[Abstract] Objective To investigate the CT features of diffuse ground glass shadow as the main manifestation of pulmonary diseases, and to improve the diagnosis and differential diagnosis of this type of pulmonary diseases. Methods We reviewed and analyzed the CT, HRCT and clinical data of 121 cases with diffuse ground glass shadow as the main manifestation of pulmonary diseases, summarized their respective CT features, and sought the CT and HRCT signs with diagnostic and differential diagnostic values. Among the 121 cases, 18 cases of interstitial pneumonia and 5 cases of connective tissue disease were found to have abnormal lung structure, and the ground glass shadows were mainly distributed in the peripheral parts of the middle and lower lungs, and all of them were accompanied by interstitial thickening and fibrosis signs. The diseases with predominantly abnormal lung cavity inflation status were allergic pneumonia in 10 cases, pulmonary hemorrhage in 5 cases, pulmonary metastases in 3 cases and alveolar carcinoma in 2 cases, and the ground glass shadows were distributed according to lobes and lung segments with or without central lobular nodules, alveolar nodules or mass lesions. Pulmonary edema had a tendency to be distributed along the hypophysis and could be accompanied by enlarged cardiac shadow and pleural effusion, while pulmonary contusion had a tendency to be distributed along the hypophysis in the lung of the trauma area. The diseases with predominantly abnormal blood perfusion were pulmonary embolism in 11 cases and Leukocyte’s syndrome in 4 cases. The ground glass shadow was located in the high perfusion zone to which the normal vessels belonged, while the low density zone was the low perfusion zone to which the embolized vessels belonged, and multiple fine vessel embolism or multiple fine arteritis could form a mosaic-like density. Chronic obstructive pulmonary disease is caused by ventilation-blood flow disorders, and its ground glass shadow and hypointense area form mosaic-like changes, often accompanied by barrel-shaped chest; while alveolar protein deposition and viral pneumonia have both airspace and intrinsic lung structure abnormalities In contrast, alveolar protein deposition and viral pneumonia have both airspace and intrinsic lung structure abnormalities, and their ground glass shadow is the result of a combination of interstitial and substantive lesions. Conclusion Diffuse ground glass shadow in both lungs is seen in many diseases, through the analysis of its morphology, distribution, concomitant signs and dynamic changes of the disease, the pathological basis and pathogenesis of its occurrence can be initially understood, and the scope of the proposed diagnosis can be narrowed down by combining with clinical practice. Lei Zhidan, Department of Radiology, Henan Provincial People’s Hospital
[Keywords] Lung disease; ground-glass shadow; body layer photography, X-ray computer
Ground-glass opacity (GGO) is a CT sign that can occur in a variety of lung diseases, and is divided into two categories: limited and diffuse. The imaging significance of GGO and its relationship with disease diagnosis have been repeatedly reported in the domestic literature [1-4], but the pathogenesis and pathological basis of diffuse ground-glass opacity (DGGO) in the lung have not been discussed in the literature. We collected a total of 121 cases of diffuse ground-glass opacity (DGGO) in 5 categories and 13 types of pulmonary diseases with pathological confirmation and clinical diagnosis in the past 6 years from January 2001 to December 2006, and analyzed their CT, HRCT and clinical data to investigate the pathogenesis and CT characteristics of DGGO, in order to improve the diagnosis and differential diagnosis of this type of disease.
