Editors: Collins, Jannette; Stern, Eric J.
Title: Chest Radiology: The Essentials, 2nd Edition
> Table of Contents > Chapter 2 - Signs and Patterns of Lung Disease
Chapter 2
Signs and Patterns of Lung Disease
P.17

A sign in chest radiology refers to a radiographic and/or computed tomographic (CT) scan finding that implies a specific pathologic process. Understanding the meaning of a sign indicates comprehension of an important concept related to the radiologic findings. Knowing the name of the sign is not as important as recognizing and understanding the meaning of the radiologic findings, but it will help in communicating with clinicians and radiologists who use the "sign" terminology. A CT "pattern" refers to a nonspecific radiologic finding or collection of findings suggesting one or more specific disease processes. The material that follows is not an all-inclusive list but represents a collection of the more common and useful signs and patterns of focal and diffuse lung disease.
Air Bronchogram Sign
This sign refers to a branching, linear, tubular lucency representing a bronchus or bronchiole passing through airless lung parenchyma (Fig. 2-1). This sign does not differentiate nonobstructive atelectasis from other abnormal parenchymal opacities such as pneumonia. An air bronchogram indicates that the underlying opacity must be parenchymal rather than pleural or mediastinal in location. Although cancers tend to be solid masses, air bronchograms are a characteristic feature of lymphoma and bronchoalveolar cell carcinoma.
Air Crescent Sign
A mass growing within a pre-existing cavity, or an area of pneumonia that undergoes necrosis and cavitates, may form a peripheral crescent of air between the intracavitary mass and the cavity wall, resulting in the air crescent sign (Fig. 2-2). Intracavitary masses are most often caused by mycetomas. In immunocompromised patients with invasive aspergillosis, the appearance of the air crescent sign, representing necrosis and cavitation, indicates recovery of the immune system and white blood cell response to the infection.
FIGURE 2-1. Air bronchogram sign. CT of the chest shows bilateral subpleural areas of airspace opacity with air bronchograms (arrows) resulting from acute eosinophilic pneumonia. Air bronchograms can also be seen with other causes of airspace disease, including infectious pneumonia, hemorrhage, edema, bronchoalveolar cell carcinoma, lymphoma, lipoid pneumonia, "alveolar" sarcoidosis, and alveolar proteinosis and can also be seen in atelectasis not caused by central obstruction. The presence of the sign indicates that the process is parenchymal in location, rather than mediastinal or pleural.
Bulging Fissure Sign
Historically, the bulging fissure sign was seen as a result of pne-umonia caused by Klebsiella pneumoniae involving the right upper lobe (Fig. 2-3). Also called Friedländer pneumonia, the disease is often confined to one lobe, with consolidation spreading rapidly, causing lobar expansion and bulging of the adjacent fissure inferiorly (1). Because of timely antibiotic treatment, pneumonia rarely progresses to this state.
Continuous Diaphragm Sign
This sign is seen as a continuous lucency outlining the base of the heart, representing pneumomediastinum (Fig. 2-4). Air in the mediastinum tracks extrapleurally, between the heart and diaphragm (2). Pneumopericardium can have a similar appearance but will show air circumferentially outlining the heart.
CT Angiogram Sign
This sign refers to the identification of vessels within an airless portion of lung on contrast-enhanced CT (Fig. 2-5). The vessels are prominently seen against a background of low-attenuation material (3,4). This sign has been associated with bronchoalveolar cell carcinoma and lymphoma, but it can also be seen with other processes, including many infectious pneumonias.
Deep Sulcus Sign
This sign refers to a deep, sometimes fingerlike collection of intrapleural air (pneumothorax) in the costophrenic sulcus as seen on the supine chest radiograph (5). In the supine patient, air rises to the nondependent anteromedial basilar pleural space and may not cause displacement of the visceral pleural line laterally or at the apex, as seen on upright chest radiographs (Figs. 2-6 and 2-7). When present, this sign may represent a pneumothorax that is much larger than initially expected.
FIGURE 2-2. Air crescent sign. CT of the chest shows bilateral pulmonary nodules in a predominantly subpleural distribution resulting from septic emboli. Some of the nodules are cavitary. A resulting crescent of air (arrows) is contained within and outlined by the thin cavity wall.
P.18

FIGURE 2-3. Bulging fissure sign. A: Posteroanterior (PA) chest radiograph shows dense opacification of the right upper lobe resulting from Klebsiella pneumonia. The inflammatory process is extensive and results in expansion of the lobe and bulging of the fissure inferiorly (arrows). B: Lateral view shows bulging of the superior portion of the major fissure inferiorly (larger arrows). The right upper lobe is outlined by the superior portion of the major fissure and the minor fissure (arrowheads). The middle lobe is outlined by the inferior portion of the major fissure (smaller arrows) and the minor fissure. The right lower lobe is outlined by the major fissure, which is divided into superior and inferior portions by the minor fissure.
FIGURE 2-4. Continuous diaphragm sign. In this patient with pneumomediastinum, a continuous lucency is seen between the heart and the diaphragm (solid arrows). Air in the mediastinum is also seen tracking into the neck bilaterally (dashed arrows).
FIGURE 2-5. CT angiogram sign. CT with intravenous contrast shows opacification of the left lower lobe from bronchoalveolar cell carcinoma. The pulmonary vessels (arrows) are seen prominently against a background of low-attenuation mucus within the tumor. Other processes producing low-attenuation material within the lung can also produce this sign, including lymphoma, lipoid pneumonia, and bacterial pneumonia.
P.19

