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Self-assessment CME RadioGraphic 自我评价式继续医学教育读物 · 第363期 · 接 · 第351期 ·  Small Airways Disease Small airways are defined as noncartilaginous airways with an internal diameter of less than 2 mm and are located from approximately the eighth generation of airways down to the terminal bronchioles (smallest airways without alveoli) and respiratory bronchioles (airways distal to terminal bronchioles that partake in gas exchange) (12). In normal patients, these small airways are not visible on CT due to their small size (13). However, in certain instances, these small airways may become visible due to underlying disease. Numerous classification systems have been used to describe small airways diseases based on clinical, imaging, and histologic findings. On a practical basis, small airways disease can be classified as a primary bronchiolar disorder, which includes constrictive bronchiolitis, cellular bronchiolitis, diffuse panbronchiolitis, respiratory bronchiolitis, mineral dust airways disease, and follicular bronchiolitis; bronchiolar involvement in diffuse interstitial lung disease, such as hypersensitivity pneumonitis; and bronchiolar involvement in large airways disease, such as bronchiectasis or asthma (1) (Table 1). Table 1: Classification of Bronchiolar Disorders 小气道解剖结构 Terminal bronchus = 终末支气管 Bronchilole = 细支气管 Terminal bronchiole = 终末细支气管 Respiratory bronchiole = 呼吸性细支气管 Alweolar duct = 肺泡管 Atrium = 房 Alveolus = 肺泡 Alveolar sac = 肺泡囊 alveolar duct = 肺泡管 ciliated cell=纤毛细胞 serous secretion = 浆液分泌 clara cell = 非纤毛上皮细胞（克拉细胞） smooth muscle = 平滑肌 basement membrane =基底膜 interstitium = 间质 Type I pneumocyte = I 型肺泡上皮细胞 Type II pneumocyte = II型肺泡上皮细胞 free alveolar macrophage = 自由肺泡巨噬细胞 小气道病变 小气道的定义是指内径小于2mm的无软骨结构的气道，约从气道的第八级分支到终末细支气管（不带肺泡的最小的气道）和呼吸性细支气管（终末细支气管的远端，参加气体交换）。在正常人，因结构太小而不能在CT上显示。但是，在一定的条件下，这些小气道由于其基础病变而变得可见。 根据临床，影像学和组织学发现，对小气道病变的分类方法很多。从临床出发，小气道疾病可以分为原发的细支气管病变，包括缩窄性细支气管炎，细胞性细支气管炎，弥漫性泛细支气管炎，呼吸性细支气管炎，矿物尘气道疾病，以及滤泡性细支气管炎；弥漫性间质性肺病变累及细支气管，如过敏性肺炎；以及大气道疾病累及细支气管，如支气管扩张或哮喘（表1）。 表1: 细支气管病变分类
Inflammatory small airways disease can be categorized by the underlying pathologic process. Causes of small airways inflammation are many and include infection (cellular bronchiolitis), cigarette smoking (respiratory bronchiolitis), inhalation of organic or inorganic antigens (hypersensitivity pneumonitis or mineral dust airways disease), and lymphoid hyperplasia (follicular bronchiolitis) (10,14–17). Although small airway inflammation can lead to permanent obstruction of the small airways, it is often a reversible process. In contrast, the submucosal and peribronchiolar fibrosis of constrictive bronchiolitis leads to irreversible obstruction of the small airways (Table 2) (18). Inflammation and/or constriction or obliteration of the small airways is a common pathologic process and leads to both direct and indirect signs of the underlying disease state (Fig 4) (19). Table 2: Causes of Constrictive Bronchiolitis 炎症性小气道疾病可根据其基础的病理过程进行归类。小气道炎症的原因有很多，且包括感染性（细胞性细支气管炎），吸烟（呼吸性细支气管炎），吸入有机物或无机物（过敏性肺炎或矿物尘气道疾病），以及淋巴增生（滤泡性细支气管炎）。虽然小气道炎症会导致小气道的永久性阻塞，但这个过程常常是可逆的。 相反，缩窄性细支气管炎，因粘膜下和细支气管周围纤维化，却向小气道不可逆性阻塞发展（表2）。小气道的炎症和/或缩窄或比赛是常见的病理过程，并导致出现基础疾病的直接和间接征象（图4）。 表2.缩窄性细支气管炎的原因