1 Data and methods
1.1 General data 121 patients with DGGO, 83 males and 38 females, aged 19-73 years old, average 47 years old. 121 patients had varying degrees of dyspnea and restrictive ventilatory dysfunction. (1) 23 cases of diseases with predominantly abnormal lung intrinsic structures: mainly including 18 cases of interstitial pneumonia and 5 cases of connective tissue disease; all 18 cases of interstitial pneumonia were confirmed by open lung biopsy, 13 cases of common interstitial pneumonia (UIP), 4 cases of nonspecific interstitial pneumonia (NSIP), and 1 case of acute interstitial pneumonia (AIP), all with varying degrees of cough, dyspnea, Velcro All five cases of connective tissue disease had more typical symptoms, signs and pulmonary function abnormalities. Two cases of desiccation syndrome were confirmed by labial gland biopsy, two cases of rheumatic pneumonia were confirmed by serological CCP examination, and one case of scleroderma was confirmed by skin biopsy. ②20 cases of diseases with abnormal lung cavity inflation status: all had dyspnea and abnormal lung function, 10 cases of allergic pneumonia were comprehensively diagnosed by serology and treatment, 5 cases of pulmonary hemorrhage were confirmed by history of typical hemoptysis and improvement of hemostatic treatment, 3 cases of pulmonary metastases and 2 cases of alveolar carcinoma were confirmed based on medical history and bronchoscopic biopsy. (iii) 26 cases of diseases with predominantly increased extravascular fluid volume in the lung: 21 cases of pulmonary edema and 5 cases of pulmonary contusion. 21 patients with pulmonary edema were confirmed to have cardiac or renal insufficiency and the DGGO disappeared after improvement of cardiac or renal function; 5 patients with pulmonary contusion had DGGO related to the site of trauma and the lesions disappeared after short-term treatment. ④15 cases of diseases with predominantly abnormal blood perfusion: 11 cases of pulmonary embolism all had typical history, symptoms, signs and abnormal pulmonary function, and all cases were confirmed by CTPA; 4 cases of leukoaraiosis syndrome all had typical symptoms and signs in the oral cavity, genitalia, eyes and lungs, and 2 cases were examined by CTPA. ⑤ Thirty-seven cases of diseases with two or more abnormal factors, 25 cases of chronic obstructive pulmonary disease all had a typical history of chronic bronchitis; among the 7 cases of alveolar protein deposition, 5 cases were confirmed by positive PAS of bronchial lavage fluid and 2 cases by open lung biopsy; 5 cases of viral pneumonia were diagnosed comprehensively based on history, symptoms, signs, treatment and serology.
1.2 Examination methods All patients in this group had chest X-ray plain film and routine CT examination, 67 had HRCT examination, 11 cases of pulmonary embolism and 2 cases of Leukocyte’s syndrome had CTPA examination, and 83 patients had chest plain film or/and CT review data after 1~3 treatments. Chest radiographs were conventional or CR or DR chest films. CT scans were performed with the company’s Light Speed Plus 4 multi-layer spiral CT machine. The layer thickness was 7.5 mm, the pitch factor was 1.5:1, the reconstruction interval was 5 mm, the standard algorithm reconstruction, the matrix was 512×512, the range was from the entrance of the thorax to the base of the lung, and the lung window and the mediastinal window were used. 59 cases of conventional high-resolution CT scans and 8 cases of volumetric reconstructed high-resolution CT (VHRCT) were used for HRCT examination, the layer thickness of conventional HRCT was 1.25 mm, the layer pitch was 10 mm, and the bone algorithm image was 10 mm. The layer thickness of conventional HRCT was 1.25 mm, the layer pitch was 10 mm, and the image was reconstructed by bone algorithm from the level of the aortic arch to the diaphragm and observed by the lung window; the layer thickness of VHRCT scan was 2.5 mm, the pitch factor was 3:1, and the thin layer was decomposed into 1.25 mm layer thickness and reconstruction interval, and reconstructed by bone algorithm image and observed by the lung window; the layer thickness of CTPA scan was 2.5 mm, the pitch factor was 3:1, and the thin layer was decomposed into 1.25 mm layer thickness and reconstruction interval The contrast agent was iohexol or Uvexan (300 mg I/ml) 100 ml, administered through an elbow vein with a high pressure syringe at a flow rate of 3.0 ml/s and a scan delay time of 18-22 s. The scan area was from 2 cm above the diaphragm to 2 cm above the aortic arch. , maximum density projection (MIP), surface masking method (SSD), volume reproduction (VR), and vascular endoscopy (VE).
