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Clinical Application of High-Resolution CT in Detection and Characterization of Diffuse Lung Diseases Using 64 Multidetector CT

Dr. Mohamed N.E Kassem

By Dr. Mohamed N.E Kassem

Consultant and Lecturer of Radiology. Department of Radiology, Damietta hospital, Al-Azhar University, Egypt. Postdoctoral Fellowship in MRI Spectroscopy and PET, UCSF, USA (1995-1997). Clinical Fellowship in DIAGNOSTIC Radiology, UWO, Canada (2000-2001). Clinical Fellowship in MRS and MR perfusion, UWO, Canada (2001-2002). MD Doctorate degree and lecturer in diagnostic radiology, Al-Azhar University, Egypt (2006).


PURPOSE: The objective of this article is to identify the role of the HRCT in the detecting and characterizing different lung diseases, to identify the ability of HRCT to detect the activity of the diseases, and to localize the sites of biopsy of certain diseases.

MATERIALS AND METHODS: Three hundred and fifty patients who had HRCT findings were retrospectively reviewed.

RESULTS: All patients had abnormal findings on HRCT at presentation. The predominant HRCT findings at presentation consisted of high attenuation pattern, low attenuation pattern, reticular pattern and nodular pattern. Each category was further divided into subgroups.

CONCLUSION: HRCT is superior to conventional CT in detecting and characterizing the abnormalities caused by diffuse lung diseases. HRCT should replace the conventional CT and used as a routine exam for detection and characterization of diffuse lung diseases. HRCT has been shown to be of great value in directing biopsy to regions with the appearance of most active disease.

Key words: HRCT, high attenuation, low attenuation.


HRCT is performed in the evaluation of patients with suspected diffuse lung disease. Up to 10% of patients with interstitial lung disease may have a normal CXR. Between 20 to 30% of these individuals will be shown to have interstitial disease by HRCT. Additionally, HRCT has been shown to be of great value in directing biopsy to regions with the appearance of most active disease. HRCT provides macroscopic, not microscopic information. Findings on HRCT do however often reflect histologic appearances and distribution of disease.

Diffuse lung diseases are categorized according to HRCT findings as follows:

High Attenuation pattern:

Ground-Glass Opacity:

Ground glass opacity is defined as a region of increased lung attenuation not obscuring the underlying vessels [1]. Acute Ground glass opacity is associated with pulmonary edema, Hemorrhage, Pneumocystic pneumonia (PCP), acute interstitial pneumonia, Hypersensitivity pneumonia, and early idiopathic pulmonary fibrosis (IPF). Chronic Ground glass opacity is associated with Desquamative interstitial pneumonitis, IPF, Alveolar proteinosis, Hypersensitivity pneumonitis, Chronic Sarcoidosis, Lipoid pneumonia, and Bronchoalveolar carcinoma.


Consolidation is synonymous with airspace disease. Causes of consolidation can be pus, edema, blood or tumor cells. Even fibrosis as in UIP, NSIP and long-standing Sarcoidosis can replace the air in the alveoli and cause consolidation. Acute consolidation is seen in Pneumonias (bacterial, Mycoplasma, PCP), Pulmonary edema due to heart failure or ARDS, Hemorrhage, Acute eosinophilic pneumonia. Chronic consolidation is seen in Organizing Pneumonia, Chronic eosinophilic pneumonia, Fibrosis in UIP and NSIP, Bronchoalveolar carcinoma (BAC) or lymphoma.

Crazy Paving:

Crazy Paving is a combination of ground glass opacity with superimposed septal thickening. Crazy Paving is seen in alveolar proteinosis, Sarcoidosis, NSIP, Organizing pneumonia (COP/BOOP), Infection (PCP, viral, Mycoplasma, bacterial), Neoplasm (Bronchoalveolar carcinoma (BAC), pulmonary hemorrhage, and Edema (heart failure, ARDS, AIP).

Mosaic Attenuation with Air Trapping:

Inhomogeneous lung attenuation seen on HRCT may reflect regional differences in pulmonary blood volume, a finding termed mosaic perfusion (The dense area is normal) [2]. Mosaic perfusion may be present in patients who have airway obstruction with reflex vasoconstriction [3, 4] or in patients with vascular obstruction such as that occurring in pulmonary embolism [5].

Low Attenuation pattern:

Abnormalities that result in decreased lung attenuation or air-filled lesions include Emphysema, Bulla, Lung cysts, lymphangioleiomyomatosis (LAM), lymphocytic interstitial pneumonia (LIP), Langerhans cell histeocytosis (LCH)}, Honeycombing, and Bronchiectasis [11]. Honeycombing indicates the presence of end-stage pulmonary fibrosis and typically predominates in the peripheral and subpleural lung.

Reticular pattern:

Intralobular Interstitial Thickening:

Thickening of the intralobular interstitium produces a fine reticular or mesh-like pattern in the subpleural lung periphery. Intralobular bronchioles are often visible in patients with this type of fibrosis because of traction bronchiolectasis.

