Chest Radiology: The Essentials
2nd Edition

Chapter 4
Alveolar Lung Disease
Alveolar lung disease (ALD) refers to filling of the airspaces with fluid or other material (water, pus, blood, cells, or protein). The airspace filling can be partial, with some alveolar aeration remaining, or complete, producing densely opacified, nonaerated lung that obscures underlying bronchial and vascular markings. ALD producing dense airspace opacity is more easily distinguished from interstitial lung disease (ILD) than lesser degrees of alveolar filling. Abnormal “hazy” lung opacification that does not obscure underlying bronchovascular markings is referred to as ground-glass opacification and can represent ILD, ALD, or both. Compared with ILD, ALD tends to produce a homogeneous appearance of parenchymal opacification, with abnormal opacities appearing more confluent. ILD produces linear, reticular, nodular, or reticulonodular opacities. There can be, and often is, overlap in the radiographic appearances of ILD and ALD.
Different causes of ALD often cannot be distinguished based on the radiographic distribution alone, but the clinical history, associated radiographic findings, and chronicity of the process can help to narrow the differential diagnosis. The processes to consider when an ALD pattern is seen are divided into those that are acute and those that are chronic. Recurrence of an acute process can mimic a chronic process (as with recurrent pulmonary hemorrhage in pulmonary–renal syndromes). In these cases, serial chest radiographs can help to show that the process is not caused by bronchoalveolar cell carcinoma, lipoid pneumonia, or lymphoma, for example, because these processes do not typically clear completely and then recur. All causes of acute ALD can resolve completely and subsequently recur, and therefore they should also be considered in the differential diagnosis of chronic ALD when serial chest radiographs or patient history suggests a chronic process with exacerbations and remissions. Although organizing pneumonia and eosinophilic pneumonia often present as ALD, they are discussed in Chapter 12 with other causes of peripheral lung disease.
Acute Alveolar Lung Disease
Pulmonary Edema
The four most common processes causing acute ALD are listed in Table 4-1. Pulmonary edema is the most common cause of ALD on chest radiographs. As mentioned in the previous chapter, on ILD, edema can be (a) hydrostatic (from cardiac failure, renal failure, or overhydration); (b) nonhydrostatic, owing to increased capillary permeability (in acute respiratory distress syndrome [ARDS] and fat embolization syndrome); or (c) inflammatory in etiology (as from chemical pneumonitis or eosinophilic pneumonitis). Fat embolization syndrome occurs most commonly after traumatic fracture of long bones, which results in liberated marrow fat entering the pulmonary arterial circulation. Hydrolysis of fat, forming free fatty acids, leads to endothelial damage and increased capillary permeability 12 to 48 hours after trauma. This entity is further discussed in Chapter 8.
The radiographic distinction of pulmonary edema as cardiogenic or noncardiogenic in etiology is not always clear cut (1). Radiographic signs of cardiogenic pulmonary edema include enlargement of the cardiac silhouette (which may be assumed as secondary to cardiomegaly in many cases but is not always distinguishable from pericardial effusion), pleural effusions, pulmonary vascular congestion and redistribution, and interstitial and alveolar opacities. Edema fluid spills into the interstitial spaces and progresses to filling of the airspaces. Often, the chest radiograph shows evidence of interstitial and airspace filling, although occasionally a predominantly interstitial pattern may be seen. Interstitial edema can result in blurring of the margins of blood vessels and hazy thickening of bronchial walls (peribronchial cuffing), thickening of fissures (subpleural edema), and edematous thickening of the interlobular septa (Kerley A and B lines). Subpleural pulmonary edema refers to fluid that accumulates in the loose connective tissue beneath the visceral pleura and is seen radiographically as a thickened fissure; this is sometimes difficult to distinguish from pleural effusion. Chest radiographs are highly sensitive for the diagnosis of pulmonary edema and can show edema in patients who have not yet developed symptoms; conversely, pulmonary edema may be visible radiographically for hours or even days after the hemodynamic factors have returned to normal (2).
