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DOI: 10.1148/rg.236035101
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(Radiographics. 2003;23:1509-1519.)
© RSNA, 2003

EDUCATION EXHIBIT

"Crazy-Paving" Pattern at Thin-Section CT of the Lungs: Radiologic-Pathologic Overview1

Santiago E. Rossi, MD, Jeremy J. Erasmus, MD, Mariano Volpacchio, MD, Tomas Franquet, MD, Teresa Castiglioni, MD and H. Page McAdams, MD

1 From the Departments of Radiology (S.E.R., M.V.) and Pathology (T.C.), Centro de Diagnostico Dr Enrique Rossi, Arenales 2777, Buenos Aires 1425, Argentina; the Department of Radiology, University of Texas M.D. Anderson Cancer Center, Houston (J.J.E.); the Department of Radiology, Hospital de Sant Pau, Universidad Autónoma de Barcelona, Spain (T.F.); and the Department of Radiology, Duke University Medical Center, Durham, NC (H.P.M.). Recipient of a Cum Laude award and an Excellence in Design award for an education exhibit at the 2002 RSNA scientific assembly. Received April 9, 2003; revision requested May 12 and received July 24; accepted July 25. Address correspondence to S.E.R. (e-mail: santirossi@cdrossi.com).


   Abstract
Top
 Abstract
Introduction
 Infection
 Neoplasm
 Idiopathic Disorders
 Inhalational Disorders
 Sanguineous Disorders
 Conclusions
 References
 
The "crazy-paving" pattern is a common finding at thin-section computed tomography (CT) of the lungs. It consists of scattered or diffuse ground-glass attenuation with superimposed interlobular septal thickening and intralobular lines. This finding has a variety of causes, including infectious, neoplastic, idiopathic, inhalational, and sanguineous disorders. Specific disorders that can cause the crazy-paving pattern include Pneumocystis carinii pneumonia, mucinous bronchioloalveolar carcinoma, pulmonary alveolar proteinosis, sarcoidosis, nonspecific interstitial pneumonia, organizing pneumonia, exogenous lipoid pneumonia, adult respiratory distress syndrome, and pulmonary hemorrhage syndromes. Knowledge of the many causes of this pattern can be useful in preventing diagnostic errors. In addition, although the causes of this pattern are frequently indistinguishable at radiologic evaluation, differences in the location of the characteristic attenuation in the lungs, as well as the presence of additional radiologic findings, the patient’s history, and the clinical presentation, can often be useful in suggesting the appropriate diagnosis.

© RSNA, 2003

Index Terms: Bronchiolitis obliterans organizing pneumonia, 60.795 • Lung, ground-glass opacification, 60.12118 • Lung, hemorrhage, 60.60 Lung, infection, 60.2075, 60.21 • Lung neoplasms, diagnosis, 60.3216 • Pneumocystis carinii, 60.2075 • Pneumonia, 60.21, 60.253, 60.795 • Pneumonia, lipoid, 60.253 • Pneumonia, nonspecific interstitial and fibrosis, 60.795 • Proteinosis, pulmonary alveolar, 60.791 • Respiratory distress syndrome, adult (ARDS), 60.413 • Sarcoidosis, 60.222


   Introduction
Top
 Abstract
 Introduction
Infection
 Neoplasm
 Idiopathic Disorders
 Inhalational Disorders
 Sanguineous Disorders
 Conclusions
 References
 
The "crazy-paving" pattern at thin-section computed tomography (CT) of the lungs is characterized by scattered or diffuse ground-glass attenuation with superimposed interlobular septal thickening and intralobular lines (Fig 1). Initially described in cases of alveolar proteinosis, this pattern has subsequently been reported in a variety of infectious, neoplastic, idiopathic, inhalational, and sanguineous disorders of the lung (Fig 2).



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  		Figure 1.  Photograph of a colonial-era pavement street in Buenos Aires, Argentina (left), drawings of the lungs (center) and lung tissue (top right), and close-up high-resolution CT scan (bottom right) show the crazy-paving pattern.

 


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  		Figure 2.  Causes of the crazy-paving pattern.