Interlobular interstitial thickening:

Smooth septal thickening is associated with pulmonary edema, Lymphangitic spread of carcinoma, lymphoma and Amyloidosis. Nodular septal thickening is associated with Lymphangitic spread of carcinoma, lymphoma, silicosis and chronic hypersensitivity pneumonitis. Irregular septal thickening is associated with asbestosis, UIP, dermatomyositis with UIP, systemic lupus erythematosis (SLE) with NSIP, scleroderma with NSIP, connective tissue disease (CTD) with NSIP or Sjogren’s syndrome with NSIP [12].

Peribronchovascular Interstitium:

The peribronchovascular interstitium appears as a thin band of low-density attenuation adjacent to the major bronchi and vessels. Diseases that spread along lymphatic channels such as lymphangitic carcinomatosis and Sarcoidosis commonly produce abnormalities of the peribronchovascular interstitium [13].

Parenchymal Bands:

The parenchymal bands are non-tapering linear densities within the lungs from 2 to 5 cm in length that are often located in the lung periphery and frequently contact the pleural surface. The bands may represent continuous thickened interlobular septa, but those that are several millimeters thick, may represent coarse scars or atelectasis.

Subpleural Lines:

A subpleural line is a thin (1-2 mm) curvilinear opacity which is less than 1 cm from the pleural surface and parallels the pleura. They represent early fibrosis with alveolar collapse. However, these lines may be seen in normal patients as a result of atelectasis within dependent lung (the abnormality disappears in these patients when placed prone).

Nodules pattern:

The distribution of pulmonary nodules on HRCT is: (1) centrilobular (including bronchiocentric and angiocentric), (2) perilymphatic, and (3) random [12].

Tree-in-bud Appearance:

On HRCT abnormal bronchioles filled with fluid, mucus, or pus can appear as centrilobular tubular, branching, or nodular structures and give “tree-in-bud” appearance. Disorders associated with a tree-in-bud appearance include infection such as endobronchial spread of mycobacterium tuberculosis (classically), atypical mycobacterial infection, as well as bacterial, viral, or fungal infection [13].

The aim of this article is to compare HRCT with other diagnostic techniques, summarize its clinical usefulness in patients with diffuse lung disease. The clinical value of HRCT is assessed in terms of its ability to detect diffuse lung disease; its accuracy in the differential diagnosis; and when biopsy is required, its ability to determine the optimal type and site of lung biopsy.

Materials and Methods

The study included 350 patients with chest complaint from Damietta city and surrounding cities who underwent HRCT (from January 2018 until January 2020) as part of the clinical evaluation in the outpatients (n = 210) or inpatients (n = 140). Table 1 shows that the Patients were grouped according to clinical diagnosis, age, sex, stage of presentation and predominant HRCT findings. The patients included 215 men and 135 women (age range, 25–82 years; mean, 53.5 years; median, 44 years), all patients had chest complaints such as (cough, shortness of breath, difficulty breathing, or hypoxia) and most of them lived in rural areas.

Chest radiographs were obtained using conventional radiography. HRCT was performed on a Philips Brilliance 64-channel scanner. The scans were obtained while the patient in supine position at end inspiration using slice thickness 1.00 mm, scan mode helical, tube voltage 120 kV, tube current automatic, filter L. The images were obtained on lung (window width, 1,000–1,500 H; level, –700 H) and mediastinal (window width, 350 H; level, 35–40 H) settings.

The HRCT scans obtained were reviewed and compared with previous radiographs and conventional CT independently and in random order and reached a decision by consensus. The HRCT scans, the radiographs and the conventional CT were assessed for the presence and distribution of abnormalities such as ground-glass opacities, consolidation, nodular opacities, septal lines, and reticular opacities and for the presence of associated hilar, mediastinal, or pleural abnormalities. Ground-glass opacities were defined as hazy areas of increased attenuation without obscuration of the underlying vessels. Consolidation was defined as homogeneous opacification of the parenchyma with obscuration of the underlying vessels. Reticular opacities were defined as linear opacities forming a mesh like pattern. Nodular opacities were defined as focal round opacities. The predominant patterns of abnormality on HRCT were classified into ground-glass opacities, consolidation, reticular opacities, or nodular opacities.

The distribution was categorized as focal, patchy, and diffuse. Focal was defined as a single focus of abnormality, patchy as more than one focus, and diffuse if bilateral and involving the equivalent of the volume of one or both lungs. Predominant distribution was also assessed as being in the upper, middle, or lower lung zones, in random, central, or peripheral (outer third of the lungs) location.

Data Analysis For data analysis, the confidence level was scored by measurement of the distance from the left end of the line to the marked point and converting the measurement to a scale from 0 to 100.


All HRCT scans were interpreted retrospectively as abnormal. The predominant HRCT findings consisted of three hundred and fifty cases. The predominant findings were classified into four categories (Fig. 1, 2); high attenuation pattern (n = 120 cases), low attenuation pattern (n = 70 cases), reticular pattern (n = 60 cases) and nodular pattern (n = 100 cases). A mixed pattern denoted a combination of ground-glass opacities, consolidation, reticulation and nodules. Each category was further divided into subgroups.