The distribution of airspace opacities in alveolar edema is usually patchy, bilateral, and widespread, and the opacities tend to coalesce. Air bronchograms may be evident, particularly when the edema is confluent. Often, alveolar accumulation of fluid in pulmonary edema is most pronounced centrally near the hila, resulting in a “bat’s wing” or “butterfly” configuration. A clue to the diagnosis of pulmonary edema, instead
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of pneumonia, for example, is rapid change on radiographs taken over short time intervals (several hours); rapid clearing is particularly suggestive of the diagnosis. Edema fluid can also change distribution or shift from one lung to the other as a result of the effect of gravity, as when a patient has been lying on one side.
TABLE 4-1 ACUTE ALVEOLAR LUNG DISEASE
“HEAP”
Hemorrhage
Edema
Alveolar proteinosis/Aspiration
Pneumonia (includes infectious, organizing, and eosinophilic pneumonias)
ARDS is the result of increased pulmonary vascular permeability and develops in response to lung injury. The more common of the many lung insults leading to ARDS include sepsis, pneumonia, aspiration of gastric contents, circulatory shock, trauma, burns, and drug overdose. Often there are multiple overlapping inciting events. The clinical syndrome of ARDS is characterized by acute, severe, progressive respiratory distress, usually requiring mechanical ventilation; widespread pulmonary opacity on chest radiographs; hypoxia despite high inspired oxygen concentration; and decreased compliance of the lungs (“stiff lungs”). Damage to the alveolar capillary membrane leads to increased capillary permeability and leakage of proteinaceous fluid into the alveoli. Eventually, alveolar disruption and hemorrhage occur, surfactant is reduced, and the alveoli tend to collapse. The stages of ARDS are outlined in Table 4-2. The radiographic features may be delayed by up to 12 hours or more following the onset of clinical symptoms—an important difference from cardiogenic pulmonary edema, in which the chest radiograph is frequently abnormal before or coincident with the onset of symptoms. Findings on chest radiography include bilateral, widespread, patchy, ill-defined opacities resembling cardiogenic pulmonary edema, but without cardiomegaly, vascular redistribution, or pleural effusion (Fig. 4-1). Although the lungs appear diffusely involved on chest radiographs, computed tomographic (CT) scanning often shows a more patchy distribution with preservation of normal lung regions (3). If an endotracheal tube is not present on the chest radiograph, the diagnosis of ARDS is unlikely, except in the later stages of healing.
FIGURE 4-1. Acute respiratory distress syndrome (ARDS). This 69-year-old man had undergone a liver transplant several years earlier and developed ARDS as a result of herpes simplex virus pneumonia. A: Anteroposterior (AP) recumbent chest radiograph shows an endotracheal tube and bilateral interstitial and alveolar lung disease. B: Computed tomographic (CT) scan shows bilateral diffuse ground-glass and reticular opacities.
TABLE 4-2 STAGES OF ACUTE RESPIRATORY DISTRESS SYNDROME
Stage 1 (first 24 hours): Capillary congestion and extensive microatelectasis with minimal fluid leakage. The chest radiograph may be normal, or it may show minimal interstitial edema or decreased lung volume.
Stage 2 (1 to 5 days): Fluid leakage and fibrin deposition and hyaline membranes develop. Alveolar consolidation by hemorrhagic fluid becomes extensive. The chest radiograph shows lung opacity (usually bilateral and symmetric), similar in appearance to cardiogenic pulmonary edema or pneumonia, which may start out patchy but rapidly coalesces.
Stage 3 (after 5 days): Alveolar cell proliferation, collagen deposition, and microvascular destruction. The chest radiograph shows a developing interstitial pattern that may result in honeycomb lung.
Reproduced with permission from Greene R. Adult respiratory distress syndrome: acute alveolar damage. Radiology. 1987;163:57–66.
Patients with ARDS typically require mechanical ventilation, sometimes with high positive end expiratory pressure because of stiff, noncompliant lungs. This predisposes to barotrauma, with rupture of alveolar walls and subsequent dissection of air into the perivascular bundle sheaths and interlobular septa, resulting in pulmonary interstitial emphysema. Discrete air-filled cysts, or “pneumatoceles,” may form in both central and subpleural locations (Fig. 4-2). These air collections can dissect into the mediastinum, causing pneumomediastinum, and can rupture into the pleural space, causing pneumothorax. The lung may be so stiff that it does not collapse easily, even when a pneumothorax is present. Air may dissect from the mediastinum into the neck and chest wall, retroperitoneum, or
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peritoneal cavity. The long-term outlook for survivors of ARDS is poorly documented. Mortality is related mainly to multiple organ failure rather than pulmonary dysfunction (4). One study of 109 survivors of ARDS showed that survivors had persistent functional disability 1 year after discharge from intensive care. Most had extrapulmonary conditions, with muscle wasting and weakness being the most prominent (5). Chest radiographs may return to normal or show varying degrees of interstitial lung disease, including pulmonary fibrosis.