 
In this article, we review the most important entities that can manifest as the crazy-paving pattern at thin-section CT. Where appropriate, the pathologic basis for this appearance is emphasized. Helpful clues for appropriately narrowing the differential diagnosis and for directing patient care are discussed.


   Infection
Top
 Abstract
 Introduction
 Infection
Neoplasm
 Idiopathic Disorders
 Inhalational Disorders
 Sanguineous Disorders
 Conclusions
 References
 
Pneumocystis carinii pneumonia is a common pulmonary infection in the severely immunocompromised patient (1,2). Symptoms include dry cough, dyspnea, and low-grade fever. Although chest radiographs are normal in up to 18% of patients, the typical radiographic manifestations are bilateral, perihilar reticular and poorly defined ground-glass opacities, which often progress to alveolar consolidation in 3–4 days (1,3,4). High-resolution CT usually reveals scattered ground-glass attenuation that can be associated with interlobular septal thickening (Fig 3a) (5,6). Histologic features contributing to the ground-glass attenuation include the foamy nature of the alveolar exudates and thickening of the alveolar walls by edema and cellular infiltrates (Fig 3b).



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  		Figure 3a.  P carinii pneumonia in a 32-year-old man with acquired immunodeficiency syndrome. (a) High-resolution CT scan shows areas of ground-glass attenuation with intralobular lines. (b) Photomicrograph (original magnification, x400; Grocott stain) of a specimen obtained with bronchoalveolar lavage shows alveolar exudates that contain cystic forms of P carinii (arrows).

 


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  		Figure 3b.  P carinii pneumonia in a 32-year-old man with acquired immunodeficiency syndrome. (a) High-resolution CT scan shows areas of ground-glass attenuation with intralobular lines. (b) Photomicrograph (original magnification, x400; Grocott stain) of a specimen obtained with bronchoalveolar lavage shows alveolar exudates that contain cystic forms of P carinii (arrows).

 

   Neoplasm
Top
 Abstract
 Introduction
 Infection
 Neoplasm
Idiopathic Disorders
 Inhalational Disorders
 Sanguineous Disorders
 Conclusions
 References
 
Bronchioloalveolar carcinoma has been classified into mucinous and nonmucinous subgroups. Mucinous bronchioloalveolar carcinoma, a well-differentiated type of adenocarcinoma, consists of mucin-producing columnar cells with moderate nuclear atypia (Fig 4) (7–9). Bronchioloalveolar carcinoma is characterized by a lepidic growth pattern through the airways and air spaces with preservation of the lung architecture. Bronchorrhea, the expectoration of copious quantities of sputum, is an uncommon but characteristic clinical feature.



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  		Figure 4a.  Diffuse mucinous bronchioloalveolar carcinoma in a 78-year-old man. (a) High-resolution CT scan shows a bilateral crazy-paving pattern and centrilobular nodules. (b) Photomicrograph (original magnification, x400; hematoxylin-eosin stain) of a specimen from open lung biopsy shows replacement of the alveolar epithelium by epithelial neoplastic cells with abundant intracytoplasmic mucin (arrows).

 


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  		Figure 4b.  Diffuse mucinous bronchioloalveolar carcinoma in a 78-year-old man. (a) High-resolution CT scan shows a bilateral crazy-paving pattern and centrilobular nodules. (b) Photomicrograph (original magnification, x400; hematoxylin-eosin stain) of a specimen from open lung biopsy shows replacement of the alveolar epithelium by epithelial neoplastic cells with abundant intracytoplasmic mucin (arrows).

 
Radiographic findings include ill-defined consolidation or ground-glass opacities that occur in a focal or multilobar distribution (10,11). Lymphadenopathy and pleural effusion occur occasionally. High-resolution CT manifestations are numerous and include alveolar consolidation and ground-glass attenuation, which occasionally manifest as a crazy-paving pattern (Fig 4). The ground-glass attenuation reflects the low-density intraalveolar material (glycoprotein), whereas the superimposed reticular attenuation is due to infiltration of the interstitium by inflammatory or tumor cells (12,13).