FIGURE 2-6. Deep sulcus sign. Anteroposterior (AP) supine chest radiograph shows bilateral pneumothoraces (intrapleural air) as a result of barotrauma from mechanical ventilation. On the right, the visceral pleura is separated from the parietal pleura by intrapleural air along the apicolateral chest wall (larger arrows). On the left, the intrapleural air is collecting at the lung base, expanding the costophrenic sulcus (smaller arrows). The stiff lungs do not collapse completely in this patient with acute respiratory distress syndrome.
FIGURE 2-7. Deep sulcus sign. AP supine chest radiograph of a patient involved in chest trauma shows a right basilar pneumothorax (arrow), which expands the costophrenic sulcus, creating a tonguelike extension of air that continues inferiorly along the right lateral chest wall. Note bilateral lung contusion, pneumomediastinum, and bilateral subcutaneous emphysema.
FIGURE 2-8. Fallen lung sign. AP supine chest radiograph of a man involved in a motor vehicle accident. There is a large pneumothorax on the right, which persists with adequate chest tube placement, as a result of a fractured right mainstem bronchus. The lung has collapsed inferiorly and laterally (arrows), instead of toward the hilum, because it is hanging from a fractured pedicle (bronchus).
Fallen Lung Sign
This sign refers to the appearance of the collapsed lung occurring with a fractured bronchus (6). The bronchial fracture results in the lung "falling" away from the hilum, either inferiorly and laterally in an upright patient (Fig. 2-8) or posteriorly, as seen on CT in a supine patient. Normally, a pneumothorax causes a lung to collapse inward toward the hilum.
Flat Waist Sign
This sign refers to flattening of the contours of the aortic knob and adjacent main pulmonary artery (Fig. 2-9). It is seen in severe collapse of the left lower lobe and is caused by leftward displacement and rotation of the heart (7).
Finger-in-Glove Sign
In allergic bronchopulmonary aspergillosis, a clinical disorder secondary to Aspergillus hypersensitivity, the bronchi become impacted with mucus, cellular debris, eosinophils, and fungal hyphae. The impacted bronchi appear radiographically as opacities with distinctive shapes (Fig. 2-10), variously described as "gloved finger," "Y," "V," "inverted V," "toothpaste," and so forth (8).
P.20

FIGURE 2-9. Flat waist sign. A: Frontal chest radiograph shows left lower lobe opacification from left lower lobe collapse. Note loss of the medial contour of the left hemidiaphragm, which is known as the silhouette sign. The left lower lobe bronchus has a more vertical course than normal (arrowheads). Leftward displacement and rotation of the heart in left lower lobe collapse results in flattening of the contours of the aortic knob and adjacent main pulmonary artery (arrows), termed the flat waist sign. B: Frontal chest radiograph obtained 1 day later shows partial re-expansion of the left lower lobe. The medial left hemidiaphragm is now visible (smaller arrows). There is a notch between the aorta and the pulmonary artery (larger arrow) and no flat waist sign.
FIGURE 2-10. Finger-in-glove sign. A: PA chest radiograph of a patient with cystic fibrosis and allergic bronchopulmonary aspergillosis. Bronchi impacted and distended with mucus, cellular debris, eosinophils, and fungal hyphae produce tubular or masslike opacities, as seen in both lower lobes (arrows). Also shown is diffuse bronchiectasis related to cystic fibrosis. B: CT scan of the same patient shows dilated and impacted central bronchi in the left lower lobe (arrow).
P.21

FIGURE 2-11. Golden S sign. A: PA chest radiograph of a man with bronchogenic carcinoma of the right upper lobe. The endobronchial tumor causes collapse of the right upper lobe, and upward displacement of the minor fissure (solid arrow). The tumor mass produces a convex margin toward the lung at the right hilum (dashed arrow). The contour of the displaced fissure and central mass creates a reverse S shape. Note the elevation of the right hemidiaphragm, another sign of right upper lobe volume loss. B: CT of the chest shows tumor encasing and occluding the right upper lobe bronchus (solid arrow) and collapse of the right upper lobe, with superior and medial displacement of the minor fissure (dashed arrow).
Golden S Sign
When a lobe collapses around a large central mass, the peripheral lung collapses and the central portion of lung is prevented from collapsing by the presence of the mass (Fig. 2-11). The relevant fissure is concave toward the lung peripherally but convex centrally, and the shape of the fissure resembles an S or a reverse S (9). This sign is important because it signifies the presence of a central obstructing mass that, in an adult, may represent bronchogenic carcinoma.
Halo Sign
This sign refers to ground-glass attenuation on CT scanning that surrounds, or forms a halo around, a denser nodule or area of consolidation (Fig. 2-12). Although most hemorrhagic pulmonary nodules produce this sign (10), when seen in patients with acute leukemia, the halo sign suggests early invasive pulmonary aspergillosis (11).
Hampton Hump Sign
Pulmonary infarction secondary to pulmonary embolism produces an abnormal area of opacification on the chest radiograph, which is always in contact with the pleural surface (Fig. 2-13). The opacification may assume a variety of shapes. When the central margin is rounded, a "hump" is produced, as described by Hampton and Castleman (12).
Juxtaphrenic Peak Sign
This sign refers to a small triangular shadow that obscures the dome of the diaphragm (Fig. 2-14), secondary to upper lobe atelectasis (13). The shadow is caused by traction on the lower end of the major fissure, the inferior accessory fissure, or the inferior pulmonary ligament.
FIGURE 2-12. Halo sign. CT shows nodular consolidation associated with a halo of ground-glass opacity (GGO) in both apices (arrows) resulting from invasive pulmonary aspergillosis. This halo represents hemorrhage and, when seen in leukemic patients, is highly suggestive of the diagnosis of invasive pulmonary aspergillosis.
P.22