The high attenuation pattern was subdivided into ground-glass opacities (n = 25), areas of consolidation (n = 50), mixture of ground-glass and consolidation (n = 15), crazy-paving appearance (n = 10) and mosaic appearance (n = 20). The low attenuation pattern was subdivided into emphysema (n = 12), bulla (n = 4), cyst (n = 8), honeycombing (n = 20) and bronchiectasis (n = 26). The reticular pattern was subdivided into smooth (interlobular or intralobular) septal thickening (n = 14), nodular (interlobular or intralobular) septal thickening (n = 18) and irregular (interlobular or intralobular) septal thickening (n = 28). The nodular pattern was subdivided into perilymphatic (n = 9), centrilobular (n = 59), random (n = 22) and tree-in-bud appearance (n = 10).

Some of these abnormalities were predominately or exclusively involved in the upper lung zones, the middle lung zones, or the lower lung zones. Some patients had a predominantly subpleural distribution, while others had either a patchy random distribution or diffuse abnormalities. In addition, some of the cases had associated ancillary findings such as pleural effusion, lymphadenopathy and pneumothorax.

High Attenuation pattern

One-hundred and twenty patients had increased lung attenuation; 25 of them had ground-glass appearance, 50 had consolidation, 15 had mixture of ground-glass and consolidation, 10 had crazy-paving and 20 had mosaic appearance. We call ground-glass-opacity (GGO) if there is a hazy increase in lung opacity without obscuration of underlying vessels and we call consolidation if the increase in lung opacity obscures the vessels. In both ground glass and consolidation, the increase in lung density is the result of replacement of air in the alveoli by fluid, cells or fibrosis. In GGO the density of the intrabronchial air appears darker as the air in the surrounding alveoli. This is called the ‘dark bronchus’ sign. In consolidation, there is exclusively air left intrabronchial. This is called the ‘air bronchogram.

Thirty-six patients with predominant ground-glass abnormalities were classified according to patient’s history into acute (n = 18) or chronic (n = 18) ground glass opacity. The acute ground glass opacity consisted of pulmonary edema caused by heart failure (n = 2) (Fig. 3) or ARDS (n = 1) (Fig. 4), pulmonary hemorrhage (n = 2) (Fig. 5), viral pneumonia (n = 4) (Fig. 6), Mycoplasma pneumonia (n = 4), and Acute hypersensitivity pneumonitis (n = 5). The chronic ground glass opacity consisted of organizing pneumonia (BOOP) (n = 3), (Fig. 7, 8), Nonspecific interstitial pneumonia (NSIP), (n = 6), Diffuse interstitial pneumonia (DIP), (n = 5) and bronchoalveolar carcinoma (BAC) (n = 4).

Forty-five patients with predominant consolidation abnormalities were classified according to patient’s history into acute (n = 31) or chronic (n = 14) consolidation. The acute consolidation consisted of bacterial pneumonias (n = 13), Mycoplasma pneumonias (n = 10), Pulmonary edema caused by heart failure (n = 4) or ARDS (n = 2), and Hemorrhage (n = 2). The chronic consolidation (n = 14) consisted of Organizing Pneumonia (n = 6), Bronchoalveolar carcinoma (BAC) (n = 3) (Fig. 9) and lymphoma (n = 5). A mixed pattern of ground-glass and consolidation abnormalities were noted (n = 9) in patients with eosinophilic pneumonia either acute (n = 3) or chronic (n = 6) stages (Fig. 10).

Ten patients had Crazy Paving, which is a combination of ground glass opacity with superimposed septal thickening. Two had alveolar proteinosis (Fig. 11), 3 had NSIP, 1 had Organizing pneumonia (COP/BOOP), 3 had Mycoplasma pneumonia, and 1 had Bronchoalveolar carcinoma (BAC).

Twenty patients had mosaic attenuation (patchy areas of black and white lung). Five patients had severe asthma (Fig. 12). Four patients had hyperperfused lung adjacent to oligemic lung due to chronic thromboembolic disease (Fig. 13). Eleven patients

had normal lung appearing relatively dense adjacent to lung with air-trapping. Eight of these patients had respiratory bronchiolitis (Fig. 14) and 3 had bronchiolitis secondary to Rheumatoid arthritis.

We used two diagnostic hints for differentiation: First we looked at the vessels size in the lucent area and the high attenuated area. If the vessels sizes were the same in the ‘black’ lung and ‘white’ lung, then the patient had infiltrative lung disease. If the vessels were difficult to see in the ‘black’ lung as compared to the ‘white’ lung, then the ‘black’ lung was abnormal, and two possibilities were considered: either obstructive bronchiolitis or chronic pulmonary embolism (Fig. 13). Second, we looked at expiratory scans for air trapping.

Seventy patients had low attenuation abnormalities. The hypoattenuated abnormalities consisted of panlobular (n = 3) or centrilobular (n = 9) emphysema, bilateral bullas (n = 4), bilateral cysts (n = 8), bilateral honeycombing (n = 20) and bronchiectasis (n = 26).