FIGURE 4-2. Acute respiratory distress syndrome. This 38-year-old man with a primary brain neoplasm developed severe respiratory distress requiring mechanical ventilation. A: AP recumbent chest radiograph shows bilateral ALD. An endotracheal tube is in place (arrowhead). Oval collections of air are present in the periphery of the lungs, representing pneumatoceles from barotrauma (arrows). A right subclavian pulmonary artery catheter was placed to measure pulmonary capillary wedge pressure. The pressure was low, consistent with noncardiogenic pulmonary edema of ARDS. The tip of the catheter is projected over the left lower lobe pulmonary artery (curved arrow). B: CT shows bilateral ALD, multiple abnormal rounded and tubular air collections within the lung representing dilated airways (arrowheads), and a peripheral pneumatocele on the left (arrows).
Pulmonary Hemorrhage
Bleeding into the lung parenchyma occurs as the result of a variety of disorders (Table 4-3). A triad of features suggesting pulmonary hemorrhage is hemoptysis, anemia, and airspace opacities on chest radiography. Bleeding into the lung, however, does not always lead to hemoptysis (6). When bleeding into the lung is widespread, the pattern is referred to as diffuse pulmonary hemorrhage (DPH). The pulmonary features of all DPH syndromes are the same, and chest radiographs are generally not helpful in distinguishing among them. Lung opacities range from patchy airspace opacities to widespread confluent opacities with air bronchograms. The lung opacities show a perihilar or middle to lower lung predominance, and they tend to be more pronounced centrally, with sparing of the costophrenic angles and apices. In general, in cases of acute pulmonary hemorrhage (if there are no complicating factors), rapid clearing in 2 to 3 days can be expected. This can aid in narrowing the differential diagnosis when chest radiography shows diffuse ALD (7). When the airspace disease clears, interstitial opacities are often seen on chest radiography, as the result of by-products of blood breakdown being taken up by the septal lymphatics.
TABLE 4-3 CAUSES OF PULMONARY HEMORRHAGE
Pulmonary–renal syndromes
Wegener granulomatosis (usually older men)
Systemic lupus erythematosus (younger women)
Goodpasture syndrome (younger men)
Other vasculitides (e.g., polyarteritis nodosa, Henoch-Schönlein purpura)
Without renal disease
Anticoagulation
Pulmonary infection or neoplasm
Pulmonary embolism
Idiopathic pulmonary hemosiderosis (childhood disease—rare in adult)
Trauma (including iatrogenic, e.g., biopsy)
Bone marrow transplantation (diffuse pulmonary hemorrhage)
Goodpasture syndrome, one of the pulmonary–renal syndromes and the most common cause of DPH, is an anti–basement membrane antibody disease manifesting as DPH and glomerulonephritis. It is a disease of young white men and is only occasionally reported in children (8). The presence of antiglomerular basement membrane antibodies in the serum is a sensitive and specific indicator of the disease. Renal biopsy shows evidence of subacute proliferative glomerulonephritis with linear IgG deposition in the glomeruli. The chest radiograph usually shows bilateral, relatively central, and symmetric ALD, but this is a nonspecific pattern (Fig. 4-3).
Many collagen vascular disorders and systemic vasculitides are associated with DPH, with or without renal disease. The association is most commonly seen with systemic lupus erythematosus (Fig. 4-4) and systemic necrotizing vasculitides of the polyarteritis nodosa type (9).