FIGURE 2-13. Hampton hump sign. A: CT with lung windowing shows a focal subpleural area of consolidation in the left lower lobe (arrows). This hump-shaped area of opacification represents pulmonary infarction secondary to pulmonary embolism. There are also small bilateral pleural effusions, which are commonly seen with acute pulmonary emboli. B: CT with mediastinal windowing shows low-attenuation filling defect, which represents a saddle embolus (arrows) bridging the lingular and left lower lobe pulmonary arteries.
Luftsichel Sign
In left upper lobe collapse, the superior segment of the left lower lobe, which is positioned between the aortic arch and the collapsed left upper lobe, is hyperinflated. This aerated segment of left lower lobe is hyperlucent and shaped like a sickle, where it outlines the aortic arch on the frontal chest radiograph (Fig. 2-15). This peri-aortic lucency has been termed the luftsichel sign, derived from the German words luft (air) and sichel (sickle) (14). Although this sign can also be seen on the right, it is more common on the left because of the difference in anatomy and the presence of a minor fissure on the right. This sign and associated findings of upper lobe collapse signify the probable diagnosis of bronchogenic carcinoma in an adult.
FIGURE 2-14. Juxtaphrenic peak sign. PA chest radiograph of a man treated with mediastinal radiation shows paramediastinal radiation fibrosis (dashed arrows) and upward retraction of both hila. There is tenting of the left hemidiaphragm (solid arrow), indicating a loss of left upper lobe volume, seen as the juxtaphrenic peak sign.
Melting Ice Cube Sign
This sign refers to the appearance of a resolving pulmonary infarct on a chest radiograph or CT scan, which looks like an ice cube that is melting peripherally to internally (Fig. 2-16). This is distinguished from the pattern of resolving pneumonia, where the opacification disappears in a patchy fashion (15).
Ring Around the Artery Sign
This sign refers to a well-defined lucency encircling the right pulmonary artery (Fig. 2-17), as seen on frontal and lateral chest radiographs, representing pneumomediastinum (16).
Silhouette Sign
Felson and Felson (17) popularized the term silhouette sign to indicate an obliteration of the borders of the heart, other mediastinal structures, or diaphragm by an adjacent opacity of similar density. An intrathoracic lesion not anatomically contiguous with a border of one of these structures will not obliterate that border. Parenchymal processes involving the medial segment of the right middle lobe obliterate the right heart border (Fig. 2-18). If the lingula is involved, the left heart border is obliterated (Fig. 2-19). Lower lobe processes involving one or more basilar segments result in obliteration of all or a part of the border of the diaphragm.
P.23

FIGURE 2-15. Luftsichel sign. A: PA chest radiograph shows a crescentic lucency adjacent to the aortic arch (arrows), representing hyperaeration of the superior segment of the left lower lobe, which is positioned between the aortic arch medially and the collapsed left upper lobe laterally. There is hazy opacification of the left lung (sparing the apex and costophrenic angle), elevation of the left hemidiaphragm, and partial obscuration of the left heart border (the silhouette sign), indicating a loss of left upper lobe volume. B: Lateral view shows anterior displacement of the major fissure (arrows). The superior extent of the displaced fissure indicates extension of the superior segment of the lower lobe to the lung apex. The luftsichel sign is just one sign of upper lobe collapse. The associated signs of volume loss make the diagnosis obvious. In an adult, left upper lobe collapse is highly suggestive of an obstructing bronchogenic carcinoma.
FIGURE 2-16. Melting ice cube sign. A: PA chest radiograph of a 69-year-old man with a 6-week history of cough, pleuritic chest pain, and hemoptysis shows bilateral, subpleural airspace opacities at the costophrenic angles (arrows), representing parenchymal infarcts. B: CT scan obtained 2 weeks later shows bilateral peripheral opacities (arrows), an appearance typical of resolving pulmonary infarcts. Note that the opacities are not wedge shaped or rounded, as expected with acute infarcts. Infarcts resolve from the periphery inward, like a melting ice cube.
P.24

FIGURE 2-17. Ring around the artery sign. A: PA chest radiograph of a patient with acute respiratory distress syndrome shows a ring of lucency around the right pulmonary artery (arrows), signifying pneumomediastinum. B: CT confirms air surrounding both pulmonary arteries (arrows).
FIGURE 2-18. Silhouette sign. A: PA chest radiograph of a patient with pneumococcal pneumonia shows opacification of the right lower lung, which partially obscures the right heart border (the silhouette sign), indicating a process involving the right middle lobe. B: Lateral view shows a triangular opacity over the heart (arrows), confirming a right middle lobe process.
P.25