The panlobular emphysema consisted of alpha-1 antitrypsin deficiency syndrome (n = 1), (Fig.15) and Sawyer’s James syndrome (n = 2) or centrilobular emphysema caused by COPD (n = 9), (Fig.16). The bulla abnormalities consisted of Marfan’s syndrome (n = 4). The cystic abnormalities consisted of lymphangioleiomyomatosis (LAM) (n = 1), (Fig.17), Lymphocytic interstitial pneumonia (LIP) (n = 3), (Fig.18), Langerhans cell histiocytosis LCH (n = 4). The honeycombing was a feature of usual interstitial pneumonia (UIP) (n = 4), (Fig.19), asbestosis (n = 2), (Fig. 20), RA (n = 5), (Fig. 21), scleroderma (n = 3), (Fig. 22), Sjogren’s syndrome (n = 1), (Fig. 23), and Systemic lupus erythematosis (SLE) (n = 5), (Fig. 24). The honeycombing represents reticular pattern recognizable on HRCT. Because of the cystic appearance, honeycombing is also discussed as low attenuation pattern. Bronchiectasis consisted of ciliary dyskinesia (n = 3), (Fig. 25), NSIP (n = 4), (Fig. 26), Hypersensitivity pneumonitis (n = 2), Tuberculosis (n = 5), Allergic bronchopulmonary Aspergilosis (n = 10), Cystic fibrosis (n = 2) (Fig. 27).

Sixty patients had reticular pattern (thickening of the interlobular septa). The reticular pattern consisted of Smooth septal thickening (n = 14), nodular septal thickening (n = 18) and irregular septal thickening (n = 28). The smooth septal thickening consisted of interstitial pulmonary edema (n = 7), lymphangitic spread of carcinoma (n = 4), (Fig. 28), and lymphoma (n = 3), (Fig. 29). The nodular septal thickening consisted of silicosis (n = 7), chronic hypersensitivity pneumonitis (n = 4), lymphangitic spread of carcinoma (n = 3), and lymphoma (n = 4). The irregular septal thickening consisted of Asbestosis (n = 4), Usual interstitial pneumonia (UIP) (n = 4), (Fig. 30), Dermatomyositis with (UIP) (n = 2), (Fig. 31), Systemic lupus erythematosus with (NSIP) (n = 4), (Fig. 30), Scleroderma with (NSIP) (n = 5), (Fig. 33), CTD with (NSIP) (n = 7), (Fig. 34), Sjogren’s syndrome with (NSIP) (n = 2), (Fig. 35).

One-hundred patients had nodular pattern. The nodules were placed into one of four categories: perilymphatic (nodules seen in relation to pleural surfaces, interlobular septa and the peribronchovascular interstitium, (n = 9), centrilobular (nodules are limited to the centrilobular region and centered 5-10 mm from fissures or the pleural surface, (n = 59), random distribution (no preference for a specific location in the secondary lobule and involve the pleural surfaces and fissures, but lack the subpleural predominance, (n = 22), and tree-in-bud appearance (n = 10).

The perilymphatic nodular pattern consisted of sarcoidosis (n = 2), (Fig. 36), lymphangitic spread of carcinoma (n = 3) and silicosis (n = 4), (Fig. 37). The centrilobular nodular pattern consisted of Subacute hypersensitivity pneumonitis (n = 6), (Fig. 38), Respiratory bronchiolitis-interstitial lung disease (RB – ILD) (n = 9), (Fig. 39), respiratory bronchiolitis with infection (n = 24), Diffuse interstitial pneumonia (DIP) (n = 8) and tuberculosis (n = 12), (Fig. 40). The random nodular pattern consisted of hematogenous metastasis (n = 10), (Fig. 41), military tuberculosis (n = 9), (Fig. 42), and Langerhans cell histeocytosis (n = 3). The Tree-in-bud appearance consisted of active TB (n = 4), (Fig. 43), and viral (H-influenzae) pneumonia (n = 6).

The location of the abnormalities in ground glass pattern or consolidation was helpful in narrowing the differential diagnosis. Upper zone predominance: PCP. Lower zone predominance: UIP, NSIP or DIP. Centrilobular distribution: Hypersensitivity pneumonitis.


The evidence from the various studies indicates that HRCT can play a major role in the assessment of diffuse lung diseases. In our study, we included 350 patients. The evidence in the literature currently suggests that HRCT can be helpful and is indicated clinically (1) in patients with signs and symptoms suggestive of diffuse lung disease but normal or nonspecific findings on conventional radiography, (2) in patients in whom the radiographic findings or the results of pulmonary function tests are not in keeping with the clinical history or symptoms, (3) before lung biopsy as a guide to the optimal type and site of biopsy in patients with infiltrative lung disease, and (4) in patients with infiltrative lung disease in whom complications (e.g., infection) are suspected. Because of the inherent nature of HRCT and low doses of radiation we support routine complete HRCT examination of the lungs without conventional CT.

High Attenuation pattern

We found that with complete HRCT scans, diagnostic accuracy comparable to that of a limited HRCT with complete conventional CT scanning can be achieved. Surprisingly, the complete HRCT did significantly improve the diagnostic accuracy. Our results found that HRCT detects early pneumonia than chest radiograph or conventional CT. These results confirmed by Claus Peter Heussel et al [17] who found that thin-section CT enables detection of an additional 20% of microbiologically proven pneumonias and allows pneumonia to be detected about 5 days earlier than when chest radiographs are used exclusively. This means that a thin-section CT study with normal findings excludes the presence of pulmonary infection in the majority of cases.

