Skip to main content

Daily Sepsis Research Analysis

3 papers

Large-scale surveillance from India quantifies CLABSI burden and extreme carbapenem resistance, informing prevention priorities. A target trial emulation suggests early albumin may increase sepsis-associated AKI without short-term survival benefit. A multi-biomarker, machine-learning classifier outperformed NEWS-2 and procalcitonin for ED sepsis identification.

Summary

Large-scale surveillance from India quantifies CLABSI burden and extreme carbapenem resistance, informing prevention priorities. A target trial emulation suggests early albumin may increase sepsis-associated AKI without short-term survival benefit. A multi-biomarker, machine-learning classifier outperformed NEWS-2 and procalcitonin for ED sepsis identification.

Research Themes

  • Healthcare-associated infection surveillance and prevention (CLABSI) with AMR profiling
  • Fluid resuscitation choices and kidney risk in sepsis (albumin and SA-AKI)
  • Composite biomarker panels with machine learning for sepsis diagnosis

Selected Articles

1. Profile of central line-associated bloodstream infections in adult, paediatric, and neonatal intensive care units of hospitals participating in a health-care-associated infection surveillance network in India: a 7-year multicentric study.

74.5Level IIICohortThe Lancet. Global health · 2025PMID: 40845882

A 7-year, multicenter surveillance across ~200 ICUs in India reported a pooled CLABSI rate of 8.83/1,000 central line-days, with the highest rate in neonatal ICUs. Klebsiella pneumoniae and Acinetobacter baumannii predominated, showing extremely high carbapenem resistance (77.7% and 87.1%). These data establish national benchmarks to target prevention and antimicrobial stewardship.

Impact: This is the first standardized, large-scale CLABSI surveillance from India, quantifying burden and resistance patterns that directly inform prevention bundles and stewardship.

Clinical Implications: Implement CLABSI bundles with emphasis on neonatal ICUs; prioritize infection control resources; tailor empiric therapy and stewardship to address high carbapenem resistance in A. baumannii and K. pneumoniae.

Key Findings

  • Pooled CLABSI rate: 8.83 per 1,000 central line-days (adult 8.68; pediatric 6.71; neonatal 13.86).
  • Predominant pathogens: K. pneumoniae (22.8%) and A. baumannii (20.4%) among 10,042 isolates.
  • Very high carbapenem resistance: A. baumannii 87.1% (1607/1846) and K. pneumoniae 77.7% (1589/2046) among tested isolates.

Methodological Strengths

  • Standardized, multicenter surveillance with centralized data quality checks
  • Large denominator data (patient-days and central line-days) enabling robust rate calculations

Limitations

  • Observational surveillance cannot infer causality or patient-level risk adjustment
  • Potential heterogeneity in practice and reporting across sites

Future Directions: Evaluate impact of targeted CLABSI prevention bundles and stewardship interventions using interrupted time series; incorporate patient-level severity and outcomes to refine risk-adjusted benchmarking.

2. Pentraxin-3, MyD88, GLP-1, and PD-L1: Performance assessment and composite algorithmic analysis for sepsis identification.

67.5Level IIICohortThe Journal of infection · 2025PMID: 40845995

In an ED cohort of 388 patients, several host-response biomarkers (notably MyD88, PD-L1, and pentraxin-3) showed strong discrimination for bacterial infection, sepsis, and 30-day mortality. A three-biomarker XGBoost classifier (pentraxin-3, MyD88, GLP-1) achieved AUROC 0.89 for sepsis, outperforming NEWS-2 (0.83) and procalcitonin (0.81).

Impact: Demonstrates a practical multi-marker algorithm that improves sepsis identification over current tools, with potential to accelerate triage and therapy.

Clinical Implications: Adopting composite biomarker panels with machine learning could enhance early sepsis recognition beyond NEWS-2 or single biomarkers, enabling earlier antibiotics and source control.

Key Findings

  • MyD88, PD-L1, and pentraxin-3 showed high AUROCs: bacterial infection ≥0.87, sepsis ≥0.81, 30-day mortality ≥0.71.
  • Seven of nine biomarkers significantly discriminated all three endpoints.
  • An XGBoost model using pentraxin-3, MyD88, and GLP-1 achieved AUROC 0.89 for sepsis, exceeding NEWS-2 (0.83) and procalcitonin (0.81).

Methodological Strengths

  • Prospective recruitment at ED presentation with predefined biomarker panel
  • Direct comparison with established clinical tools (NEWS-2) and a standard biomarker (procalcitonin)

Limitations

  • Single-cohort study with modest sample size (n=388) and need for external validation
  • Algorithm performance may depend on assay platform and local prevalence; implementation logistics not addressed

Future Directions: Externally validate and calibrate the classifier across diverse ED settings; assess impact on time-to-antibiotics and outcomes in a pragmatic trial.

3. Early use of albumin may increase the risk of sepsis-associated acute kidney injury in sepsis patients: a target trial emulation.

65.5Level IIICohortMilitary Medical Research · 2025PMID: 40841985

Using a clone-censor-weight target trial emulation over 2008–2022, early albumin administration was associated with a 3.47% higher risk of SA-AKI without a meaningful 7-day survival benefit. Findings were robust across sensitivity analyses, emphasizing careful risk-benefit assessment of albumin in sepsis resuscitation.

Impact: Challenges routine early albumin use by linking it to higher SA-AKI risk using state-of-the-art causal inference, with immediate implications for fluid strategies.

Clinical Implications: De-emphasize routine early albumin in sepsis resuscitation absent clear indications; monitor renal function closely if albumin is used; prioritize trials to confirm harm or identify subgroups who may benefit.

Key Findings

  • Early albumin administration increased SA-AKI risk by 3.47% (95% CI 1.76–5.23) versus no albumin.
  • No meaningful difference in 7-day all-cause mortality (relative difference 0.05%, 95% CI −2.30 to 2.45).
  • Robustness demonstrated via clone-censor-weight adjustment, new-user design, competing risk analyses, and sensitivity checks.

Methodological Strengths

  • Target trial emulation with clone-censor-weight method to mitigate immortal time bias
  • New-user design and competing risk analyses with extensive sensitivity analyses

Limitations

  • Observational emulation susceptible to residual confounding and indication bias
  • Single-center dataset may limit generalizability; exposure timing and dose details may vary

Future Directions: Conduct randomized trials or instrumental-variable analyses to confirm causality and explore effect heterogeneity by baseline kidney function and hemodynamics.