FIGURE 2-19. Silhouette sign. A: PA chest radiograph of a patient with pneumonia shows opacification of the left lower lung partially obscuring the left heart border (silhouette sign), indicating a lingular process. Note that the left hemidiaphragm is not obscured, as would be seen with a process involving any of the basilar segments of the lower lobe. B: Lateral view shows an opacity over the heart (arrows), confirming the lingular location of the pneumonia.
Split Pleura Sign
Normally, the thin visceral and parietal pleura cannot be distinguished as two separate structures on CT scanning. With an exudative pleural effusion, such as empyema (Fig. 2-20), the fluid separates or "splits" the thickened and enhancing pleural layers (18).
Westermark Sign
This sign refers to oligemia of the lung beyond an occluded vessel in a patient with pulmonary embolism (Fig. 2-21) (19).
FIGURE 2-20. Split pleura sign. CT with intravenous contrast shows empyema in an intrapleural location with associated thickening, contrast enhancement, and separation of the visceral and parietal pleura (arrows).
Spine Sign
Lower lobe pneumonia may be poorly visualized on a posteroanterior (PA) chest radiograph. In such cases, the lateral view is often helpful when it shows the spine sign, which is an interruption in the progressive increase in lucency of the vertebral bodies from superior to inferior (Fig. 2-22) (20).
Patterns
The following patterns are not always isolated findings on chest radiographs or CT scans. They commonly occur in combination with other patterns and findings and may or may not represent the predominant imaging feature.
Honeycomb Pattern
Honeycombing is characterized by the presence of cystic airspaces with thick, clearly definable fibrous walls lined by bronchiolar epithelium. It results from destruction of alveoli and loss of acinar architecture and is associated with pulmonary fibrosis. The cysts are typically layered along the pleural surface, helping to distinguish them from the nonlayered subpleural lucencies seen with paraseptal emphysema.
Honeycombing produces a characteristic appearance on CT that allows a confident diagnosis of lung fibrosis (Fig. 2-23) (21). On CT, the cystic spaces usually average 1 cm in diameter, although they can range from several millimeters to several centimeters in size. They have clearly definable walls that are 1 to 3 mm thick, they are air-filled, and they appear lucent in comparison to normal lung parenchyma. Honeycombing is usually associated with other findings of lung fibrosis, such as architectural distortion, intralobular interstitial thickening, traction bronchiectasis, and irregular linear opacities. Honeycombing on CT usually represents idiopathic pulmonary fibrosis,
P.26

P.27

collagen vascular disease, asbestosis, chronic hypersensitivity pneumonitis, or drug-related fibrosis (Table 2-1).
FIGURE 2-21. Westermark sign. A: PA chest radiograph shows oligemia of the right lung, the so-called Westermark sign. Note how the vessels on the right are diminutive compared with those on the left. As a result, the right hemithorax appears hyperlucent. B: CT with lung windowing better shows the diminution of vessels on the right compared with the left. There is also a right pleural effusion. C: CT with mediastinal windowing shows thrombus expanding and filling the main and right pulmonary arteries (arrows).
FIGURE 2-22. Spine sign. A: PA chest radiograph of a patient with left lower lobe pneumonia shows abnormal opacity in the left lower lung. B: Lateral view shows this opacity projected over the lower spine (arrows). Normally, the spine becomes progressively more lucent from the top to the bottom on the lateral view. The presence of increased opacity over the lower spine is an indication of a lower lobe process, typically pneumonia, and is called the spine sign.
FIGURE 2-23. Honeycomb pattern. CT shows layers of subpleural cysts (solid arrows) representing the honeycomb pattern of pulmonary fibrosis. Also shown is traction bronchiectasis (dashed arrow), another sign of pulmonary fibrosis.
TABLE 2-1 DIFFERENTIAL DIAGNOSIS OF PATTERNS OF DISEASE ON CT OF THE LUNGS
Honeycomb
Idiopathic pulmonary fibrosis
Collagen vascular diseases
Asbestosis
Chronic hypersensitivity pneumonitis
Drug-related fibrosis
Interlobular septal thickening
Smooth
Pulmonary edema
Pulmonary hemorrhage
Lymphangitic spread of carcinoma
Infectious pneumonia
Lymphoma and leukemia
Amyloidosis
Beaded
Lymphangitic spread of carcinoma
Lymphoma
Sarcoidosis
Silicosis and coal worker's pneumoconiosis
Lymphocytic interstitial pneumonitis
Amyloidosis
Cystic
Langerhan cell histiocytosis
Lymphangioleiomyomatosis
Sarcoidosis
Lymphocytic interstitial pneumonitis
Collagen vascular diseases
Pneumocystis pneumonia
Honeycombing
Centrilobular emphysema
Nodular
Perilymphatic
Sarcoidosis
Random
Silicosis and coal worker's pneumoconiosis
Tuberculosis and fungal infection
Metastases
Langerhan cell histiocytosis
Centrilobular
Subacute hypersensitivity pneumonitis
Respiratory bronchiolitis
Bronchovascular
Lymphoproliferative disorders
Leukemia
Kaposi sarcoma
Cavitating
Metastases
Wegener granulomatosis
Septic emboli
Mycobacterial or fungal infection
Ground-glass opacity
Infectious pneumonia
Pulmonary edema
Pulmonary hemorrhage
Acute or subacute hypersensitivity pneumonitis
Desquamative interstitial pneumonitis
Pulmonary alveolar proteinosis
Inadvertent exhalation
Mosaic lung attenuation
Infiltrative lung processes
Small airway disease
Pulmonary vascular disease
Tree-in-bud
Infection
Aspiration
Allergic bronchopulmonary aspergillosis
Cystic fibrosis
Diffuse panbronchiolitis
Obliterative bronchiolitis
Asthma
Septal Thickening
An interlobular septum marginates part of a secondary pulmonary lobule and contains pulmonary veins and lymphatics. These septa measure approximately 0.1 mm in thickness and are occasionally seen on normal thin-section CT scans. Abnormal thickening of interlobular septa is caused by fibrosis, edema, or infiltration by cells or other material. Within the peripheral lung, thickened septa 1 to 2 cm in length may outline part or all of a secondary pulmonary lobule, perpendicular to the pleural surface. They represent the CT counterpart of Kerley B lines seen on chest radiographs.
Interlobular septal thickening can be smooth (Fig. 2-24) or nodular (22) (Table 2-1). Smooth thickening is seen in patients with pulmonary edema or hemorrhage, lymphangitic spread of carcinoma, lymphoma, leukemia, interstitial infiltration associated with amyloidosis, and some pneumonias. Nodular or "beaded" thickening occurs in lymphangitic spread
P.28