   Idiopathic Disorders
Top
 Abstract
 Introduction
 Infection
 Neoplasm
 Idiopathic Disorders
Inhalational Disorders
 Sanguineous Disorders
 Conclusions
 References
 
Pulmonary Alveolar Proteinosis
Initially described in 1958, pulmonary alveolar proteinosis manifests as filling of the alveoli by a proteinaceous material that is positive at periodic acid–Schiff staining and rich in lipid, in association with an inflammatory response in the adjacent interstitium (Fig 5) (14–18). Pulmonary alveolar proteinosis is most common in adults between 20 and 50 years of age, although it has been reported in a wide range of ages (15,19). Dyspnea and nonproductive cough are the most common associated symptoms, whereas pleuritic chest pain, malaise, and low-grade fever are less common (14,15,19).



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  		Figure 5a.  Alveolar proteinosis in a 37-year-old woman with a nonproductive cough and dyspnea. (a) Posteroanterior chest radiograph shows bilateral reticular areas of increased opacity, which occur predominantly in the lower zones. (b) High-resolution CT scan shows diffuse geographic ground-glass attenuation with superimposed intra- and interlobular septal thickening (arrowhead). Note the polygonal appearance, which represents the secondary pulmonary lobule. (c, d) Photomicrographs (original magnification, x400; hematoxylin-eosin [c] and periodic acid-Schiff [d] stains) of a specimen from transbronchial biopsy show alveolar spaces filled by a dense, eosinophilic, granular proteinaceous material (*) that is positive for periodic acid-Schiff stain.

 


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  		Figure 5b.  Alveolar proteinosis in a 37-year-old woman with a nonproductive cough and dyspnea. (a) Posteroanterior chest radiograph shows bilateral reticular areas of increased opacity, which occur predominantly in the lower zones. (b) High-resolution CT scan shows diffuse geographic ground-glass attenuation with superimposed intra- and interlobular septal thickening (arrowhead). Note the polygonal appearance, which represents the secondary pulmonary lobule. (c, d) Photomicrographs (original magnification, x400; hematoxylin-eosin [c] and periodic acid-Schiff [d] stains) of a specimen from transbronchial biopsy show alveolar spaces filled by a dense, eosinophilic, granular proteinaceous material (*) that is positive for periodic acid-Schiff stain.

 


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  		Figure 5c.  Alveolar proteinosis in a 37-year-old woman with a nonproductive cough and dyspnea. (a) Posteroanterior chest radiograph shows bilateral reticular areas of increased opacity, which occur predominantly in the lower zones. (b) High-resolution CT scan shows diffuse geographic ground-glass attenuation with superimposed intra- and interlobular septal thickening (arrowhead). Note the polygonal appearance, which represents the secondary pulmonary lobule. (c, d) Photomicrographs (original magnification, x400; hematoxylin-eosin [c] and periodic acid-Schiff [d] stains) of a specimen from transbronchial biopsy show alveolar spaces filled by a dense, eosinophilic, granular proteinaceous material (*) that is positive for periodic acid-Schiff stain.

 


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  		Figure 5d.  Alveolar proteinosis in a 37-year-old woman with a nonproductive cough and dyspnea. (a) Posteroanterior chest radiograph shows bilateral reticular areas of increased opacity, which occur predominantly in the lower zones. (b) High-resolution CT scan shows diffuse geographic ground-glass attenuation with superimposed intra- and interlobular septal thickening (arrowhead). Note the polygonal appearance, which represents the secondary pulmonary lobule. (c, d) Photomicrographs (original magnification, x400; hematoxylin-eosin [c] and periodic acid-Schiff [d] stains) of a specimen from transbronchial biopsy show alveolar spaces filled by a dense, eosinophilic, granular proteinaceous material (*) that is positive for periodic acid-Schiff stain.

 
The classic radiographic finding is bilateral, symmetric alveolar consolidation or ground-glass opacity, particularly in a perihilar or hilar distribution resembling pulmonary edema (Fig 5a) (14,18–21). High-resolution CT typically shows diffuse ground-glass attenuation with superimposed intra- and interlobular septal thickening, often in polygonal shapes representing the secondary pulmonary lobule (Fig 5b) (17,21). The diagnosis is established with bronchoalveolar lavage (19).