Wegener granulomatosis (WG) is characterized pathologically by necrotizing granulomatous vasculitis of the upper and lower respiratory tracts, a disseminated small-vessel vasculitis involving both arteries and veins, and a focal, necrotizing glomerulonephritis (10). Mean age at presentation is 50, and there is a slight male predominance. Upper airway involvement with sinusitis, rhinitis, and otitis is the most common clinical presentation. More than 90% of patients with active multiorgan WG have a positive test for cytoplasmic antineutrophil cytoplasmic antibodies (11). There are two characteristic pulmonary radiologic findings: (i) nodules, multiple
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or single, ranging from 3 mm to 10 cm in diameter, which may cavitate; and (ii) diffuse areas of lung opacity, representing pulmonary hemorrhage (Fig. 4-5). Occasionally, ill-defined nodular opacities may be present, sometimes appearing as areas of pleural-based, wedge-shaped consolidation, resembling pulmonary infarcts.
FIGURE 4-3. Goodpasture syndrome. This 21-year-old man presented with recurrent pulmonary hemorrhage. PA (A) and lateral (B) chest radiographs show bilateral ALD involving predominantly the middle and lower lungs.
DPH can occur as a result of various coagulopathies, including thrombocytopenia (such as in leukemia or after bone marrow transplantation), anticoagulation, coronary thrombolysis, and diffuse intravascular coagulation. Infectious hemorrhagic necrotizing pneumonias or hemorrhagic neoplasms can result in diffuse, focal, or multifocal patchy areas of pulmonary hemorrhage. Pulmonary hemorrhage related to chest trauma is discussed in Chapter 8.
FIGURE 4-4. Systemic lupus erythematosus (SLE) with recurrent pulmonary hemorrhage. This 25-year-old woman presented with hemoptysis. A: PA chest radiograph shows focal ALD at the right lung base, with a rounded configuration (arrows), suggesting rounded pneumonia. Bronchoalveolar lavage showed evidence of pulmonary hemorrhage and no infectious organisms. The radiographic abnormality cleared in 4 days, consistent with hemorrhage. B: Radiograph of the right shoulder, providing a clue to the diagnosis, shows flattening, sclerosis, and collapse of the right humeral head as a result of avascular necrosis, a complication of chronic steroid treatment for SLE.
Alveolar Proteinosis
Alveolar proteinosis typically presents in a patient who feels relatively well, in striking contrast to the markedly abnormal radiograph, which shows bilateral diffuse or multifocal patchy opacities. The opacities represent a phospholipoproteinaceous material that fills the alveolar spaces and clears after bronchioalveolar lavage (12). Recurrence of disease can result in a chronic pattern of ALD, with serial chest radiographs showing varying patterns of recurrent ALD with interval clearing (Fig. 4-6). Alveolar proteinosis is associated with an increased incidence of lymphoma and infection with Nocardia (13,14).
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FIGURE 4-5. Wegener granulomatosis. This 19-year-old man, rather young in view of the age group in which this disorder most commonly appears, presented with hemoptysis and shortness of breath. AP chest radiograph shows a nonspecific pattern of bilateral ALD, predominantly involving the middle and lower lungs.
FIGURE 4-6. Pulmonary alveolar proteinosis. This 27-year-old man presented with recurrent alveolar proteinosis, which was treated with bronchoalveolar lavage. A: PA chest radiograph shows bilateral mixed interstitial and alveolar opacities involving predominantly the right middle and both lower lungs. Alveolar proteinosis is often associated with a prominent component of interstitial opacities, especially on CT. These opacities cleared after bronchoalveolar lavage. B: PA chest radiograph obtained 1 year later shows recurrent diffuse bilateral ALD, which cleared after treatment with bronchoalveolar lavage. C: PA chest radiograph 1 year after (B) shows recurrent diffuse bilateral ALD, which cleared after treatment with bronchoalveolar lavage. D: PA chest radiograph obtained 2 years after (C) shows clearing of both lungs.
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FIGURE 4-7. Bacterial pneumonia. This 58-year-old man presented with diabetic ketoacidosis, fever, cough, and elevated white blood cell count. A: PA chest radiograph shows ALD in the left lower lobe (circle). B: Lateral view shows ALD overlying the spine posteriorly (the so-called “spine sign”; circle).
FIGURE 4-8. Pulmonary blastomycosis. This 43-year-old man presented with an infected finger and an abnormal chest radiograph (not shown). CT scan shows focal airspace opacity in the left lower lobe.
