Abstract
Study ObjectivesTo evaluate sepsis-associated encephalopathy (SAE) research and to quantitatively and qualitatively predict research hot spots using bibliometric analysis.MethodsWe extracted relevant publications from the Web of Science Core Collection on July 28, 2021. We investigated the retrieved data by bibliometric analysis (e.g. co-cited and cluster analysis, keyword co-occurrence) using the software CiteSpace and VOSviewer, the Online Analysis Platform of Literature Metrology (http://bibliometric.com/) and Bibliometrix to analyse and predict the trends and hot spots in this field.Main ResultsWe identified 1,582 published articles and reviews on SAE from 2001 to 2021. During this period, the number of manuscripts on SAE increased steadily and peaked in 2021. The USA and China were the leading countries that had a critical impact on SAE research. Among all institutions, Vanderbilt University and Pittsburgh University held leading positions and became central in the collaboration network. Among all the journals, Critical Care Medicine published the maximum number of manuscripts in the field of SAE within 20 years. Dal-Pizzol Felipe was the most productive author (61 papers) and received the largest number of citations (930 citations). Co-citation cluster analysis revealed that the most popular terms on SAE in the manner of cluster labels were critical illness, sepsis-associated encephalopathy, polymicrobial sepsis, posterior reversible encephalopathy syndrome, rat brain, intensive care unit, prior sepsis, molecular hydrogen, inflammation drive, metabolic encephalopathies, delirium pathophysiology, and clinical neuroscience. Keyword burst detection indicated that neuroinflammation, blood-brain barrier (BBB) and mitochondria dysfunction were the current research hot spots.ConclusionsOur study revealed that neuroinflammation, blood-brain barrier, and mitochondria dysfunction had been the research foci of SAE over the past 20 years. These have emerged as the basis for transformation from basic research to clinical application in finding effective methods for the prevention and treatment of SAE.
Highlights
Sepsis-associated encephalopathy (SAE) is defined as a state of diffuse cerebral dysfunction caused by the inflammatory response of the body to various infections; this inflammatory process does not directly affect the central nervous system (CNS) and presents primarily symptom as a disturbed level of consciousness
The use of CiteSpace to generate the author collaboration network of SAE research resulted in 657 nodes and 944 links (Supplementary Figure 1D)
Zhan et al [63] demonstrated that Sh-LncRNA-5657 transfection decreased the expression of LncRNA-5657 in LPS-treated glial cells and decreased the mRNA and protein levels of tumor necrosis factor (TNF)-α, IL-1β, and IL-6; these results suggested that LncRNA-5657 expression can significantly reduce the inflammatory reaction in SAE and induce protective effects against this condition
Summary
Sepsis-associated encephalopathy (SAE) is defined as a state of diffuse cerebral dysfunction caused by the inflammatory response of the body to various infections; this inflammatory process does not directly affect the central nervous system (CNS) and presents primarily symptom as a disturbed level of consciousness. SAE was reported by some studies to have an incidence of as high as 42% [6], with a higher case fatality rate of 28–180 days, compared with that of non-SAE. When SAE appears as one of the main manifestations of multiple organ dysfunction, the case fatality rate can reach 70% [2]. SAE increases short-term morbidity and length of stay but may lead to long-term physical and cognitive impairment. Residual cognitive impairment after surviving sepsis is present in 12.5–21% of patients and includes disorders in attention, processing speed, association learning, visual perception, working memory, and language memory
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