Sarcoidosis
Sarcoidosis is a systemic entity characterized by the development of noncaseating granulomatous inflammation (22). Although the most common parenchymal findings include irregular thickening of the bronchovascular bundles and small nodules along vessels, alveolar sarcoidosis can manifest as ground-glass attenuation and crazy-paving attenuation (Fig 6) (22).



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  		Figure 6.  Sarcoidosis in a 25-year-old asymptomatic man. High-resolution CT scan shows scattered bilateral areas of ground-glass attenuation associated with inter- and intralobular lines. (Reprinted, with permission, from reference 22.)

 
Nonspecific Interstitial Pneumonia
Nonspecific interstitial pneumonia (NSIP) is a term used to describe interstitial inflammation and fibrosis with temporal and spatial uniformity that does not fulfill clinicopathologic criteria for usual interstitial pneumonia, desquamative interstitial pneumonia, or acute interstitial pneumonia (Fig 7). The initial concept of NSIP as a mixture of entities has evolved into the concept of NSIP as a clinicopathologic entity (23). The clinical presentation is similar to that of interstitial pulmonary fibrosis, although NSIP is associated with a much better prognosis (24).



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  		Figure 7a.  Methotrexate-induced NSIP in a 41-year-old woman with rheumatoid arthritis who presented with dyspnea and decreased diffusing capacity of the lungs for carbon monoxide (DLCO). (a) High-resolution CT scan shows scattered ground-glass attenuation and thickened inter- and intralobular lines (arrow). (b) Photomicrograph (original magnification, x400; hematoxylin-eosin stain) of a specimen from lung biopsy shows patchy interstitial fibrosis, expansion of the interstitium by chronic inflammatory infiltrates, and reactive hyperplastic type II pneumonocytes (arrow), findings consistent with NSIP induced by the pulmonary toxic effects of methotrexate.

 


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  		Figure 7b.  Methotrexate-induced NSIP in a 41-year-old woman with rheumatoid arthritis who presented with dyspnea and decreased diffusing capacity of the lungs for carbon monoxide (DLCO). (a) High-resolution CT scan shows scattered ground-glass attenuation and thickened inter- and intralobular lines (arrow). (b) Photomicrograph (original magnification, x400; hematoxylin-eosin stain) of a specimen from lung biopsy shows patchy interstitial fibrosis, expansion of the interstitium by chronic inflammatory infiltrates, and reactive hyperplastic type II pneumonocytes (arrow), findings consistent with NSIP induced by the pulmonary toxic effects of methotrexate.

 
Chest radiographic findings of bilateral pulmonary opacities, which are mainly localized in the middle and lower zones, are the predominant feature (23). The most common CT abnormality (80% of cases) is ground-glass attenuation. The ground-glass attenuation is usually bilateral and symmetric with a tendency to subpleural and basal predominance. Other findings include consolidation and irregular reticular lines that can be superimposed on a background of ground-glass attenuation (Figs 7a, 8) (24). Honeycombing is typically absent; this characteristic can be useful in narrowing the differential diagnosis with the other interstitial pneumonias.



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  		Figure 8.  Amiodarone-induced NSIP in an 88-year-old man with severe dyspnea. High-resolution CT scan shows bilateral diffuse ground-glass attenuation and inter- and intralobular lines. Note the traction bronchiectasis.

 
Organizing Pneumonia
Organizing pneumonia, also known in the past as bronchiolitis obliterans organizing pneumonia, is a chronic inflammatory process characterized by focal plugs of granulation tissue (Masson bodies) in the lumina of distal small airways, often extending into the alveolar spaces, associated with intraalveolar foamy macrophages and an interstitial cellular response (Fig 9) (25). Most cases of organizing pneumonia are idiopathic (cryptogenic organizing pneumonia). An association with collagen-vascular diseases (rheumatoid arthritis, mixed connective-tissue disease), infection, and toxic effects of drugs (bleomycin [Fig 10], methotrexate, cyclophosphamide, gold salts, topotecan [Fig 9], amiodarone) has been reported (26). Patients usually present with cough, dyspnea, fever of several weeks duration, and leukocytosis. Response to steroid therapy is typical.



