Farthmann E H, Schöffel U
Chirurgische Universitätsklinik, Universität Freiburg, Germany.
Infection. 1998 Sep-Oct;26(5):329-34. doi: 10.1007/BF02962266.
Intraabdominal infection continues to be one of the major challenges in general surgery. Whilst the term "peritonitis" means an inflammation of the peritoneum regardless of its etiology, intraabdominal infections encompass all forms of bacterial peritonitis, of intraabdominal abscesses and of infections of intraabdominal organs. Several classification systems have been suggested for peritonitis and intraabdominal infections, respectively. However, neither phenomenological classifications nor classification systems with respect to the origin of bacterial contamination have a proven relevance for the clinical course of this disease. Moreover, most of the studies dealing with secondary peritonitis or intraabdominal infections are ill-comparable because of wide variations of inclusion criteria. Thus the true incidence of secondary bacterial peritonitis is difficult to assess. With respect to its etiology perforation of hollow viscus is the leading cause followed by postoperative peritonitis, ischemic damage of bowel wall, infection of intraabdominal organs and translocation in nonbacterial peritonitis. The anatomic origin of bacterial contamination and microbiological findings are no major predictors of outcome. However, the preoperative physiological derangement, the surgical clearance of the infectious focus and the response to treatment are established prognostic factors. The pathogenesis of intraabdominal infections is determined by bacterial factors which influence the transition from contamination to infection. Intraabdominal adjuvants and the local host response are additionally important. Bacterial stimuli lead to an almost uniform activation response which is triggered by reaction of mesothelial cells and interspersed peritoneal macrophages and which also involves plasmatic systems, endothelial cells and extra- and intravascular leukocytes. The local consequences of this activation are the transmigration of granulocytes from peritoneal capillaries to the mesothelial surface and a dilatation of peritoneal blood vessels resulting in enhanced permeability, peritoneal edema and lastly the formation of protein-rich peritoneal exudate.
腹腔内感染仍然是普通外科的主要挑战之一。虽然“腹膜炎”一词意味着无论病因如何，腹膜都会发生炎症，但腹腔内感染涵盖了所有形式的细菌性腹膜炎、腹腔内脓肿以及腹腔内器官感染。针对腹膜炎和腹腔内感染，分别提出了几种分类系统。然而，无论是现象学分类还是基于细菌污染来源的分类系统，都未被证明与该疾病的临床病程相关。此外，由于纳入标准差异很大，大多数关于继发性腹膜炎或腹腔内感染的研究难以进行比较。因此，继发性细菌性腹膜炎的真实发病率难以评估。就其病因而言，中空脏器穿孔是主要原因，其次是术后腹膜炎、肠壁缺血性损伤、腹腔内器官感染以及非细菌性腹膜炎中的细菌移位。细菌污染的解剖学来源和微生物学发现并非预后的主要预测因素。然而，术前的生理紊乱、感染灶的手术清除以及对治疗的反应是已确定的预后因素。腹腔内感染的发病机制由影响从污染到感染转变的细菌因素决定。腹腔内佐剂和局部宿主反应也很重要。细菌刺激会引发几乎一致的激活反应，这种反应由间皮细胞和散在的腹膜巨噬细胞的反应触发，还涉及血浆系统、内皮细胞以及血管外和血管内白细胞。这种激活的局部后果是粒细胞从腹膜毛细血管迁移到间皮表面，以及腹膜血管扩张，导致通透性增强、腹膜水肿，最终形成富含蛋白质的腹膜渗出液。