Infectious Pneumonia Causing Alveolar Lung Disease
Infectious pneumonia is the most common cause of focal ALD, and bacteria are the most common inciting agents. Fungal, mycobacterial, parasitic, and even viral pneumonias can all produce focal or diffuse airspace opacities on chest radiography (Figs. 4-7, 4-8, 4-9). Opacity of more than half a lobe with no loss of volume is virtually diagnostic of pneumonia, and common causes are Streptococcus pneumoniae or Mycoplasma pneumoniae (Figs. 4-10 and 4-11). Lobar consolidation with expansion of the lobe, although uncommon, strongly suggests bacterial pneumonia (particularly S. pneumoniae, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Staphylococcus aureus pneumonias). A round consolidative process is likely to be caused by pneumonia (Fig. 4-12). Organisms most likely to cause round pneumonia are S. pneumoniae, S. aureus, K. pneumoniae, P. aeruginosa, Legionella pneumophila or L. micdadei, Mycobacterium tuberculosis, and several fungi. The development of air–fluid levels within an area of consolidation that is known or presumed to be pneumonia strongly suggests necrotizing pneumonia with abscess formation, and likely pathogens include S. aureus, Klebsiella sp, Proteus sp, and Pseudomonas
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sp, as well as mixed infections (Fig. 4-13). Multifocal pneumonia can be caused by numerous organisms, but the “bat’s wing pattern” in the immunocompetent patient should suggest aspiration pneumonia, Gram-negative bacterial pneumonia (Fig. 4-14), and nonbacterial pneumonias such as mycoplasma, viral, and rickettsial pneumonia. Pneumonia in the immunocompromised host often results in the bat’s wing pattern from opportunistic organisms such as Pneumocystis jiroveci and various fungi.
FIGURE 4-9. Legionella pneumonia. This 53-year-old woman with rheumatoid arthritis presented with fever, cough, shortness of breath, nausea and vomiting, and an elevated white blood cell count. A: PA chest radiograph shows bilateral peripheral ALD in the upper and middle lungs. The appearance was suggestive of organizing pneumonia. B: CT scan confirms bilateral subpleural areas of dense airspace opacity with air bronchograms.
FIGURE 4-10. Pneumococcal pneumonia. This 22-year-old man presented with cough and fever. A: PA chest radiograph shows patchy ALD in the left lung, sparing the apex. B: Lateral view shows ALD confined to the left upper lobe, outlined posteriorly by the left major fissure (arrows).
FIGURE 4-11. Mycoplasma pneumonia. This 22-year-old man presented with cough, fever, shortness of breath and hypoxemia. A: PA chest radiograph shows diffuse, nonspecific bilateral ALD. B: CT scan shows diffuse, nonspecific bilateral ground-glass opacity and areas of dense airspace opacity.
FIGURE 4-12. Pneumococcal pneumonia. A: PA chest radiograph shows a rounded area of ALD in the right middle lung (arrows). B: Lateral view shows that the ALD (solid arrows) is confined to the right upper lobe, as outlined by the minor fissure (dashed arrows).
Aspiration
The radiologic manifestation of aspirated material into the lungs is dependent on the type and volume of material aspirated, the immune status of the patient, and the presence or absence of pre-existing lung disease. Aspiration of bland substances such as blood or neutralized gastric contents does not incite an inflammatory process, and associated lung opacities clear rapidly with ventilation therapy or coughing. Aspiration of acidic gastric contents and other irritating substances causes inflammation of the lung. Within several hours of aspirating such substances, chest radiographs usually show progressive airspace opacity in the gravitationally dependent regions of the lungs (Fig. 4-15). Radiologic improvement is generally seen within a few days unless the patient develops superimposed infection or ARDS.
FIGURE 4-13. Necrotizing Pseudomonas pneumonia. A: PA chest radiograph shows ALD in the right upper and middle lung. B: CT shows numerous lucent areas with air–fluid levels (arrows) within the densely opacified lung, consistent with lung necrosis. Also shown are prominent air bronchograms.
Nasogastric or endotracheal intubation, diminished levels of consciousness, and supine positioning predispose patients to aspirate. Acute aspiration may be accompanied by fever, shortness of breath, and hypoxemia, which can make aspiration difficult to distinguish from bacterial pneumonia.