N L Muller, et al [19] stated that High-resolution CT allows confident diagnosis of UIP in most cases. The remaining idiopathic interstitial pneumonias have nonspecific CT findings. The results of this study proved that HRCT is superior to the conventional CT in detecting early changes of pulmonary hemorrhage. These findings were confirmed by the results of Steven et al [21], who stated that diffuse pulmonary hemorrhage (DPH) is characterized by anemia and diffuse air-space consolidation.

Masanori Akira, et al [22] stated that HRCT was more sensitive and more accurate than plain radiography and conventional CT in the evaluation of parenchymal abnormalities in summer-type hypersensitivity pneumonitis. In this study, we found that HRCT may be more useful than conventional radiography, not only in the differential diagnosis but also in the evaluation of responses to therapy or provocation tests.

J. Michael Holbert, ea al [24] stated that patients with pulmonary alveolar proteinosis present with a combination of ground-glass and interlobular opacities, often in a crazy paving pattern with geographic involvement.

Christoph Engelke, et al [30] proved that using inspiratory and expiratory HRCT with contrast is superior to conventional CT in detection of pulmonary embolism and parenchymal changes resulted from it.

Low Attenuation pattern

W. Richard Webb, et al [32] stated that HRCT can reveal morphologic abnormalities associated with obstructive lung disease with a greater accuracy than plain radiographs. In our study, we found that HRCT is more sensitive than radiographs in showing emphysema, large airways abnormalities such as bronchiectasis, and small airways abnormalities such as bronchiolectasis and the tree-in-bud appearance.

Reticular pattern

H. M. Fenlon, et al [37] addressed HRCT findings in patients with ankylosing spondylitis, which revealed a spectrum of pulmonary abnormalities unlike that found on plain chest radiographs alone. This spectrum included nonapical ILD, Bronchiectasis, tracheobronchomegaly, and mediastinal lymphadenopathy, in addition to the well-documented association with apical fibrosis. Our results confirmed presence of ILD in the apical segments in all patients with ankylosing spondylitis.

Jean M. SeeIy, et al [38] showed that HRCT is much more sensitive than chest radiography for the detection of interstitial lung disease in systemic scleroderma patients and should be considered in the initial assessment. Our data reinforce the concept that alveolitis may be a prominent feature in young patients in early stages of disease and suggest that early treatment and recognition of disease may be beneficial in preventing irreversible disease.

H. M. Fenlon, et al [39] stated that HRCT findings in SLE show that airways disease, lymphadenopathy, and interstitial lung disease are common thoracic manifestations of SLE, whereas pleural abnormalities are less common than previously suggested. In 21 % of our patients, HRCT showed definitive evidence of interstitial lung disease despite a normal chest radiograph and uncertain pulmonary function results.

Nodular pattern

In our study, in which HRCT and the conventional CT scans were analyzed separately, it was clear that, although small nodular opacities are easier to distinguish from vessels on the conventional CT scans, they are clearly identified on the HRCT scans also. This is an agreement with recent studies that show that HRCT scans can be used to identify clearly and characterize small nodular opacities in sarcoidosis [41] and various pneumoconioses [42].


Ground-glass opacity is nonspecific, but highly significant finding since 60-80% of patients with ground-glass opacity on HRCT have an active and potentially treatable lung disease. In the other 20-40% of the cases the lung disease is not treatable, and the ground-glass pattern is the result of fibrosis. In those cases there are usually associated HRCT findings of fibrosis, such as traction bronchiectasis and honeycombing.

HRCT has greater spatial resolution and thus allows better assessment of parenchymal detail than does conventional CT. The greater confidence in making a specific diagnosis in patients with chronic infiltrative lung disease in the present study was due to the greater ease in identifying interlobular septal thickening in lymphangitic carcinomatosis. The results of our study show that HRCH should replace conventional CT for all patients with chronic infiltrative lung disease.

We conclude that in most patients with acute or chronic diffuse infiltrative lung disease, the correct diagnosis can be made by obtaining complete HRCT scans without obtaining conventional CT. It allows pneumonia to be detected about 5 days earlier than when chest radiographs are used exclusively.

Therefore, unless there is a suspicion of primary or metastatic neoplasm, we recommend that HRCT at 10-mm intervals be performed in the initial evaluation of patients under 40 years old, while men 40 years or older and women 50 years or older, particularly those presenting with severe recurrent respiratory infections or hemoptysis, should undergo MDCT in the evaluation of suspected bronchiectasis.

For further research, pooling of data is necessary to adequately determine the natural history of malignancies diagnosed in these solid nodules and in their more detailed subtypes.


We thank all radiology technicians for collection of data.


Table 1: Patients were grouped according to clinical diagnosis, age, sex, stage of presentation and predominant HRCT findings.