1.3 Analysis methods GGO is a lung shadow with mildly increased lung density without obscuring the pulmonary vessels and bronchi [1. 2], and the author refers to lesions involving both lungs or more than two lobes of one lung as DGGO, and to lesions distributed far from the bronchovascular bundle and in the dirty subpleural area as peripheral distribution, while those distributed along the bronchovascular bundle as central distribution or medial distribution. Those with lesions located in the inner zone around the pulmonary hilum on chest radiographs were referred to as central distribution, while those with lesions mainly in the outer zone were referred to as peripheral distribution. For the analysis, two radiologists who both had extensive experience in chest radiology and were unaware of the diagnostic results first analyzed the chest films, CT and HRCT data of 121 patients, summarized the respective imaging features and classified them according to five pathogenic mechanisms, and then three physicians compared the pathology, CTPA and clinical data with the above imaging features and classification to explore the CT diagnosis and differential diagnosis of DGGO diagnostic value.
2 Results
2.1 Types and distribution of DGGO The 121 cases of DGGO were classified into 5 major categories with a total of 13 pulmonary diseases, namely: 23 cases of diseases with abnormalities in the intrinsic lung structure, including 18 cases of interstitial pneumonia and 5 cases of connective tissue disease; 20 cases of diseases with abnormalities in the inflation status of pulmonary air cavities, including 10 cases of allergic pneumonia, 5 cases of pulmonary hemorrhage, 3 cases of pulmonary metastases and 2 cases of alveolar carcinoma; 26 cases of diseases with extravasation in the lung There were 26 cases of diseases with mainly increased volume of body fluid, including 21 cases of pulmonary edema and 5 cases of pulmonary contusion; 15 cases of diseases with mainly abnormal blood perfusion, which were 11 cases of pulmonary embolism and 4 cases of Leukocyte’s syndrome; 37 cases of diseases with abnormalities of two or more factors, which were 25 cases of chronic obstructive pulmonary disease, 7 cases of alveolar protein deposition and 5 cases of viral pneumonia. All of the DGGO in this group were distributed in more than two lung lobes, and the distribution of each type of disease had certain characteristics, and the distribution characteristics in both lungs and each lung lobe are shown in Table 1.
Table 1 Types and distribution of DGGO in 121 cases (cases)
Classification Number of cases Bilateral lungs One lung Peripheral part Central part Both peripheral central involvement
Abnormal lung intrinsic structure 23 21 2 23 7 7
Abnormal air cavity inflation status 20 19 1 13 20 13
Increased extravascular body fluid volume 26 23 3 26 26 26
Abnormal blood perfusion 15 13 2 15 4 4
Abnormalities of two or more factors 37 37 – 34 8 5
2.2 Imaging characteristics and concomitant signs of DGGO ① Among the 18 cases of interstitial pneumonia (Figure 1), 15 cases of DGGO were distributed in the peripheral parts of the bilateral lower and middle lungs, 3 cases had both central and peripheral distribution but the peripheral parts were still predominant, 18 cases were accompanied by reticular shadows, lobular septal thickening and distended bronchial dilatation, 13 cases were accompanied by foveal shadows, 1 case was seen with pneumothorax; 2 cases of rheumatic pneumonia showed Two cases of rheumatic pneumonia showed bilateral DGGO in the lower and middle lungs with alveolar nodules, lobular shadows, lung segmental shadows, reticular shadows and interstitial fibrosis; two cases of desiccation syndrome (Figure 2) and one case of scleroderma had DGGO distributed in the center and periphery of the lobes of the lower and middle lungs, but the peripheral part was still predominant, along with marked interstitial fibrosis and mild distension of the bronchioles. (2) Ten cases of allergic pneumonia (Figure 3a,b) showed DGGO distributed in the center and periphery of the lung lobes, but predominantly in the center, with scattered lobular central nodules and alveolar nodules within the GGO, with blurred nodule margins and variable morphology and location of the GGO; five cases of pulmonary hemorrhage (Figure 4a,b) showed DGGO distributed mainly around the bronchovascular bundles with blurred margins, without interstitial thickening and Three cases of pulmonary metastases (Figure 5) showed scattered nodules and masses in both lungs with