Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Jun 22;10(12):e33458.
doi: 10.1016/j.heliyon.2024.e33458. eCollection 2024 Jun 30.

Research progress in the pathogenesis of sepsis-associated encephalopathy

Yue Zhou  1 , Lu Bai  2 , Wenjing Tang  3 , Weiying Yang  3 , Lichao Sun  3
Affiliations
Review

Research progress in the pathogenesis of sepsis-associated encephalopathy

Yue Zhou et al. Heliyon. .

Abstract

Sepsis is a syndrome that causes dysfunction of multiple organs due to the host's uncontrolled response to infection and is a significant contributor to morbidity and mortality in intensive care units worldwide. Surviving patients are often left with acute brain injury and long-term cognitive impairment, known as sepsis-associated encephalopathy (SAE). In recent years, researchers have directed their focus towards the pathogenesis of SAE. However, due to the complexity of its development, there remains a lack of effective treatment measures that arise as a serious issue affecting the prognosis of sepsis patients. Further research on the possible causes of SAE aims to provide clinicians with potential therapeutic targets and help develop targeted prevention strategies. This paper aims to review recent research on the pathogenesis of SAE, in order to enhance our understanding of this syndrome.

Keywords: Epigenetics; Hyperammonemia; Intestinal flora disorder; Neuroinflammation; Sepsis; Sepsis-associated encephalopathy.

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
The pathogenesis of sepsis-associated encephalopathy.
See this image and copyright information in PMC

References

    1. Catarina A.V., Branchini G., Bettoni L., De Oliveira J.R., Nunes F.B. Sepsis-associated encephalopathy: from pathophysiology to progress in experimental studies. Mol. Neurobiol. 2021;58(6):2770–2779. doi: 10.1007/s12035-021-02303-2. - DOI - PubMed
    1. Herridge M.S., Azoulay E. Outcomes after critical illness. N. Engl. J. Med. 2023;388(10):913–924. doi: 10.1056/NEJMra2104669. - DOI - PubMed
    1. Yende S., Austin S., Rhodes A., Finfer S., Opal S., Thompson T., Bozza F.A., LaRosa S.P., Ranieri V.M., Angus D.C. Long-term quality of life among survivors of severe sepsis: analyses of two international trials. Crit. Care Med. 2016;44(8):1461–1467. doi: 10.1097/CCM.0000000000001658. - DOI - PMC - PubMed
    1. Andonegui G., Zelinski E.L., Schubert C.L., Knight D., Craig L.A., Winston B.W., Spanswick S.C., Petri B., Jenne C.N., Sutherland J.C., Nguyen R., Jayawardena N., Kelly M.M., Doig C.J., Sutherland R.J., Kubes P. Targeting inflammatory monocytes in sepsis-associated encephalopathy and long-term cognitive impairment. JCI Insight. 2018;3(9) doi: 10.1172/jci.insight.99364. - DOI - PMC - PubMed
    1. Giridharan V.V., Generoso J.S., Lence L., Candiotto G., Streck E., Petronilho F., Pillai A., Sharshar T., Dal-Pizzol F., Barichello T. A crosstalk between gut and brain in sepsis-induced cognitive decline. J. Neuroinflammation. 2022;19(1):114. doi: 10.1186/s12974-022-02472-4. - DOI - PMC - PubMed

LinkOut - more resources