Clinical diagnosis
Patient No.
Stage of presentation
Predominant HRCT findings
Pulmonary edema 2                      4                    20 Acute GG                       Consolidation                                  regular reticular pattern
Acute respiratory distress syndrome (ARDS) 1 Acute GG
  2 Chronic Consolidation
Hemorrhage due to MCA 2 Acute GG
Hemorrhage due to Wegener’s disease 2 Chronic Consolidation
Viral pneumonia 4 Acute GG
Bacterial pneumonia 15 Acute Consolidation
Mycoplasma pneumonia 11             4                       3 Acute Chronic Chronic GG Consolidation                                      Crazy-paving
Hypersensitivity pneumonitis 2             3                         5                      6 Chronic Chronic Chronic GG                                      honeycombing                               Bronchiectasis               centrilobular nodules
 Brochiolitis obliterance with organizing pneumonia (BOOP) 3            6                       1 Chronic Chronic Chronic GG
Lung fibrosis (usual interstitial pneumonia, UIP) 4                  4              2                    13 Chronic Chronic Chronic Chronic GG                            Consolidation       honeycombing                                     Bronchiectasis
Bronchalveolar carcinoma (BAC) 2            3                       1 Chronic Chronic Chronic GG                        Consolidation                                      Crazy paving
Lymphoma 5              13                     5 Chronic Chronic Chronic Consolidation
regular reticular pattern
irregular reticular pattern
Eosinophilic pneumonia 5                    10 Acute    Chronic Mixed
Pulmonary alveolar proteinosis (PAP) 2 Chronic Crazy paving
Lung fibrosis (nonspecific interstitial pneumonitis, NSIP) 3 Chronic Crazy paving
Asthma 5 Chronic Mosaic with air-trapping
Respiratory bronchiolitis 4                    40 Chronic Mosaic with air-trapping centrilobular nodules
Rheumatoid arthritis bronchiolitis 3                      4 Chronic Chronic Mosaic with air-trapping honeycombing
Thromboembolic disease 8 Chronic Mosaic without air-trapping
Alpha-one antitrypsin deficiency 1 Chronic Panlobular emphysema
Swyer-james syndrome 2 Chronic Panlobular emphysema
 Chronic obstructive pulmonary disease (COPD, cigarette smoking) 9 Chronic centrilobular emphysema
Marfan’s syndrome 4 Chronic Bulla
Lymphangioleiomyomatosis (LAM) 3 Chronic cyst
Lymphomatous interstitial pneumonitis (LIP) 2 Chronic cyst
Langerhans cell histeocytosis (LCH) 3                      3 Chronic Chronic cyst                                            random nodules
Scleroderma 3 Chronic honeycombing
Drug reaction 3 Chronic honeycombing
Asbestosis 5 Chronic honeycombing
Sarcoidosis 2                      2 Chronic      Chronic Bronchiectasis                      perilymphatic nodules
Allergic bronchopulmonary Aspergilosis (ABPA) 4 Chronic Bronchiectasis
Cystic fibrosis 2 Chronic Bronchiectasis
Lymphangitic carcinomatosis 4            3                      3 regular reticular pattern              irregular reticular pattern perilymphatic nodules
Silicosis 15                    4 irregular reticular pattern perilymphatic nodules
Tuberculosis (TB) 13                    9 centrilobular nodules                        random nodules
Hematogenous Metastasis 10 random nodules
Fungal infection, miliary pattern 10 random nodules


Figure 1: The predominant HRCT findings at presentation consisted of high attenuation pattern (n = 120 cases), low attenuation pattern (n = 70 cases), reticular pattern (n = 60 cases) and nodular pattern (n = 100 cases). Each category was further divided into subgroups. The high attenuation pattern was subdivided into ground-glass opacities (n = 36), areas of consolidation (n = 45), crazy-paving appearance (n = 10) and mosaic appearance (n = 20). The low attenuation pattern was subdivided into emphysema (n = 12), bulla (n = 4), cyst (n = 8), honeycombing (n = 20) and bronchiectasis (n = 26). The reticular pattern was subdivided into smooth (interlobular or intralobular) septal thickening (n = 14), nodular (interlobular or intralobular) septal thickening (n = 18) and irregular (interlobular or intralobular) septal thickening (n = 28). The nodular pattern was subdivided into perilymphatic (n = 9), centrilobular (n = 59), random (n = 22) and tree-in-bud (n = 22).

Figure 2: The percentage of HRCT findings at presentation consisted of high attenuation pattern (n = 120 cases, 34%), low attenuation pattern (n = 70 cases, 20%), reticular pattern (n = 60 cases, 17%) and nodular pattern (n = 100 cases, 29%).

Fig. 3. A 71-year-old woman with fluid overload and cardiac failure. HRCT scan shows bat wing alveolar edema with a central distribution and sparing of the lung cortex.

Fig. 4A. A 47-year-old man with severe acute respiratory syndrome. HRCT scan shows focal ground-glass opacities in right upper lobe.
Fig. 4B. HRCT scan obtained 12 h later on same day as A shows mixed pattern that includes ground-glass opacities, band like areas of consolidation, and reticulation in right upper lobe.

Note cephalic displacement of minor fissure (straight arrows) and anterior displacement of major fissure (curved arrow), consistent with volume loss.