of carcinoma (Fig. 2-25) or lymphoma, sarcoidosis, silicosis or coal worker's pneumoconiosis, lymphocytic interstitial pneumonia, and amyloidosis.
FIGURE 2-24. Smooth septal thickening. CT shows smooth thickening of the interlobular septae (arrows) in this patient with pulmonary edema. There are also small pleural effusions and scattered areas of GGO, which support the diagnosis.
Cystic Pattern
The term "cyst" is nonspecific and refers to a thin-walled (usually less than 3 mm thick), well-defined, well-circumscribed, air- or fluid-containing lesion, 1 cm or more in diameter, that has an epithelial or fibrous wall. A cystic pattern results from a heterogeneous group of diseases that have in common the presence of focal, multifocal, or diffuse parenchymal lucencies and lung destruction (Table 2-1). Pulmonary Langerhan cell histiocytosis, lymphangioleiomyomatosis, sarcoidosis, lymphocytic interstitial pneumonitis, collagen vascular diseases, Pneumocystis pneumonia, and honeycombing can manifest a cystic pattern on CT. Although they do not represent true cystic disease, centrilobular emphysema and cystic bronchiectasis mimic cystic disease on chest CT scans.
In cases of Langerhan cell histiocytosis, the cysts are often confluent, usually thin-walled, and often associated with pulmonary nodules 1 to 5 mm in diameter that may or may not be cavitary (Fig. 2-26). The intervening lung parenchyma is typically normal, without evidence of fibrosis or septal thickening. The distribution of findings is usually upper lungs, with sparing of the costophrenic sulci. The cysts are distributed diffusely throughout the lungs in lymphangioleiomyomatosis (Fig. 2-27), and nodules are not a common feature. The "cystic" spaces seen with centrilobular emphysema often contain a small nodular opacity representing the centrilobular artery (Fig. 2-28). This finding is helpful in distinguishing emphysema from lymphangioleiomyomatosis and Langerhan cell histiocytosis.
FIGURE 2-25. Nodular septal thickening. CT shows nodular thickening of the septae (arrows), other scattered small nodules, and areas of GGO, involving only the right lung. These findings are highly suggestive of this patient's diagnosis: lymphangitic carcinomatosis associated with primary bronchogenic carcinoma involving the right lung. Lymphangitic carcinomatosis from an extrathoracic malignancy usually involves both lungs.
Nodular Pattern
A nodular pattern refers to multiple round opacities, generally ranging in diameter from 1 mm to 1 cm, that may be very difficult to separate from one another as individual nodules on a
P.29

