiolar disorders: state of the art. Am J Respir Crit Care Med 2003; 168:1277–1292 10. Seo JB, Im JG, Goo JM, et al. Atypical pulmonary metastases: spectrum of radiologic findings. RadioGraphics 2001; 21:403–417

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This article has been cited by: 1. Aws Alfahad, Paul Jennings, Simmon Smith, Nikta Niktash, John Curtin. 2016. An interesting finding of multiple calcified pulmonary nodules in a patient with rheumatoid arthritis. BJR|case reports 2, 20150116. [CrossRef] 2. Richard C. Cabot, Eric S. Rosenberg, Nancy Lee Harris, Jo-Anne O. Shepard, Alice M. Cort, Sally H. Ebeling, Emily K. McDonald, Barry S. Shea, Amita Sharma, Eugene J. Mark. 2015. Case 14-2015. New England Journal of Medicine 372, 1749-1758. [CrossRef] 3. T. Hilal. 2015. Diffuse unresolving pulmonary nodules in a patient with a history of cervical carcinoma. Case Reports 2015, bcr2014208959-bcr2014208959. [CrossRef] 4. J. Caleb Richards, David Lynch, Jonathan H. Chung. 2015. Cystic and Nodular Lung Disease. Clinics in Chest Medicine . [CrossRef] 5. S. K. Mandal, S. Ghosh, S. S. Mondal, S. Chatterjee. 2014. Coexistence of pulmonary tuberculosis and sarcoidosis: a diagnostic dilemma. Case Reports 2014, bcr2014206016-bcr2014206016. [CrossRef] 6. Pritinanda Mishra, Sajini Elizabeth Jacob, Debdatta Basu, Manoj Kumar Panigrahi, Vishnukanth Govindaraj. 2014. Bilateral Spontaneous Pneumothorax in Chronic Silicosis: A Case Report. Case Reports in Pathology 2014, 1-3. [CrossRef] 7. Mohamed Sayyouh, Dharshan R Vummidi, Ella A Kazerooni. 2013. Evaluation and management of pulmonary nodules: stateof-the-art and future perspectives. Expert Opinion on Medical Diagnostics 7, 629-644. [CrossRef] 8. R. Ysamat Marfá, A. Benito Ysamat, S. Espejo Pérez, M. Blanco Negredo, R. Roldán Molina. 2013. Lung disease associated with connective tissue disease. Radiología (English Edition) 55, 107-117. [CrossRef] 9. R. Ysamat Marfá, A. Benito Ysamat, S. Espejo Pérez, M. Blanco Negredo, R. Roldán Molina. 2013. La patología pulmonar asociada a las enfermedades del tejido conectivo. Radiología 55, 107-117. [CrossRef]

Diffuse Pulmonary Nodules

Diffuse Pulmonary Nodules

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