Fig. 5. A 27 year old woman with no history of previous diseases or smoking reported cough and hemoptysis beginning 48 hours prior to hospital admission. HRCT scan shows mixed and diffuse infiltrate, primarily in the lower lobes. Bronchofiberoscopy showed presence of blood along the entire respiratory tract also the bronchial lavage was hemorrhagic indicating acute pulmonary hemorrhage.

Fig. 6. A 46-year-old man with dyspnea. He had influenza for one week. HRCT scan shows diffuse ground-glass attenuation with some irregular linear areas of increased attenuation in both lungs indicating Pneumonia due to influenza virus.
Fig. 7. A 51-year-old man with cough. HRCT scan shows subpleural, patchy consolidations with air bronchograms. Patchy areas of ground-glass are also seen. Peribronchial thickening. Lung biopsy proved bronchiolitis obliterans organizing pneumonia.
Fig. 8. A 49-year-old man was receiving sulfasalazine for treatment of ulcerative colitis for a long period. HRCT scan shows subpleural, patchy consolidations with air bronchograms. Patchy areas of ground-glass are also seen. Peribronchial thickening.  Lung biopsy proved bronchiolitis obliterans organizing pneumonia. Sulfasalazine can result in BOOP.
Fig. 9. A 42-year-old man with dyspnea. HRCT scan shows multiple poorly marginated lung nodules, some of which appear cavitary. The findings mimic a pulmonary infectious process. Lung biopsy proved bronchoalveolar carcinoma.


Fig. 10. A 49-year-old man was receiving amiodarone over 3 months. HRCT scan shows patchy ground-glass opacities with consolidations and thin intralobular reticulations. These radiological abnormalities have been decreased after cessation of amiodarone and corticotherapy.
Fig. 11. A 38-year-old man presenting with worsening dyspnea on exertion. HRCT scan shows widespread bilateral ground-glass opacities with superimposed interlobular opacities giving crazy paving appearance (a characteristic appearance of pulmonary alveolar proteinosis).
Fig. 12. A 55-year-old woman with a history of asthma. A, Inspiratory HRCT scan at lung base shows no abnormalities. B, Expiratory HRCT scan at same level as A shows patchy areas of low attenuation due to air trapping.
Fig. 13 A. A 66-year-old man presented with acute shortness of breath. HRCT scan shows clot (arrowhead) in posterior segmental arteries of right upper lobe.


Fig.13 B. Inspiratory HRCT scan shows inhomogeneous lung attenuation (arrows) in both upper lobes. Vessel size in lower attenuation areas is reduced, thus indicating mosaic perfusion as possible cause of inhomogeneous lung attenuation.


Fig. 13 C. Expiratory HRCT scan obtained at same level as B shows air trapping associated with mosaic perfusion in both upper lobes. Air trapping in left upper lobe closely corresponds to area of low attenuation seen on inspiratory scan (B). In right upper lobe, area of air trapping appears larger than area of mosaic perfusion seen on inspiratory scan.
Fig. 14. A 29-year-old male smoker. A, HRCT scan obtained through upper lobes with patient supine shows patchy, ground glass opacities in the RT lung. B, HRCT scan obtained with patient prone shows small centrilobular opacities (curved arrows) scattered throughout lung in a nonuniform distribution.

Biopsy was performed and proved respiratory bronchiolitis.

Fig.15. A 40-year-old woman presented with alpha1-antiprotease deficiency and worsening dyspnea on exertion. HRCT scan shows diffuse low attenuation and thinned out vascular structures in both lungs indicating panlobular emphysema.
Fig. 16. A 67-year-old man with a long history of cigarette smoking and worsening cough. HRCT scan shows bilateral upper lobes multiple well-defined, confluent lucencies (white arrows), most without defined margins, which are surrounded by patchy areas of more normal-appearing parenchyma (black arrows) indicating centrilobular emphysema.
Fig. 17. A 40- year-old woman with Lymphangioleiomyomatosis and a 10-year history of dyspnea dating back to her first pregnancy. HRCT scan shows bulla-like cysts with diffuse bilateral cystic lucencies in the lower lungs with smooth, thin walls. There are no pleural effusions.


Fig. 18. A 60-year-old woman with LIP caused by Sjögren syndrome. HRCT scan obtained with patient prone shows diffuse ground-glass opacification and multiple lung cysts (arrows).
Fig. 19. A 43-year-old man with severe shortness of breath. HRCT scan shows subpleural cystic change. The reticulated shadowing with septal thickening, subpulmonary lines and subpulmonary cystic change. The findings are characteristic of UIP
Fig. 20. A 60-year-old man with history of an asbestos exposure complains of dyspnea. HRCT scan shows subpleural honeycombing (open arrows), interlobular septal thickening (solid arrows), and subpleural nodular opacities (arrowheads). These findings suggesting asbestosis.
Fig. 21. A 33-year-old woman with a long history of Rheumatoid arthritis and cough. HRCT scan shows honeycombing and reticulation predominantly in the lung periphery indicating pulmonary fibrosis.
Fig. 22. A 34-year-old woman with a long history of scleroderma and cough. HRCT scan shows patchy areas of diffuse honeycombing at the lung bases.
Fig. 23. A 31-year-old woman with a long history of Sjögren syndrome and cough. HRCT scan shows subpleural ground-glass attenuation, irregular linear hyperattenuating areas, and honeycombing. Traction bronchiectasis is also visible (arrows).
Fig. 24. A 26-year-old woman with a long history of SLE and cough. HRCT scan shows subpleural honeycombing, irregular linear hyperattenuating areas, and ground-glass attenuation in the basal areas of both lungs.
Fig. 25. A 43-year-old woman with primary ciliary dyskinesia. HRCT scan shows bronchiectasis distributed in typical pattern in the lower lobes. Peribronchial consolidation and collapse are evident in left lower lobe.