图4. Selected pathologic features of small airway obstruction that can lead to mosaic attenuation on CT/ 小气道阻塞的病理征象，在CT上可以引起马赛克征 (a) Photomicrograph from a patient with constrictive bronchiolitis shows obliteration of a small airway due to fibrous tissue (arrows). The adjacent pulmonary artery is normal (*). (Original magnification, ×100; hematoxylin-eosin [H-E] stain.) 缩窄性细支气管炎患者的病理图片，显示小气道因纤维组织（箭）而致闭塞。邻近的肺动脉正常（*）（放大倍数×100，HE染色） (b) Photomicrograph from a patient with severe asthma shows a membranous bronchiole with hypertrophy of the smooth muscle layer (*) and a few scattered eosinophils (arrows). L = lumen. (Original magnification, ×120; H-E stain.) 严重哮喘患者的病理图片，显示细支气管粘膜呈平滑肌层增生（*），并有少数散在的嗜酸性粒细胞（箭）。L=管腔 （放大倍数×120，HE染色）
(c) Photomicrograph from a patient with hypersensitivity pneumonitis shows airway-centered chronic interstitial inflammation with narrowing of the airway lumen (arrows) due to submucosal expansion by the chronic inflammatory infiltrates (*). (Original magnification, ×100; H-E stain.) 过敏性肺炎患者的病理图片，显示以气道为中心的慢性间质性炎症伴有气道管腔狭窄（箭），后者由慢性炎症浸润（*）在粘膜下蔓延所致。（放大倍数×100，HE染色） Pulmonary Vascular Disease Primary pulmonary vascular disease results in mosaic attenuation due to regional differences in lung perfusion. Mosaic attenuation is most commonly seen in association with pulmonary hypertension, which will lead to enlargement of the pulmonary trunk and remodeling of the right heart, including right ventricular enlargement and hypertrophy (20). Although any cause of pulmonary hypertension can lead to mosaic attenuation, chronic thromboembolic pulmonary hypertension (CTEPH) and primary pulmonary arterial hypertension (PAH) (previously referred to as primary pulmonary hypertension), are the most common vascular causes of this finding (3). However, mosaicism can also be seen in patients with pulmonary hypertension due to long-standing cardiac shunts (21). Pulmonary hypertension due to left heart disease or lung disease and/or hypoxia are less likely causes of a mosaic pattern (21). These can usually be identified at imaging by the presence of ancillary findings (eg, dilated left heart; septal thickening; presence of severe emphysema or fibrosis). Pulmonary veno-occlusive disease (PVOD) and pulmonary capillary hemangiomatosis (PCH) can also lead to mosaic attenuation but are rare and are associated with additional parenchymal findings (discussed later). Vasculitis can also lead to mosaic attenuation, but this is often due to increased ground-glass opacity from areas of pulmonary hemorrhage and is also discussed separately (22). 肺血管性疾病 原发性肺血管病引起马赛克改变是由于在不同的区域间肺的灌注有差别。马赛克征最常见于伴有肺动脉高压者，肺动脉高压导致肺动脉干的增粗和右心的形态重构，包括右心室增大和肥厚。虽然任何导致肺动脉高压的原因都可引起马赛克征，但慢性血栓栓塞性肺动脉高压（CTEPH）和原发性肺动脉高压（PAH，以前称原发性肺高压），是马赛克征最常见的血管性病因。 然而，马赛克征也可见于因长期心脏分流产生肺高压的患者。因左心疾病或肺疾病以及/或低氧血症而导致肺高压者多不是出现马赛克征的原因。这些疾病常可在影像学上借助辅助征象进行甄别（如，左心扩张，间隔增厚，出现严重的肺气肿或纤维化等）。 肺静脉阻塞性疾病（PVOD）和肺毛细血管多发血管瘤病（PCH）也可导致马赛克征，但较罕见，且伴有其他的实质性表现（后述）。血管炎也可引起马赛克征，但更多是由于肺出血的病变区使磨玻璃影增多所致，这点也将分别论述。 Ground-Glass Opacity At CT, ground-glass opacity occurs when there is increased lung attenuation through which the underlying airway and vessels remain visible (23). Diffuse ground-glass opacity is a nonspecific finding with numerous causes (Table 3). In many cases, it may be easy to distinguish the abnormally high-attenuation lung from normal surrounding lung parenchyma, but in other cases differentiation of normal lower-attenuation parenchyma from increased ground-glass opacity can be difficult. However, there are certain findings (discussed later) that can help differentiate between the different causes and narrow the differential diagnosis. Table 3: Causes of Mosaic Attenuation Due to Diffuse Ground-Glass Opacity
磨玻璃密度 在CT上，当肺的密度增加，但透过增加的密度其内的气道和血管影依然可见，则称为磨玻璃密度。弥漫性磨玻璃密度是一种非特异性表现，可由多种原因引起（表3）。在很多情况下，被正常肺包围的异常高密度影更容易被发现，但在某些情况下，在密度较高的磨玻璃影中指出正常而密度较低的肺实质会出现困难。但无论如何，有一些征象（后述）有助于对不同病因进行鉴别，有助于缩小鉴别诊断的范围。 |
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