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  		Figure 9a.  Topotecan-induced organizing pneumonia in a 45-year-old woman with small cell lung cancer who presented with increasing dyspnea. (a) High-resolution CT scan shows diffuse ground-glass attenuation and septal thickening in a crazy-paving pattern in the right upper lobe (arrows). (b) Photomicrograph (original magnification, x400; hematoxylin-eosin stain) of a specimen from wedge resection biopsy of the right upper lobe shows scattered interstitial inflammation and occlusion of terminal bronchioles and alveolar ducts by plugs of loose connective tissue (*), findings typical of organizing pneumonia.

 


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  		Figure 9b.  Topotecan-induced organizing pneumonia in a 45-year-old woman with small cell lung cancer who presented with increasing dyspnea. (a) High-resolution CT scan shows diffuse ground-glass attenuation and septal thickening in a crazy-paving pattern in the right upper lobe (arrows). (b) Photomicrograph (original magnification, x400; hematoxylin-eosin stain) of a specimen from wedge resection biopsy of the right upper lobe shows scattered interstitial inflammation and occlusion of terminal bronchioles and alveolar ducts by plugs of loose connective tissue (*), findings typical of organizing pneumonia.

 


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  		Figure 10.  Bleomycin-induced organizing pneumonia in a 44-year-old woman with Hodgkin lymphoma who presented with a nonproductive cough, dyspnea, and decreased DLCO. High-resolution CT scan shows ground-glass attenuation and scattered areas of focal consolidation peripherally. Note the intralobular lines superimposed on the ground-glass attenuation. The diagnosis of organizing pneumonia was confirmed with transthoracic biopsy; there was improvement in the symptoms and radiologic findings after discontinuation of the bleomycin therapy and initiation of corticosteroid therapy.

 
Chest radiographs and CT frequently show scattered and asymmetric consolidation bilaterally. In over one-half of patients, the consolidation is predominantly peripheral (Fig 10), and high-resolution CT commonly shows subpleural as well as peribronchovascular consolidation. The crazy-paving pattern is uncommon (Figs 9, 10) (27).


   Inhalational Disorders
Top
 Abstract
 Introduction
 Infection
 Neoplasm
 Idiopathic Disorders
 Inhalational Disorders
Sanguineous Disorders
 Conclusions
 References
 
Exogenous lipoid pneumonia is a pulmonary disorder resulting from chronic aspiration or inhalation of animal, vegetable, or petroleum-based oils or fats (28,29). Predisposing factors such as structural abnormalities of the pharynx, esophageal disorders (achalasia, Zenker diverticulum, hiatus hernia, and reflux), neurologic defects, and chronic illness are common (30–33). However, in many cases, no predisposing condition is found (28).

Histopathologically, exogenous lipoid pneumonia manifests acutely as intraalveolar macrophages containing abundant cytoplasmic lipoproteinaceous material within normal-appearing alveoli. Subacute manifestations include larger vacuoles within the alveoli, often surrounded by macrophages, and inflammatory infiltrates of alveolar walls and interlobular septa (Fig 11). Repeated episodes of aspiration can result in pulmonary fibrosis (30). Symptoms include cough, mild fever, shortness of breath, and chest discomfort (30).



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  		Figure 11a.  Lipoid pneumonia in a 64-year-old woman with a 20-year history of scleroderma who presented with progressive dyspnea and a dry cough. (a) Posteroanterior chest radiograph shows bilateral, asymmetric, scattered areas of increased opacity in the air space, which have a predominantly perihilar and basal distribution. (b) High-resolution CT scan shows geographic ground-glass attenuation in association with interlobular thickening and intralobular lines (arrow). The results of bronchoalveolar lavage and transbronchial biopsy were nondiagnostic. (c) Photomicrograph (original magnification, x250; hematoxylin-eosin stain) of a specimen from open lung biopsy shows numerous lipid-laden macrophages that fill and distend the alveoli (arrow) and interstitium.