Fig. 26. A 61 year-old man with NSIP presented with dyspnea.  HRCT scan shows bilateral subpleural reticulation, traction bronchiectasis (curved arrow), and honeycombing (straight arrows).
Fig. 27. A 43 year-old man with a history of productive cough, fevers, shortness of breath since infancy, history of diarrhea and weight loss for several years and Insulin Dependent Diabetes.  HRCT scan shows tram tracking bronchiectasis, Peribronchial cuffing and nodules.
Fig. 28. A 42-year-old woman with a history of breast cancer. HRCT scan shows nodular interlobular septal thickening in both lungs with peribronchovascular thickening and minor fissure thickening indicating lymphangitic spread of breast cancer.


Fig. 29. A 37-year-old woman with non-Hodgkin’s lymphoma who developed adenovirus pneumonia 1 year after allogeneic peripheral blood stem cell transplantation. HRCT scan shows extensive and patchy ground-glass opacities (arrows) associated with interlobular septal thickening (arrowheads) and intralobular linear opacities in both upper lobes, forming crazy paving appearance. A small amount of left pleural effusion is also noted.
Fig. 30. A 60 year old woman with a chronic respiratory condition. HRCT scan shows reticulated shadowing with subpleural septal thickening, and subpleural cystic change (honeycombing). This disease heterogeneity is typical of usual interstitial pneumonia (UIP).
Fig. 31. A 64-year-old woman with Dermatomyositis presenting with dyspnea. HRCT scan shows patchy areas of ground-glass attenuation and irregular linear hyperattenuating areas with random distribution in both lungs.
Fig. 32. A 57-year-old woman with Systemic lupus erythematosis. HRCT scan shows ground-glass attenuation and irregular linear hyperattenuating areas in the subpleural areas of both lower lung zones, as well as traction bronchiectasis.


Fig. 33. A 49-year-old woman with Progressive systemic sclerosis presenting with dyspnea. HRCT shows patchy areas of ground-glass attenuation, irregular linear hyperattenuating areas, and traction bronchiectasis.


Fig. 34. A 54-year-old woman with Mixed connective tissue disease presenting with dyspnea. HRCT subpleural areas of ground-glass attenuation, irregular linear hyperattenuating areas, and traction bronchiectasis and bronchiolectasis.
Fig. 35. A 30-year-old woman with Sjögren syndrome presenting with dyspnea. HRCT scan obtained at the level of the lower lobar bronchus shows subpleural ground-glass attenuation, irregular linear hyperattenuating areas, and honeycombing. Traction bronchiectasis.
Fig. 36. A 40 year-old woman with erythema nodosurn, fever, and Polyarthropathy. HRCT scan shows dense peribronchovascular nodularity with fibrosis and traction bronchiectasis.


Fig. 37. A 54-year-old man who worked for 20 years as a stonecutter. HRCT shows multiple small nodules with similar shape and attenuation throughout the upper lobes of both lungs.


Fig. 38. A 38-year-old woman with progressive dyspnea. She had recently acquired several birds as pets. HRCT shows extensive bilateral diffuse, poorly defined centrilobular nodular areas of ground glass opacification. Hypersensitivity pneumonitis (subacute stage) was suspected. The patient sold her birds and her symptoms resolved following a course of corticosteroids.
Fig. 39. A 41-year-old man with 30 pack-year history of cigarette smoking. HRCT scan shows widespread ground-glass opacification, with some poorly defined centrilobular nodules (arrowheads).


Fig. 40. A 25-year-old man presented with cough, fever and weight loss.  HRCT scan shows foci of nodular lesions markedly variable in size in anterior segment of upper lobe of right lung and superior segment of lower lobe of left lung. Lesions consist of branching linear structures (arrowheads), 2-3- mm poorly defined centrilobular peribronchiolar nodules (straight arrows), 4-10-mm acinar shadows (curved arrows), and larger lobular consolidation.
Fig. 41. A 59-year-old woman had had a thyroid malignancy treated with surgical excision and radioactive iodine.  HRCT scan shows innumerable miliary metastases scattered throughout both lungs.
Fig. 42.  A 50-year-old man with a history of fever, weight loss and shortness of breath. HRCT shows uniform-sized small nodules randomly distributed throughout both lungs. Note subpleural and subfissural nodules (arrows).
Fig. 43. A 18-year-old man with active tuberculosis.  HRCT scan shows severe changes of bronchiolar dilatation and impaction. Tree-in-bud pattern is seen in right lower lobe (arrow) and represents endobronchial spread of tuberculosis. Direct signs of bronchiolar involvement are also seen in left upper and lower lobes.



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