chest radiograph because of superimposition but which are accurately diagnosed on CT. Nodular opacities may be described as miliary (1 to 2 mm, the size of millet seeds), small, medium, or large as the diameter of the opacity increases. Nodules can be further characterized according to their margins (e.g., smooth or irregular), presence or absence of cavitation, attenuation characteristics (such as ground-glass opacity [GGO] or calcification), and distribution (e.g., centrilobular, perilymphatic, or random) (23) (Table 2-1).
FIGURE 2-26. Cystic pattern. A: CT of this patient with Langerhan cell histiocytosis shows irregular, variably sized cysts with definable walls (solid arrow) and scattered small nodules (dashed arrow) involving both upper lungs. B: CT at a level inferior to A shows normal lower lungs. The sparing of the lower lungs and the combination of cysts and nodules is highly suggestive of Langerhan cell histiocytosis.
FIGURE 2-27. Cystic pattern. CT scan of a woman with lymphangioleiomyomatosis shows fairly homogeneous thin-walled cysts with normal intervening lung parenchyma. The cysts involve the upper and lower lungs equally (not shown).
Multiple small smooth or irregularly marginated nodules in a perilymphatic distribution are characteristic of sarcoidosis (Fig. 2-29). The nodules represent the coalescence of microscopic noncaseating granulomas distributed along the bronchoarterial bundles, interlobular septa, and subpleural regions. A similar appearance can be seen with silicosis or coal worker's pneumoconiosis, although with the latter, the distribution of nodules is random, with predominant upper lung zone involvement. Within affected areas, the nodules of silicosis can show a predominantly posterior distribution. As disease progresses, coalescence of the silicotic nodules leads to progressive massive fibrosis. Numerous small nodules of GGO in a centrilobular distribution are characteristic of the acute or subacute stage of extrinsic allergic alveolitis (Fig. 2-30) or respiratory bronchiolitis. The nodules are poorly defined and usually measure less than 3 mm in diameter. A random distribution of miliary nodules can be seen with hematogenous spread of tuberculosis (Fig. 2-31), fungal infection, or metastases from a variety of primary sources. When associated with irregularly shaped, thin-walled cysts, randomly distributed nodules suggest Langerhan cell histiocytosis. Multiple cavitary nodules can be seen with metastases (usually of squamous cell histology), Wegener granulomatosis, rheumatoid lung disease, septic emboli, and multifocal infection (typically of fungal or mycobacterial etiology). Multiple irregular nodules in a bronchovascular distribution are characteristic of benign lymphoproliferative disorders (Fig. 2-32), lymphoma, leukemia, and Kaposi sarcoma.
FIGURE 2-28. Cystic pattern look-alike. CT scan shows lucent areas throughout both lungs, which can occasionally be confused with true lung cysts. However, the lucent areas do not have circumferential walls and in some areas, the centrilobular artery is visible within the area of lucency (arrows). These findings, along with a distribution that is predominantly in the upper lungs, are typical of centrilobular emphysema.
FIGURE 2-29. Perilymphatic nodular pattern. CT scan of a young man with sarcoidosis shows numerous small nodules distributed along the bronchovascular bundles (solid arrow) and subpleural lung (dashed arrows). This is a perilymphatic distribution, which is typical of sarcoidosis.
FIGURE 2-30. Centrilobular nodular pattern. CT scan of a man with acute hypersensitivity pneumonitis (also called extrinsic allergic alveolitis) shows numerous ill-defined ground-glass nodules in a centrilobular distribution. This appearance is highly suggestive of the diagnosis but can also be seen in respiratory bronchiolitis. A history of exposure and the presence or absence of cigarette smoking help to make the correct diagnosis.
P.30

FIGURE 2-31. Random nodular pattern. CT scan of a patient with miliary tuberculosis shows a pattern of diffuse, randomly distributed, well-defined small pulmonary nodules. Some of the nodules appear centrilobular and some are subpleural in location. The same pattern can be seen with fungal infection or pulmonary metastases.
Ground-Glass Pattern
GGO is defined as “hazy increased attenuation of lung, with preservation of bronchial and vascular margins; caused by partial filling of airspaces, interstitial thickening, partial collapse of alveoli, normal expiration, or increased capillary blood volume; not to be confused with consolidation, in which bronchovascular margins are obscured; may be associated with an air bronchogram” (24). GGO is a common but nonspecific finding on CT that reflects the presence of abnormalities below the limit of CT resolution (Table 2-1). In one investigation of patients with chronic infiltrative lung disease in whom lung biopsy was performed in areas of GGO, the pattern was shown to be caused by predominantly interstitial diseases in 54% of cases, equal involvement of the interstitium and airspaces in 32%, and predominantly airspace disease in 14% (25). GGO is an important finding. In certain clinical circumstances, it can suggest a specific diagnosis, indicate a potentially treatable disease, and guide a bronchoscopist or surgeon to an appropriate area for biopsy (26).
FIGURE 2-32. Bronchovascular nodular pattern. CT scan of a patient with benign posttransplant lymphoproliferative disorder shows multiple ill-defined nodules distributed along the bronchovascular bundles (arrows). This appearance can also be seen with malignant lymphoma, leukemia, and Kaposi sarcoma.
FIGURE 2-33. Ground-glass pattern. CT scan of a patient with diffuse pneumonia shows extensive bilateral GGO. Note that the pulmonary vessels and bronchi are still visible. This is a nonspecific pattern that is also commonly seen with pulmonary hemorrhage and pulmonary edema.
Acute lung diseases characteristically associated with diffuse GGO include pneumonia (Fig. 2-33), pulmonary hemorrhage, and pulmonary edema. In patients with acquired immunodeficiency syndrome, the presence of focal or diffuse GGO on CT is highly suggestive of Pneumocystis pneumonia. In patients with lung transplants, GGO is very suggestive of Cytomegalovirus pneumonia or acute rejection. When diffuse GGO is seen in the first month after bone marrow transplantation, both infection and diffuse alveolar hemorrhage should be considered.
Diffuse or patchy GGO is frequently the main abnormality seen in the acute or subacute phase of extrinsic allergic alveolitis. It is also the predominant finding in patients with desquamative interstitial pneumonia, in which it reflects the presence of mild interstitial thickening and filling of the airspaces with macrophages. In pulmonary alveolar proteinosis, the areas of GGO usually have a patchy or geographic distribution. Although the abnormality consists mainly of filling of airspaces with proteinaceous material, interlobular septal thickening is frequently identified on CT in the areas of GGO, creating a "crazy paving" pattern (Fig. 2-34). Solitary small areas of GGO can signify early stage bronchioloalveolar carcinoma or atypical adenomatous hyperplasia (AAH).
FIGURE 2-34. "Crazy paving" pattern. CT scan of a patient with pulmonary alveolar proteinosis shows patchy areas of GGO associated with septal thickening, so-called “crazy paving.” This is a characteristic but not pathognomonic finding of pulmonary alveolar proteinosis.
P.31

