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Histopathological changes of organ dysfunction in sepsis
Intensive Care Medicine Experimental Pub Date : 2019-07-01 , DOI: 10.1186/s40635-019-0236-3
Antonio M Garofalo 1, 2 , Marta Lorente-Ros 3 , Gesly Goncalvez 1 , Demetrio Carriedo 1 , Aída Ballén-Barragán 1 , Ana Villar-Fernández 1 , Óscar Peñuelas 1, 4 , Raquel Herrero 1, 4 , Rosario Granados-Carreño 1, 2 , José A Lorente 1, 2, 4
Affiliation  

Sepsis is a highly lethal disorder. Organ dysfunction in sepsis is not defined as a clinicopathological entity but rather by changes in clinical, physiological, or biochemical parameters. Pathogenesis and specific treatment of organ dysfunction in sepsis are unknown. The study of the histopathological correlate of organ dysfunction in sepsis will help understand its pathogenesis. We searched in PubMed, EMBASE, and Scielo for original articles on kidney, brain, and liver dysfunction in human sepsis. A defined search strategy was designed, and pertinent articles that addressed the histopathological changes in sepsis were retrieved for review. Only studies considered relevant in the field were discussed. Studies on acute kidney injury (AKI) in sepsis reveal that acute tubular necrosis is less prevalent than other changes, indicating that kidney hypoperfusion is not the predominant pathogenetic mechanism of sepsis-induced AKI. Other more predominant histopathological changes are apoptosis, interstitial inflammation, and, to a lesser extent, thrombosis. Brain pathological findings include white matter hemorrhage and hypercoagulability, microabscess formation, central pontine myelinolysis, multifocal necrotizing leukoencephalopathy, metabolic changes, ischemic changes, and apoptosis. Liver pathology in sepsis includes steatosis, cholangiolitis and intrahepatic cholestasis, periportal inflammation, and apoptosis. There is no information on physiological or biochemical biomarkers of the histopathological findings. Histopathological studies may provide important information for a better understanding of the pathogenesis of organ dysfunction in sepsis and for the design of potentially effective therapies. There is a lack of clinically available biomarkers for the identification of organ dysfunction as defined by the histological analysis.

中文翻译:

脓毒症器官功能障碍的组织病理学变化

败血症是一种高度致命的疾病。脓毒症的器官功能障碍并不被定义为临床病理学实体,而是通过临床、生理或生化参数的变化来定义。脓毒症器官功能障碍的发病机制和具体治疗尚不清楚。研究脓毒症器官功能障碍的组织病理学相关性将有助于了解其发病机制。我们在 PubMed、EMBASE 和 Scielo 中搜索了有关人类脓毒症肾、脑和肝功能障碍的原始文章。设计了明确的搜索策略,并检索了解决脓毒症组织病理学变化的相关文章以供审查。仅讨论了被认为与该领域相关的研究。对脓毒症中急性肾损伤(AKI)的研究表明,急性肾小管坏死比其他变化较少发生,表明肾脏灌注不足并不是脓毒症诱发 AKI 的主要发病机制。其他更主要的组织病理学变化是细胞凋亡、间质炎症,以及较小程度的血栓形成。脑病理结果包括白质出血和高凝状态、微脓肿形成、脑桥中央髓鞘溶解、多灶性坏死性白质脑病、代谢变化、缺血性变化和细胞凋亡。脓毒症的肝脏病理包括脂肪变性、胆管炎和肝内胆汁淤积、门静脉周围炎症和细胞凋亡。没有关于组织病理学结果的生理或生化生物标志物的信息。组织病理学研究可能为更好地了解脓毒症器官功能障碍的发病机制和设计潜在有效的疗法提供重要信息。缺乏临床上可用的生物标志物来识别组织学分析所定义的器官功能障碍。
更新日期:2019-07-01
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