blurred margins and non-lobular lamellar GGO around them; two cases of alveolar carcinoma (Figure 6) showed DGGO mainly in the center of the lobes of the middle and lower lungs on the peg side, with more corn nodules and lobular center nodules in the GGO and enlarged hilar and mediastinal lymph nodes. (iii) 21 cases of pulmonary edema (Figure 7a,b), all of which showed bilateral pulmonary DGGO with a gradual increase in shadow density from top to bottom and from anterior to posterior, solid shadows in the dorsal and posterior segments of the lower lobes in 8 cases, mild thickening of pulmonary vessels in 19 cases, a small amount of bilateral pleural effusion in 18 cases, enlarged cardiac shadow in 17 cases, and normal cardiac shadow with thickening of large vessels in 4 cases; 5 cases of pulmonary contusion (Figure 8) had DGGO distributed in the injured area, and 3 In 5 cases of pulmonary contusion (Figure 8), the DGGO was distributed in the injured area, and in 3 cases, a top-to-bottom and anterior-to-posterior density change was formed locally, pleural effusion was seen in 3 cases and rib fracture was seen in 1 case. In 11 cases of pulmonary embolism (Figure 9a,b), the DGGO showed mosaic-like changes in 7 cases, and in 4 cases of trunk and lobe pulmonary artery embolism, the DGGO was located in the lobe to which the unembolized pulmonary artery belonged, while the embolized lobe showed hypodensity. The DGGO of 4 cases of Leukocerebrok’s syndrome (Figure 10a,b) also showed mosaic-like changes, small and medium-sized pulmonary arteries in 3 cases showed aneurysm formation of various sizes, and 1 case showed irregular thinning of the pulmonary artery. In 25 cases of chronic obstructive pulmonary disease, the DGGO density was lower than that of other diseases and showed mosaic-like changes. 25 cases had obvious signs of emphysema and 17 cases had signs of pulmonary heart disease (Figure 11). In five cases of viral pneumonia, the DGGO showed a central and peripheral distribution, while all five cases showed different degrees of interstitial thickening and fibrosis, three cases showed central lobular nodules within the GGO, and two cases showed “tree bud signs” scattered along the central lobules (Figure 13).
2.3 Dynamic changes of DGGO Among the 83 cases reviewed, 9 cases of interstitial pneumonia, after comprehensive treatment with pirfenidone and hormone, the reticular shadow and surrounding DGGO of UIP basically disappeared in 6 cases, but the foveal shadow and its surrounding ground glass shadow still existed, and only a little striated shadow remained in 3 cases of NSIP; 2 cases of dry syndrome and 2 cases of rheumatic pneumonia also remained only fibrous striated shadow after treatment. 8 cases The DGGO disappeared after hormone treatment in 8 cases of allergic pneumonia and after hemostatic treatment in 5 cases of pulmonary hemorrhage. 21 cases of pulmonary edema were treated with cardiac and diuretic therapy, and the DGGO was rapidly absorbed as cardiac and renal function improved. 5 cases of pulmonary contusion were treated with hemostatic therapy and short-term absorption. 11 cases of pulmonary embolism and 4 cases of Leukocyte’s syndrome were treated with thrombolytic therapy, and the DGGO was gradually absorbed. 10 cases of chronic obstructive pulmonary disease were treated with anti-infection and respiratory training. In 10 cases of chronic obstructive pulmonary disease, after anti-infection, respiratory training and other treatments, the change of DGGO was not obvious; in 3 cases of alveolar protein deposition, after bronchopulmonary lavage and other comprehensive treatments, the lung DGGO gradually decreased; in 3 cases of viral pneumonia, after hormone and antiviral drugs and other comprehensive treatments, the DGGO disappeared and only a little fibrous streak shadow remained.
3 Discussion
3.1 Mechanism of lung density alteration Lung density is composed of four factors: the density of air spaces in the lung, the density of intrinsic lung tissue, the amount of extravascular body fluid in the lung, and pulmonary blood volume. Thus, any disease that causes changes in these factors will definitely cause changes in lung density, but most commonly, lung diseases cause changes in air cavity density, intra-pulmonary extravascular fluid volume and blood volume, which are the basic pathological basis of lung density changes [5. 6]. And all the four factors mentioned above are altered to varying degrees by the diseases in this group respectively, which leads to the formation of DGGO.