 


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  		Figure 11b.  Lipoid pneumonia in a 64-year-old woman with a 20-year history of scleroderma who presented with progressive dyspnea and a dry cough. (a) Posteroanterior chest radiograph shows bilateral, asymmetric, scattered areas of increased opacity in the air space, which have a predominantly perihilar and basal distribution. (b) High-resolution CT scan shows geographic ground-glass attenuation in association with interlobular thickening and intralobular lines (arrow). The results of bronchoalveolar lavage and transbronchial biopsy were nondiagnostic. (c) Photomicrograph (original magnification, x250; hematoxylin-eosin stain) of a specimen from open lung biopsy shows numerous lipid-laden macrophages that fill and distend the alveoli (arrow) and interstitium.

 


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  		Figure 11c.  Lipoid pneumonia in a 64-year-old woman with a 20-year history of scleroderma who presented with progressive dyspnea and a dry cough. (a) Posteroanterior chest radiograph shows bilateral, asymmetric, scattered areas of increased opacity in the air space, which have a predominantly perihilar and basal distribution. (b) High-resolution CT scan shows geographic ground-glass attenuation in association with interlobular thickening and intralobular lines (arrow). The results of bronchoalveolar lavage and transbronchial biopsy were nondiagnostic. (c) Photomicrograph (original magnification, x250; hematoxylin-eosin stain) of a specimen from open lung biopsy shows numerous lipid-laden macrophages that fill and distend the alveoli (arrow) and interstitium.

 
Chest radiographs are usually nonspecific, demonstrating bilateral lower-lobe air-space opacities (Fig 11a), mixed alveolar and interstitial opacities, and occasionally poorly marginated focal masslike lesions that mimic pulmonary neoplasms (28,29,34). Chest high-resolution CT usually reveals consolidation that is characteristically low in attenuation (-35 to -75 HU), indicating the presence of lipid deposition (35,36). However, exogenous lipoid pneumonia can also manifest as geographic ground-glass attenuation associated with interlobular septal thickening within areas of ground-glass attenuation (Fig 11b) (28,29). This crazy-paving pattern reflects intraalveolar and interstitial accumulation of lipid-laden macrophages and hyperplasia of type II pneumocytes in the alveolar lining (28).

Diagnosis can be difficult, since many patients do not recall a history of ingestion or inhalation of mineral oil substances. Bronchoalveolar lavage, transbronchial biopsy, or open lung biopsy combined with a history of oil ingestion and radiographic studies are usually diagnostic (28).


   Sanguineous Disorders
Top
 Abstract
 Introduction
 Infection
 Neoplasm
 Idiopathic Disorders
 Inhalational Disorders
 Sanguineous Disorders
Conclusions
 References
 
Adult Respiratory Distress Syndrome
Adult respiratory distress syndrome is a form of pulmonary edema characterized by refractory hypoxemia and respiratory distress. Numerous causes have been reported, including shock, contusion, infection, sepsis, aspiration, drug abuse, and inhalation of noxious substances (37). Diagnosis is based on impaired diffusion capacity (DLCO), reduced compliance of the lung, and typical radiologic findings.

Chest radiographs typically show bilateral homogeneous pulmonary opacities. Cardiomegaly and upper-lobe blood diversion are usually absent in these patients (38,39). High-resolution CT reveals bilateral consolidation and ground-glass attenuation (37). Other findings such as reticular and linear attenuation can be seen (Fig 12). Adult respiratory distress syndrome may progress to architectural distortion, consolidation with bronchiectasis, and honeycombing (37). Histologic features include edema of the alveoli and perivascular spaces with filling of the alveoli by a protein-rich fluid (22).



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  		Figure 12.  Adult respiratory distress syndrome in a 27-year-old man who developed barotrauma and pulmonary interstitial emphysema. High-resolution CT scan shows scattered ground-glass attenuation and thickening of the intra- and interlobular septa (crazy-paving pattern). Note the air within the areas of interlobular thickening, a finding indicative of pulmonary emphysema. (Reprinted, with permission, from reference 43.)