FIGURE 2-35. Mosaic perfusion pattern. CT scan of a patient with sickle cell disease shows a mosaic pattern of lung attenuation. The abnormal lucent areas represent decreased perfusion secondary to microvascular occlusion.
Mosaic Pattern of Lung Attenuation
Lung attenuation normally increases during exhalation. In the presence of airway obstruction and air trapping, lung remains lucent on exhalation and shows little change in cross-sectional area; this is best appreciated when patchy and compared to normal lung. Areas of air trapping are seen as relatively low in attenuation on expiratory CT scans. Areas of air trapping can be patchy and nonanatomic; can correspond to individual secondary pulmonary lobules, segments, and lobes; or may involve an entire lung. Air trapping in a lobe or lung is usually associated with large airway or generalized small airway abnormalities, whereas lobular or segmental air trapping is associated with diseases that affect small airways. Bronchiolectasis is a common associated finding. Pulmonary vessels within the low-attenuation areas of air trapping often appear small relative to vessels in the more opaque normal lung regions (27). This finding is also seen with vascular disease, such as chronic thromboembolic disease, as a result of decreased perfusion to affected areas of lung.
The presence of heterogeneous lung attenuation on inspiratory scans - the so-called mosaic pattern of lung attenuation - can result from infiltrative processes, airway obstruction and reflex vasoconstriction, mosaic perfusion resulting from vascular obstruction (e.g., chronic thromboembolic disease; Fig. 2-35), or a combination of these (Table 2-1). In patients with GGO from infiltrative processes, expiratory CT shows a proportional increase in attenuation in areas of both increased and decreased opacity. In patients with mosaic attenuation resulting from airway disease, such as obliterative bronchiolitis or asthma, attenuation differences are accentuated or seen only on expiration (Fig. 2-36). In patients with mosaic perfusion caused by vascular disease, air trapping can be seen but is not a dominant feature on expiratory CT.
FIGURE 2-36. Mosaic attenuation pattern. A: Inspiratory CT scan of a patient with asthma shows a homogeneous pattern of lung attenuation. B: Expiratory CT scan shows a mosaic pattern of lung attenuation. The abnormal lucent areas represent air trapping related to the patient's asthma. Note the anterior bowing of the posterior membranous trachea (arrow), indicating expiration.
FIGURE 2-37. Tree-in-bud pattern. Maximum-intensity projection axial CT image of a patient with bacterial bronchiolitis shows a pattern of small nodular and linear branching opacities, predominantly in the periphery of the lung (arrows). This is a bronchiolar distribution. The most common etiologies for this pattern are infection and aspiration.
Tree-in-Bud Pattern
The CT pattern of centrilobular nodular and branching linear opacities has been likened to the appearance of a budding tree. Many disorders can result in this pattern, the most common being infectious processes with endobronchial spread of disease (Fig. 2-37) (28,29) (Table 2-1). The common CT features of all processes producing the tree-in-bud pattern are (a) bronchiolar
P.32