3.2 Imaging features, concomitant signs and formation mechanisms of DGGO He Wen classified the main etiologies of GGO into three major categories: interstitial diseases, substantial diseases and ventilation-blood flow disorders [2], which play a positive role in the diagnosis and differential diagnosis of pulmonary GGO to a greater extent. However, based on the distribution and imaging characteristics of our group with DGGO as the main manifestation of lung diseases, there are still 2 major categories of diseases that cannot be explained by the above etiology. In order to comprehensively discuss the formation mechanism of DGGO, we believe that we should argue from 5 major categories of diseases based on the 4 factors that lead to increased lung density. (1) In 18 cases of interstitial pneumonia and 5 cases of connective tissue disease in our group, the DGGO was distributed in the peripheral part or predominantly in the peripheral part of the middle and lower lungs, and thus this type of DGGO was mainly distributed around the interstitium and was accompanied by thickening, fibrosis and even honeycomb formation of the interstitium, so that the formation of the DGGO was related to interstitial inflammation. Interstitial inflammation results in interstitial inflammatory exudate and interstitial fibrosis, and the exudate causes an increase in interstitial density and widening of the diameter, while it can enter the alveolar cavity and form a partial filling of the air cavity, while both interstitial thickening and fibrosis can cause deformation and destruction of the intrinsic lung structure and an increase in the density of the intrinsic lung tissue, and the deformation and destruction of the intrinsic lung structure can lead to a change in the inflation status of the air cavity. lead to a mild increase in lung density thus forming a GGO, which produces a DGGO of the lung due to the more extensive occurrence of the lesion [7. 8]. (ii) Ten cases of allergic pneumonia and five cases of pulmonary hemorrhage showed predominantly central DGGO without significant interstitial thickening or fibrosis, and scattered lobular central nodules and alveolar nodules were seen within the GGO of allergic pneumonia, thus the DGGO was the result of diffuse partial filling of air spaces with exudate or blood resulting in a mild increase in lung density [1. 9]; the DGGO of three cases of pulmonary metastases was the result of tumor hemorrhage, The DGGO of three cases of pulmonary metastases was formed by partial filling of the mass margins and surrounding air spaces by tumor hemorrhage, mucus secretion, and secondary infection [6]; two cases of alveolar carcinoma showed bilateral DGGO in the middle and lower lungs, mainly in the center of the lobes, with more corn nodules, lobular center nodules, and enlarged hilar and mediastinal lymph nodes in the GGO, so the DGGO was a result of partial filling of the alveolar cavity with cancer cells and mucus and dissemination, as well as secondary hemorrhage and inflammatory exudate [10]. related [10]. (iii) Twenty-one cases of pulmonary edema showed DGGO in both lungs, with a gradual increase in shadow density from top to bottom and from front to back, accompanied by solid shadows in the dorsal and posterior segments of the lower lobes, thickened pulmonary vessels, enlarged cardiac shadow, or thickened large vessels, indicating that the increase in extravascular fluid due to cardiac and renal insufficiency and other etiological factors was distributed in the interstitial and alveolar cavities, and accumulated diffusely along the inferior air spaces due to gravity. The typical distribution of DGGO along the hypoplasia was also formed due to extensive partial filling of the airspace [11]; 5 cases of pulmonary contusion DGGO were distributed in the injured region, and again the mechanism of their formation was the result of extensive partial filling of the airspace in the region with exudate or leaky fluid from the injured region [12]. ④ Among the 11 pulmonary embolisms, 7 cases of DGGO showed mosaic-like changes as a result of inhomogeneous perfusion of pulmonary blood, i.e., increased pulmonary blood volume in the high perfusion zone resulted in a mild increase in lung density in this zone, and decreased pulmonary blood volume in the low perfusion zone resulted in a decrease in lung density, and an extensive mosaic of the two densities formed to produce mosaic-like changes [5. 