Fair Game

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Fair Game

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Case 37

Thymic Mass (Thymic Carcinoma)

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Case 38

Subcarinal Lymph Node Enlargement Secondary to Metastatic Disease

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Case 39

Silicosis

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Silicosis is a fibrotic lung disease related to the inhalation of dust containing either free crystalline silica or silicon dioxide. Occupational settings related to silica exposure include heavy metal mining, sandblasting, foundry work, and stone masonry. Silicosis is usually a slowly progressive chronic lung disease with a latency period of at least 20 years.

Chronic silicosis is classified into simple and complicated forms. Simple silicosis is asymptomatic and typically presents radiographically with multiple small, nodular opacities, ranging in size from 1 to 10 mm in diameter. The nodules usually have an upper lung zone predominance and frequently calcify. Enlarged nodes are often present and may demonstrate a characteristic peripheral eggshell pattern of calcification, as shown in the first figure.

Complicated silicosis is associated with symptoms and reduced pulmonary function. It is characterized by one or more areas in which silicotic nodules have become confluent, measuring more than 1 cm. Such opacities may be observed in the periphery of the upper lung zone or in the middle lung zone. Over time, these opacities migrate toward the hila, with residual emphysema in the remaining portions of the lungs. In both figures, note the large vertically oriented opacities in the upper and middle lung zones, which are typical of the complicated form of silicosis. As progressive massive fibrosis becomes more extensive, the nodularity in the remaining portions of the lungs usually becomes less apparent.

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Case 40

Interstitial Lung Disease Secondary to Progressive Systemic Sclerosis (Scleroderma)

Comment

The HRCT images demonstrate a subpleural distribution of irregular linear opacities, ground-glass attenuation, and traction bronchiolectasis. The last term refers to the small, discrete, cystic lucencies in the lung periphery (best demonstrated in the right lower lobe in the first figure [arrows]), which represent dilated bronchioles. A subpleural and basilar predominance of infiltrative lung disease is characteristic of UIP and NSIP.

UIP is characterized histologically by a variegated pattern composed of foci of normal lung, interstitial cellular infiltrates, and intervening zones of active fibrosis and end-stage fibrosis. UIP is associated with a variety of chronic infiltrative lung diseases, including idiopathic pulmonary fibrosis, asbestosis, connective tissue disorders, and drug toxicity. Characteristic HRCT findings in patients with UIP include a subpleural and basilar predominant distribution of irregular linear opacities, ground-glass attenuation, traction bronchiectasis and bronchiolectasis, and honeycombing.

NSIP is characterized by a subpleural and basilar predominant distribution of ground-glass attenuation, irregular linear opacities, and traction bronchiectasis. In contrast to UIP, honeycombing is typically absent in cases of NSIP.

Progressive systemic sclerosis (also referred to as scleroderma), is a connective tissue disorder that is characterized by fibrosis and atrophy of numerous organ systems, including the skin, lungs, gastrointestinal tract, heart, and kidneys. Pulmonary manifestations include interstitial fibrosis, pulmonary vascular disease, and pleural thickening. Other common manifestations include esophageal dilation and dysmotility, enlarged mediastinal lymph nodes, and calcinosis in the skin and subcutaneous tissues.

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Case 42

Interstitial Edema

Comment

The chest radiograph in the second figure demonstrates several typical findings of interstitial edema, including indistinctness of the pulmonary vessels, peribronchial cuffing, and thickened septal (Kerley) lines. The presence of a recent normal baseline radiograph (first figure) confirms that this is an acute process. Significant ancillary findings include interval slight increase in heart size and increased caliber of upper lobe vessels (cephalization).

Cardiogenic pulmonary edema refers to excess extravascular fluid within the lungs secondary to increased pulmonary microvascular pressure, which is usually due to diseases of the left side of the heart such as left ventricular failure. Cardiogenic pulmonary edema usually follows a typical course. It begins in the interstitial compartment and extends into the alveolar compartment as it increases in severity.

The characteristic radiographic findings of pulmonary venous hypertension and congestive heart failure have been shown to correlate with physiologic parameters such as the PVWP. Normally, the PVWP is lower than 12 mm Hg. As PVWP rises to between 13 and 17 mm Hg, you should expect to see vascular redistribution. At PVWP higher than 17 mm Hg, Kerley lines are usually visible. At PVWP values higher than 20 mm Hg, a right-sided pleural effusion is often evident. When PVWP rises above 25 mm Hg, you should expect to see airspace opacities, usually most prominent in the central, perihilar regions of the lungs.

The chest radiographic features may lag behind the clinical status of the patient as pulmonary edema resolves. Radiographic findings of pulmonary edema may persist despite a return to normal wedge pressure measurements.

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Case 43

Bronchiectasis in a Patient With Marfan’s Syndrome

Comment

Bronchiectasis is defined as abnormal, irreversible dilation of the bronchi. Bronchiectasis may arise secondary to a wide variety of congenital and acquired abnormalities. Cystic fibrosis is the most common associated congenital abnormality, and prior infection, especially childhood viral illnesses, is the most common acquired abnormality. Bronchiectasis is a rare complication of Marfan’s syndrome. Note the characteristic elongated thorax of this patient on the lateral radiograph.