dilatation and (b) impaction of bronchioles with mucus, pus, or other material. The CT findings are nonspecific, but a specific diagnosis can occasionally be suggested when the findings are correlated with patient history, clinical information, associated CT scan findings, and chronicity of disease.
FIGURE 2-38. Tree-in-bud pattern. CT scan of a patient with cystic fibrosis shows bilateral bronchiectasis and bronchiolectasis, along with "tree-in-bud" opacities in the periphery of the right lung (arrow). The opacities represent mucoid impaction of the bronchioles.
The term tree-in-bud dates back to the bronchogram descriptions of normal respiratory bronchioles by Twining and Kerley (30) but has been more recently popularized by Im et al (31) to describe the CT appearance of the endobronchial spread of Mycobacterium tuberculosis.
Numerous noninfectious disorders are associated with the tree-in-bud pattern. In allergic bronchopulmonary aspergillosis, immunologic responses to the endobronchial growth of Aspergillus sp result in damage to the bronchial wall, central bronchiectasis, and the formation of mucous plugs that contain fungus and inflammatory cells. The tree-in-bud pattern is seen when the process extends to the bronchioles. In cystic fibrosis, an abnormally low water content of airway mucus is at least partially responsible for decreased mucous clearance, mucous plugging of small and large airways, and an increased incidence of bacterial airway infection. Bronchial wall inflammation progresses to bronchiectasis, and bronchiolar secretions result in a tree-in-bud pattern (Fig. 2-38). The tree-in-bud pattern can also be seen with aspiration of infected oral secretions or other irritant material (Fig. 2-39), diffuse panbronchiolitis (Fig. 2-40), obliterative bronchiolitis, and asthma.
FIGURE 2-39. Tree-in-bud pattern. CT scan of a patient who aspirated shows extensive tree-in-bud pattern (arrow) bilaterally.
FIGURE 2-40. Tree-in-bud pattern. CT scan of a patient with diffuse panbronchiolitis shows tree-in-bud pattern (solid arrow) and dilated, nonimpacted bronchioles (dashed arrows).
References
1. Felson LB, Rosenberg LS, Hamburger M. Roentgen findings in acute Friedlander's pneumonia. Radiology. 1949; 53:559–565.
2. Levin B. The continuous diaphragm sign: a newly recognized sign of pneumomediastinum. Clin Radiol. 1973;24:337–338.
3. Im JG, Han MC, Yu EJ. Lobar bronchioloalveolar carcinoma: "angiogram sign" on CT scans. Radiology. 1990;176:749–753.
4. Vincent JM, Ng YY, Norton AJ, et al. CT "angiogram sign" in primary pulmonary lymphoma. J Comput Assist Tomogr. 1992;16:829–831.
5. Gordon R. The deep sulcus sign. Radiology. 1980;136:25–27.
6. Oh KS, Fleischner FG, Wyman SM. Characteristic pulmonary finding in traumatic complete transection of a main stem bronchus. Radiology. 1969;92:371–372.
7. Armstrong P. Basic patterns in lung disease. In: Armstrong P, Wilson AG, Dee P, Hansell DM, eds. Imaging of Diseases of the Chest. 2nd ed. St. Louis, MO: Mosby; 1995:89.
8. Gefter WB. The spectrum of pulmonary aspergillosis. J Thorac Imaging. 1992;7:56–74.
9. Golden R. The effect of bronchostenosis upon the roentgen-ray shadows in carcinoma of the bronchus. Am J Roentgenol. 1925;13:21–30.
10. Primack SL, Hartman TE, Lee KS, Müller NL. Pulmonary nodules and the CT halo sign. Radiology. 1994;190:513–515.
11. Kuhlman JE, Fishman EK, Siegelman SS. Invasive pulmonary aspergillosis in acute leukemia: characteristic findings on CT, the CT halo sign, and the role of CT in early diagnosis. Radiology. 1985;157:611–614.
12. Hampton AO, Castleman B. Correlations of post mortem chest teleroentgenograms with autopsy findings with special reference to pulmonary embolism and infarction. Am J Roentgenol. 1940;43:305–326.
13. Kattan KR, Eyler WR, Felson B. The juxtaphrenic peak in upper lobe collapse. Semin Roentgenol. 1980;15:187–193.
14. Burgel E, Oleck HG. Ueber die rechtsseitige paramediastinale Luftsichel bei Oberlappenschrumpfung. Rofo. 1960;93:160–163.
15. Woesner ME, Sanders I, White GW. The melting sign in resolving transient pulmonary infarction. Am J Roentgenol. 1971;111:782–790.
16. Hammond DI. The "ring around the artery" sign in pneumomediastinum. J Can Assoc Radiol. 1984;35:88–89.
17. Felson B, Felson H. Localization of intrathoracic lesions by means of the postero-anterior roentgenogram: the silhouette sign. Radiology. 1950;55:363–374.
18. Stark DD, Federle MP, Goodman PC, et al. Differentiating lung abscess and empyema: Radiography and computed tomography. Am J Roentgenol. 1983;141:163–167.
19. Westermark N. On the roentgen diagnosis of lung embolism. Acta Radiol. 1938;19:357–372.
P.33

20. Ely JW, Berbaum KS, Bergus GR, et al. Diagnosing left lower lobe pneumonia: usefulness of the ‘spine sign’ on lateral chest radiographs. J Fam Pract. 1996;43:242–248.
21. Müller NL, Miller RR, Webb WR, et al. Fibrosing alveolitis: CT-pathologic correlation. Radiology. 1986;160:585–588.
22. Kang EY, Grenier P, Laurent F, et al. Interlobular septal thickening: patterns at high-resolution computed tomography. J Thorac Imaging. 1996;11:260–264.
23. Gruden JF, Webb WR, Naidich DP, et al. Multinodular disease; anatomic localization at thin-section CT: multireader evaluation of a simple algorithm. Radiology. 1999;210:711–720.
24. Austin JHM, Müller NL, Friedman PJ, et al. Glossary of terms for CT of the lungs: recommendations of the nomenclature committee of the Fleischner Society. Radiology. 1996;200:327–331.
25. Leung AN, Miller RR, Müller NL. Parenchymal opacification in chronic infiltrative lung diseases: CT-pathologic correlation. Radiology. 1993;188:209–214.
26. Collins J, Stern EJ. Ground-glass opacity at CT: the ABCs. Am J Roentgenol. 1997;169:355–367.
27. Stern EJ, Webb WR. Dynamic imaging of lung morphology with ultrafast high-resolution computed tomography. J Thorac Imag. 1993;8:273–282.
28. Collins J, Blankenbaker D, Stern EJ. CT patterns of bronchiolar disease: what is "tree-in-bud"? Am J Roentgenol. 1998;171:365–370.
29. Aquino SL, Gamsu G, Webb WR, Kee ST. Tree-in-bud pattern: frequency and significance on thin section CT. J Comput Assist Tomogr. 1996;20:594–599.
30. Twining E, Kerley P. Textbook of X-Ray Diagnosis. 2nd ed. London: Lewis; 1951:208.
31. Im JG, Itoh H, Shim YS, et al. Pulmonary tuberculosis: CT findings - early active disease and sequential change with antituberculous therapy. Radiology. 1993;186:653–660.