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FIGURE 4-14. Legionella pneumonia. This 57-year-old woman presented with severe shortness of breath and hypoxemia. PA chest radiograph shows bilateral ALD in a “bat’s wing” pattern and prominent air bronchograms (arrows).
FIGURE 4-15. Aspiration. This 21-year-old quadriplegic man had a gastric bleed and aspirated blood. A: Baseline PA chest radiograph prior to aspiration shows clear lungs. B: PA chest radiograph obtained 1 day later, after aspiration, shows ALD in the right lung base.
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TABLE 4-4 CAUSES OF CHRONIC ALVEOLAR LUNG DISEASE
“BALLS”
Bronchoalveolar cell carcinoma
Alveolar proteinosis
Lymphoma
Lipoid pneumonia
Sarcoidosis
Chronic Alveolar Lung Disease
Processes that result in a chronic pattern of ALD are listed in Table 4-4. Determining that the process is chronic requires serial chest radiographs showing a static appearance or progression of ALD, typically over several months. Two neoplastic processes should be considered in the differential diagnosis of chronic ALD: lymphoma (Figs. 4-16 and 4-17) and bronchoalveolar cell carcinoma (a type of primary bronchogenic adenocarcinoma) (Figs. 4-18 and 4-19). These are discussed in Chapters 6 and 15, respectively. Alveolar proteinosis has been discussed along with other causes of acute ALD, but it can be recurrent. Sarcoidosis can result in myriad chest radiographic patterns, both typical and atypical. Chronic ALD, although not a common pattern of sarcoidosis, should be considered in a young, relatively asymptomatic patient (Fig. 4-20). Although the chest radiographic appearance mimics ALD, sarcoidosis involves only the interstitial compartment of the lung. Areas of airspace opacity, so-called “alveolar sarcoidosis,” represent a conglomeration of interstitial granulomas. This disorder is discussed further in Chapter 10.
FIGURE 4-16. Pulmonary lymphoma. Chest CT shows bilateral foci of ALD, with prominent air bronchograms (arrows).
FIGURE 4-17. Burkitt lymphoma. A: PA chest radiograph shows bilateral ALD, most prominent on the left. B: CT scan shows bilateral ALD with prominent air bronchograms (arrow).
Lipoid pneumonia results from aspiration of vegetable, animal, or mineral oil, usually in elderly or debilitated patients, patients with neuromuscular disease or swallowing abnormalities, or patients taking mineral oil as therapy for chronic constipation. Most patients are relatively asymptomatic. Chest radiographs show homogeneous segmental areas of lung opacification, or circumscribed masses (“paraffinomas”) that remain stable or slowly progress over a period of months and can be similar in appearance to bronchogenic carcinoma. Because of the lipid content, these areas of opacification may be of relatively low attenuation on CT scans of the chest, which may help suggest the correct diagnosis. Dilated colon and chronic stool retention seen on chest or abdominal radiographs may also provide clues to a patient who chronically aspirates mineral oil.
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FIGURE 4-18. Bronchoalveolar cell carcinoma. This 56-year-old man presented with chronic ALD on serial chest radiographs. A: PA chest radiograph shows bilateral ALD, which appears “hazy” in some areas and is difficult to discern as interstitial or alveolar. The opacity in the left upper lobe is more confluent. B: PA chest radiograph obtained 16 months later shows progression of ALD.
FIGURE 4-19. Bronchoalveolar cell carcinoma. This 75-year-old man presented with cough and mild shortness of breath. A: PA chest radiograph shows ALD in the left lower lobe (circle). B: Lateral view shows that the ALD is posterior, in the left lower lobe (circle). C: CT shows focal ALD in the left lower lobe and prominent air bronchograms.
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FIGURE 4-20. Sarcoidosis. This 29-year-old man presented with mild cough and shortness of breath. A: AP chest radiograph shows patchy ALD in the upper lungs (circles). B: CT shows bilateral upper lobe ALD. Although the appearance on imaging is that of ALD, sarcoidosis involves only the interstitial space. When the disease is profuse, as in this case, the interstitial granulomas compress and obliterate the adjacent alveolar spaces.
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