Chest radiographs are frequently normal in patients with mild degrees of bronchiectasis but may occasionally reveal parallel thickened bronchial walls, also referred to as a tram-track appearance. With cystic bronchiectasis, radiographs may reveal clusters of air-filled cysts, often with fluid levels. HRCT is highly sensitive and specific for diagnosing bronchiectasis. Findings include a bronchial wall diameter greater than its adjacent artery (resulting in a “signet-ring” sign when the dilated bronchus and accompanying artery are viewed in cross-section), identification of bronchi within the peripheral centimeter of the lung, lack of normal bronchial tapering, bronchial wall thickening, and strings or clusters of cysts. Because bronchial wall thickening may also be seen in other forms or airways disease, it should not be used as a sole criterion for diagnosis bronchiectasis. Complications of bronchiectasis include recurrent infections, hemoptysis, mucoid impaction, and atelectasis (note the left lower lobe atelectasis in the second figure).

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Case 44

Arteriovenous Malformation

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Case 45

Saccular Aortic Aneurysm

Comment

Vascular abnormalities, including aneurysms and vascular variants, are an important cause of middle mediastinal masses. You should consider the diagnosis of an aortic aneurysm whenever you detect a mass in close proximity to the aorta, particularly if a border of the mass is indistinguishable from the aortic contour. The diagnosis can be confirmed with either contrast-enhanced CT or MRI.

A thoracic aortic aneurysm is an abnormal dilation of the aorta. Aortic aneurysms can be classified according to shape, integrity of the aortic wall, and location. With regard to shape, aneurysms may be classified as either saccular or fusiform. Saccular aneurysms are characterized by a focal outpouching of the aorta, as demonstrated in the second figure. Such aneurysms are often traumatic or infectious in etiology. Fusiform aneurysms, conversely, are characterized by cylindrical dilation of the entire aortic circumference. This configuration is typical of atherosclerotic aneurysms.

Based on the integrity of the aortic wall, aneurysms may be classified as either true or false. True aneurysms have an intact aortic wall. The most common cause of a true aneurysm is an atherosclerotic aneurysm. In contrast, false aneurysms are associated with a disrupted aortic wall. Examples of false aneurysms include infectious (mycotic) and posttraumatic aneurysms.

Regarding location, aneurysms may be classified as involving primarily the ascending aorta, aortic arch, or descending aorta. Aneurysms that classically involve the ascending aorta include those related to cystic medial necrosis and syphilis. Other causes of aneurysms, including atherosclerotic, mycotic, and posttraumatic etiologies, most often affect the descending thoracic aorta and aortic arch.

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Case 48

Traumatic Aortic Transection

Comment

Acute thoracic aortic injury is a serious complication of blunt chest trauma, with an associated high mortality rate. The majority of affected patients die before reaching the hospital, and approximately half of those who present to the hospital die within 1 week without appropriate treatment.

MDCT plays an important role in screening trauma patients for evidence of mediastinal hematoma, an important indirect sign of aortic injury. Although mediastinal hemorrhage is sensitive for detecting aortic injury, it is not very specific. For example, mediastinal hematoma may be associated with injuries to other arterial and venous structures as well as with nonvascular injuries, such as sternal and spinal fractures. When hemorrhage is localized to the periaortic region (first figure), it is more specific for aortic injury. When you identify hemorrhage, you should look carefully for direct signs of aortic injury.

Direct signs of aortic injury include deformity of the aortic contour (second figure), intimal flap (arrow in the second figure), intraluminal thrombus, pseudoaneurysm, and frank extravasation of contrast. Multiplanar and three-dimensional reconstructions provide important complementary information to axial CT images including distance of injury from aortic arch branch vessels, length of injury, aortic diameter above and below the site of injury, and coexisting vascular anomalies. Precise characterization of the injury is important for guiding treatment decisions, including surgical repair and stent placement.

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Case 50

Lipoid Pneumonia

Comment

Exogenous lipoid pneumonia is associated with the inadvertent aspiration of oily substances such as mineral oil. On conventional radiographs, lipoid pneumonia typically appears as chronic alveolar consolidation, which is usually most prominent in the lung bases. Lipoid pneumonia infrequently presents as a focal masslike opacity.

On CT examination, the areas of consolidation are characterized by low density, reflecting their fatty composition. The identification of negative CT density numbers in the range of fatty tissue (e.g., –50 to –150 Hounsfield units) within the consolidation is pathognomonic for lipoid pneumonia. Less characteristically, exogenous lipoid pneumonia may manifest on HRCT as geographic ground-glass attenuation with superimposed smooth septal thickening (“crazy paving” pattern) due to intraalveolar and interstitial accumulation of lipid-laden macrophages and hyperplasia of type II pneumocytes along the alveolar lining.

Affected patients are frequently asymptomatic, but a minority of patients present with chronic symptoms of cough and dyspnea. Such symptoms generally resolve once the patient discontinues using the offending substance.

With regard to the differential diagnosis of chronic alveolar consolidation, you may narrow the differential diagnosis by assessing whether the process is focal or diffuse. Focal areas of chronic consolidation may be seen in lipoid pneumonia, BAC) and lymphoma. Diffuse chronic consolidation can be seen in BAC, alveolar proteinosis, alveolar sarcoid, and lipoid pneumonia. Lipoid pneumonia typically has a dependent distribution, which is not typical of other causes of chronic diffuse alveolar consolidation.

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Case 52

Left Upper Lobe Collapse Secondary to Lung Cancer

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Case 53

Wegener’s Granulomatosis

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Case 54

Invasive Aspergillus

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Case 55

Lymphangioleiomyomatosis

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Case 56

Community-Acquired Bacterial Pneumonia

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Case 58

Pneumocystis jiroveci Pneumonia