Evidence map›Paper›PMID 33495934›Full record

ReviewMolecular neurobiology2021

Sepsis-Associated Encephalopathy: from Pathophysiology to Progress in Experimental Studies.

Anderson Velasque Catarina, Gisele Branchini, Lais Bettoni, Jarbas Rodrigues De Oliveira, Fernanda Bordignon Nunes

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
15.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Observational
  7. Transcriptomics and metabolomics reveal the protective effect of β-hydroxybutyrate on sepsis associated encephalopathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Anderson Velasque CatarinaPrograma de Pós-graduação em Patologia, Universidade Federal de Ciências da Saúde de Porto Alegre - UFCSPA, Porto Alegre, RS, 90050-170, Brazil. anderson.catarina@acad.pucrs.br.ORCID http://orcid.org/0000-0003-4148-3857
Gisele BranchiniPrograma de Pós-graduação em Patologia, Universidade Federal de Ciências da Saúde de Porto Alegre - UFCSPA, Porto Alegre, RS, 90050-170, Brazil.
Lais BettoniPrograma de Pós-graduação em Patologia, Universidade Federal de Ciências da Saúde de Porto Alegre - UFCSPA, Porto Alegre, RS, 90050-170, Brazil.
Jarbas Rodrigues De OliveiraLaboratório de Biofísica Celular e Inflamação, Pontifícia Universidade Católica do Rio Grande do Sul - PUCRS, Porto Alegre, Brazil.
Fernanda Bordignon NunesPrograma de Pós-graduação em Patologia, Universidade Federal de Ciências da Saúde de Porto Alegre - UFCSPA, Porto Alegre, RS, 90050-170, Brazil.
Universidade Federal de Ciências da Saúde de Porto Alegre · BRPontifícia Universidade Católica do Rio Grande do Sul · BR

Funding

CAPES 001
6 · The paper itself

Abstract

Sepsis is an organ dysfunction caused by an uncontrolled inflammatory response from the host to an infection. Sepsis is the main cause of morbidity and mortality in intensive care units (ICU) worldwide. One of the first organs to suffer from injuries resulting from sepsis is the brain. The central nervous system (CNS) is particularly vulnerable to damage, mediated by inflammatory and oxidative processes, which can cause the sepsis-associated encephalopathy (SAE), being reported in up to 70% of septic patients. This review aims to bring a summary of the main pathophysiological changes and dysfunctions in SAE, and the main focuses of current experimental studies for new treatments and therapies. The pathophysiology of SAE is complex and multifactorial, combining intertwined processes, and is promoted by countless alterations and dysfunctions resulting from sepsis, such as inflammation, neuroinflammation, oxidative stress, reduced brain metabolism, and injuries to the integrity of the blood-brain barrier (BBB). The treatment is limited once its cause is not completely understood. The patient's sedation is far to provide an adequate treatment to this complex condition. Studies and experimental advances are important for a better understanding of its pathophysiology and for the development of new treatments, medicines, and therapies for the treatment of SAE and to reduce its effects during and after sepsis.

Indexed as

AnimalsBrainDisease Models, AnimalHumansModels, BiologicalOxidative StressSepsis-Associated EncephalopathyBrainEncephalopathyExperimental studiesSepsis

Identifiers

PMID33495934
OpenAlexW3122275326

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.