# Propofol provides a significant survival advantage in sepsis-associated encephalopathy: A retrospective cohort study investigating one-year all-cause mortality

**Authors:** Yuan Li, Han Huang, Bingxing Shuai

PMC · DOI: 10.1371/journal.pone.0340371 · PLOS One · 2026-02-05

## TL;DR

This study found that using propofol as a sedative in patients with sepsis-associated encephalopathy significantly lowers their risk of dying within one year.

## Contribution

The study reveals that propofol monotherapy reduces one-year mortality in sepsis-associated encephalopathy patients.

## Key findings

- Propofol monotherapy was associated with a 49% reduction in one-year all-cause mortality in SAE patients.
- The protective effect of propofol was more pronounced in patients receiving ventilation support.
- Propensity score matching confirmed the robustness of the observed mortality reduction.

## Abstract

Considering the high incidence, mortality, and long-term effects of sepsis-associated encephalopathy (SAE), along with the availability of sedation therapy data and the significance of distress management, this study investigated the relationship between sedation therapy and one-year all-cause mortality in patients with SAE.

This retrospective cohort study utilized the Medical Information Market for Intensive Care (MIMIC-IV) database. We gathered demographic data, vital signs, laboratory test results, microbial findings, comorbidities, scoring systems, treatments administered within the first 24 hours of patient admission to the intensive care unit (ICU), and follow-up data from 24 hours after ICU admission to one year. Cox regression models were employed to evaluate the relationship between sedation therapy and one-year all-cause mortality among patients with SAE. Propensity score matching (PSM) and subgroup analyses were used to assess the robustness of the findings.

Four thousand six hundred eighteen patients with SAE were enrolled, including 3,343 in the sedative group and 1,275 in the non-sedative group; additionally, 511 pairs were matched. A protective correlation was observed between propofol monotherapy and one-year all-cause mortality in patients with SAE, with hazard ratios (HRs) of 0.51 (95% confidence interval (CI), 0.40–0.65), P < 0.001. Furthermore, the interaction between propofol monotherapy and ventilation support significantly increased one-year all-cause mortality, yielding an HR of 0.70 (95% CI, 0.49–1.00) with P for interaction = 0.041. The results of PSM remained robust.

Our study indicated that compared to patients with SAE who did not receive sedation, administering propofol alone significantly reduced one-year all-cause mortality among patients with SAE. For patients undergoing ventilation support on the first day of ICU admission, the interaction between sedation therapy and ventilation support significantly influenced the one-year all-cause mortality of patients with SAE.

## Linked entities

- **Chemicals:** propofol (PubChem CID 4943)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** Wernicke's encephalopathy (MESH:D014899), liver or kidney diseases (MESH:D008107), SAE (MESH:D065166), delirium (MESH:D003693), death (MESH:D003643), cognitive dysfunction (MESH:D003072), agitation (MESH:D011595), coma (MESH:D003128), inattention (MESH:D001308), memory loss (MESH:D008569), cerebral embolism (MESH:D020766), diabetes (MESH:D003920), septic (MESH:D001170), intestinal infections (MESH:D007410), electrolyte imbalances (MESH:D014883), anxiety (MESH:D001007), urea cycle disorders (MESH:D056806), altered consciousness (MESH:D003244), inflammation (MESH:D007249), meningitis (MESH:D008580), CNS (MESH:D002493), brain injuries (MESH:D001930), pain (MESH:D010146), structural injury (MESH:D020914), glycemic disturbances (MESH:D014832), brain dysfunction (MESH:D001927), hypertensive encephalopathy (MESH:D020343), hyperglycemia (MESH:D006943), renal failure (MESH:D051437), cerebrovascular diseases (MESH:D002561), central nervous system (CNS) infection (MESH:D002494), hypernatremia (MESH:D006955), dyspnea (MESH:D004417), hypoglycemic coma (MESH:C000721848), mental disorders (MESH:D001523), ischemic stroke (MESH:D002544), hepatic encephalopathy (MESH:D006501), acute kidney injury (MESH:D058186), confusional (MESH:D003221), alcohol intoxication (MESH:D000435), traumatic brain injury (MESH:D000070642), infection (MESH:D007239), intracerebral hemorrhage (MESH:D002543), hypoglycemia (MESH:D007003), epilepsy (MESH:D004827), encephalitis (MESH:D004660), neurological diseases (MESH:D020271), critical illness (MESH:D016638), metabolic encephalopathy (MESH:D001928), SIRS (MESH:D018746), chronic hepatic or renal disorders (MESH:D006521), hyponatremia (MESH:D007010), organ failure (MESH:D009102), skin and soft tissue infections (MESH:D018461), respiratory failure (MESH:D012131), SEPSIS (MESH:D018805), chronic alcohol or drug abuse (MESH:D019966)
- **Chemicals:** oxygen (MESH:D010100), potassium (MESH:D011188), Propofol (MESH:D015742), haloperidol (MESH:D006220), norepinephrine (MESH:D009638), benzodiazepine (MESH:D001569), carbon dioxide (MESH:D002245), glucose (MESH:D005947), lipid (MESH:D008055), midazolam (MESH:D008874), lactate (MESH:D019344), sodium (MESH:D012964), creatinine (MESH:D003404), PaCO2 (-), dexmedetomidine (MESH:D020927)
- **Species:** Escherichia coli (E. coli, species) [taxon 562], Homo sapiens (human, species) [taxon 9606], Staphylococcus aureus (species) [taxon 1280]

## Full text

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## Figures

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## References

33 references — full list in the complete paper: https://tomesphere.com/paper/PMC12875438/full.md

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Source: https://tomesphere.com/paper/PMC12875438