13], and 4 cases of trunk and lobe pulmonary artery embolism had DGGO located in the lobe to which the unembolized pulmonary artery belonged The DGGO in the four cases of Leukocerebrokia syndrome also showed mosaic-like changes due to the redistribution of reduced blood from the embolized area to the lobe of the unembolized pulmonary artery, resulting in an increase in blood volume in this area and a corresponding increase in lung density; the DGGO in the four cases of Leukocerebrokia syndrome also showed mosaic-like changes due to the uneven perfusion of pulmonary blood caused by extensive small and medium-sized arteritis [5]. ⑤ The DGGO of 25 cases of COPD showed mosaic-like changes due to extensive uneven perfusion of pulmonary air and blood caused by two factors of ventilation-blood flow disorders [2. 5 ]; the map-like distribution and “paving stone” changes in the DGGO of 7 cases of alveolar protein deposition were due to the presence of phospholipid-rich The DGGO of the air spaces is confined by the thickened interstitium and mixed with normal lung parenchyma or compensatory emphysema to form typical imaging changes, thus the DGGO is the result of extensive partial and heterogeneous filling of the air spaces with surface active substances and interstitial thickening resulting in structural changes of the lung [5.14] In five cases of viral pneumonia, the DGGO was centrally and peripherally distributed, with varying degrees of interstitial thickening and fibrosis, central lobular nodules, and scattered “bud signs” along the center of the lobules, and the DGGO was the result of extensive interstitial thickening, small airway obstruction, and partial filling of air spaces [15. 16].
3.3 Dynamic characteristics of DGGO changes Among the 83 cases reviewed after treatment, the foveal shadow and the surrounding ground glass shadow of UIP persisted in 6 cases and the DGGO of COPD did not change significantly in 10 cases, suggesting that the destruction of lung structures due to fovea and the obstruction of ventilation and blood flow due to COPD are irreversible damages and the resulting GGO is not easily absorbed. In the remaining 67 cases of pulmonary disease, the lung density returned to normal after treatment, when the bleeding stopped, interstitial and alveolar inflammation disappeared, perfusion returned to normal, the amount of extravascular body fluid in the lung returned to normal due to normal cardiac and renal function, and the filling in the airspace disappeared, so the factors producing DGGO disappeared.
3.4 Diagnostic and differential diagnosis of DGGO Based on the mechanism of DGGO formation, the author believes that the diagnostic and differential diagnosis of DGGO should be combined with the morphology, distribution, accompanying signs, dynamic changes of lesions and clinical data. When DGGO is distributed along the peripheral part of the lung with interstitial thickening and fibrosis, it can be considered as a disease causing structural changes in the lung, such as interstitial pneumonia and connective tissue disease, which often has more obvious pulling bronchial dilatation and honeycomb shadow, while honeycomb shadow in connective tissue disease is uncommon and often accompanied by alveolar nodules, lobular shadow, lung segment shadow and serological abnormalities. When the distribution of DGGO is central or predominantly central, with lobar central nodules and alveolar nodules, substantive diseases with predominantly air-filled lungs, such as allergic pneumonia, pulmonary hemorrhage, alveolar carcinoma, and transbronchial metastases, should be considered. Allergic pneumonia may be accompanied by pleural effusion and eosinophilia, and pulmonary hemorrhage is often associated with hemoptysis. When DGGO shows a top-down, anterior-to-posterior gradient curve, it should be considered as pulmonary edema, pulmonary contusion, and other diseases that cause increased extravascular fluid volume. When DGGO presents with mild hyperdensity in one or more lobes of the lung and decreased density in the rest of the lung, with or without enlargement of the main pulmonary artery and right heart, a lobar or one-sided pulmonary artery embolism should be considered. When DGGO shows mosaic-like changes, it should be considered as segmental and subsegmental pulmonary embolism, chronic obstructive pulmonary disease, and alveolar protein deposition. DGGO with alveolar protein deposition often presents with a typical map-like distribution and typical “pavement”-like changes. Viral pneumonia, especially cytomegalovirus pneumonia, should be considered when DGGO is associated with central lobular nodules, alveolar nodules, lobular shadows, positive “buds” and more extensive interstitial fibrosis without foveal shadowing [15. 16].
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