Harley R A
Department of Pathology, Medical University of South Carolina, Charleston 29425.
Semin Respir Infect. 1988 Dec;3(4):291-7.
The pleura is protected by several tissue boundaries of differing degrees of strength. Penetration of the pleural space by mediastinal infection occurs more easily than from the lung, which in turn occurs more easily than through the diaphragm or chest wall. Infectious organisms of all classes, including bacteria, viruses, fungi, and protozoa are capable of causing pleural infection. The basic tissue response in the pleura is similar to that seen in other tissues but is modified by the peculiar anatomy of the pleura, flat serosal surfaces in constant motion against each other. Most pleural infections are initiated in the lung. Some of the most spectacular pathologic lesions are caused by aspergillus where vasculoinvasive fungi cause infected infarcts that result in round visceral pleural lesions. These in turn result in "kissing lesions" of the parietal diaphragmatic surfaces which are of the same size and shape as the visceral pleural lesions, indicating attachment and splinting of the pleural surfaces in these loci. Studies in rabbit demonstrate rapid resolution of experimental empyema with a standardized series of pathologic responses. In uncomplicated empyema, the end result is an extremely thin, almost undetectable scar. Thick fibrotic pleural lesions suggest a complicated course with continuing infection.
胸膜受到几种强度不同的组织边界的保护。纵隔感染穿透胸膜腔比肺部感染更容易发生，而肺部感染又比通过膈肌或胸壁感染更容易发生。包括细菌、病毒、真菌和原生动物在内的各类感染性生物体都能够引起胸膜感染。胸膜的基本组织反应与其他组织相似，但会因胸膜独特的解剖结构而有所改变，即扁平的浆膜表面相互不断摩擦。大多数胸膜感染始于肺部。一些最引人注目的病理病变是由曲霉菌引起的，血管侵袭性真菌导致感染性梗死，进而形成圆形的脏层胸膜病变。这些病变继而导致膈胸膜表面出现“亲吻病变”，其大小和形状与脏层胸膜病变相同，表明这些部位的胸膜表面相互附着并固定在一起。对兔子的研究表明，标准化的一系列病理反应可使实验性脓胸迅速消退。在无并发症的脓胸中，最终结果是形成极其薄的、几乎难以察觉的瘢痕。厚的纤维化胸膜病变提示病程复杂且存在持续感染。