 
Pulmonary Hemorrhage Syndromes
Pulmonary hemorrhage syndromes include a wide spectrum of diseases, including idiopathic pulmonary hemosiderosis, Wegener granulomatosis, Churg-Strauss syndrome, Goodpasture syndrome, collagen-vascular disease (systemic lupus erythematosus [Fig 13], rheumatoid arthritis, systemic sclerosis, polymyositis, and mixed connective-tissue disease), drug-induced coagulopathy, and hemorrhage associated with malignancy (Fig 14) (40,41). Diffuse parenchymal bleeding may be secondary to either hemodynamic modifications of the capillary pulmonary blood flow or pathologic changes in the alveolar wall. Patients typically present with hemoptysis, dyspnea, and anemia (40). The diagnosis can be established by recovery of blood with bronchoalveolar lavage or evaluation of the iron content of alveolar macrophages.



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  		Figure 13a.  Acute diffuse pulmonary hemorrhage in a 53-year-old woman with systemic lupus erythematosus and massive hemoptysis. (a) High-resolution CT scan shows geographic areas of ground-glass attenuation with interlobular septal thickening. (b) Photomicrograph (original magnification, x250; hematoxylin-eosin stain) shows acute intraalveolar hemorrhage.

 


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  		Figure 13b.  Acute diffuse pulmonary hemorrhage in a 53-year-old woman with systemic lupus erythematosus and massive hemoptysis. (a) High-resolution CT scan shows geographic areas of ground-glass attenuation with interlobular septal thickening. (b) Photomicrograph (original magnification, x250; hematoxylin-eosin stain) shows acute intraalveolar hemorrhage.

 


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  		Figure 14a.  Primary lung adenocarcinoma in a 54-year-old man with hemoptysis. (a) Posteroanterior chest radiograph shows a centrally located mass adjacent to an area of diffuse ground-glass opacity in the right upper lobe. Note the air trapping in the lung base. (b) CT scan shows typical crazy-paving ground-glass attenuation associated with septal thickening surrounding the mass, which is perihilar. Adenocarcinoma with surrounding pulmonary hemorrhage was confirmed at surgery.

 


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  		Figure 14b.  Primary lung adenocarcinoma in a 54-year-old man with hemoptysis. (a) Posteroanterior chest radiograph shows a centrally located mass adjacent to an area of diffuse ground-glass opacity in the right upper lobe. Note the air trapping in the lung base. (b) CT scan shows typical crazy-paving ground-glass attenuation associated with septal thickening surrounding the mass, which is perihilar. Adenocarcinoma with surrounding pulmonary hemorrhage was confirmed at surgery.

 
Diffuse pulmonary hemorrhage occurs in up to 2% of patients with systemic lupus erythematosus, typically in the context of established disease associated with extrapulmonary manifestations such as glomerulonephritis. Forty-two percent to 66% of patients do not have hemoptysis at presentation (42). Chest radiographic and CT manifestations are symmetric acinar and ground-glass opacities or attenuation and the crazy-paving pattern (Fig 13).


   Conclusions
Top
 Abstract
 Introduction
 Infection
 Neoplasm
 Idiopathic Disorders
 Inhalational Disorders
 Sanguineous Disorders
 Conclusions
References
 
The crazy-paving pattern, characterized by scattered or diffuse ground-glass opacities or attenuation with superimposed interlobular septal thickening and intralobular lines, is a common radiologic manifestation. Often considered to have a limited differential diagnosis—pulmonary alveolar proteinosis, lipoid pneumonia, bronchioloalveolar cell malignancy—this pattern is now recognized as a CT manifestation of many diverse entities. Knowledge of the many causes of this pattern can be useful in preventing diagnostic errors. In addition, although causes of this pattern are frequently indistinguishable at radiologic evaluation, differences in the location of the characteristic opacities or attenuation in the lungs as well as presence of additional radiologic findings, together with the history and clinical presentation, can often be useful in suggesting the appropriate diagnosis.


   Footnotes
 
Abbreviations: DLCO = diffusing capacity of the lungs for carbon monoxide, NSIP = nonspecific interstitial pneumonia


   References
Top
 Abstract
 Introduction
 Infection
 Neoplasm
 Idiopathic Disorders
 Inhalational Disorders
 Sanguineous Disorders
 Conclusions
 References
 

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