# Prognostic value of serial alactic base excess measurements in patients with sepsis: a retrospective cohort study

**Authors:** Dursun Elmas, Muhammet Cemal Kizilarslanoglu

PMC · DOI: 10.3389/fmed.2026.1755874 · Frontiers in Medicine · 2026-03-13

## TL;DR

This study shows that tracking changes in a blood measure called alactic base excess over 48 hours can predict survival in sepsis patients.

## Contribution

The study introduces serial alactic base excess as a novel independent predictor of mortality in sepsis patients.

## Key findings

- Patients with persistently low alactic base excess had a 52.9% mortality rate, significantly higher than those with normalized values.
- Each 1 mmol/L increase in alactic base excess over 48 hours was linked to a 25% lower mortality risk.
- Alactic base excess showed better, though not statistically significant, discrimination for mortality than base excess at ICU admission.

## Abstract

This study evaluated the prognostic significance of serial alactic base excess (ABE) measurements in patients with sepsis.

We conducted a retrospective cohort study including 521 adult patients with sepsis. Arterial blood gas analyses obtained at 0, 6, 12, 24, and 48 h were used to calculate ABE. Patients were classified into three trajectory groups: persistently low ABE (ABE < 0 at all time points), normalizing ABE (initial ABE < 0 with recovery to ≥0 by 48 h), and normal ABE (ABE ≥ 0 at admission). The primary outcome was 28-day mortality.

Overall 28-day mortality was 35.9%. Non-survivors exhibited more severe metabolic derangement at admission, with higher lactate levels (median 4.22 [2.89–5.31] vs. 3.66 [2.31–4.82] mmol/L) and more negative base excess values (median −6.00 [−8.54 to −3.88] vs. −5.09 [−7.63 to −2.71] mmol/L) (both p < 0.001). Admission ABE was significantly lower in non-survivors and remained consistently reduced throughout the first 48 h (all p < 0.001). Patients with a persistently low ABE trajectory experienced the highest mortality compared with those whose ABE normalized (52.9% vs. 19.8%, p < 0.001). In multivariable Cox regression adjusted for age, sex, baseline eGFR, SOFA score, and APACHE II score, persistently low ABE independently predicted 28-day mortality (adjusted HR 2.539; 95% CI 1.510–4.267; p < 0.001). Furthermore, each 1 mmol/L increase in ΔABE over 48 h was associated with a 25% relative reduction in mortality risk (adjusted HR 0.750; 95% CI 0.633–0.889; p = 0.001). At ICU admission, ABE showed numerically higher discrimination for 28-day mortality than BE (AUC 0.671 vs. 0.639), although this difference did not reach statistical significance (p = 0.057).

Serial ABE trajectories provide independent prognostic information in sepsis. Failure to normalize ABE within the first 48 h identifies a high-risk phenotype associated with markedly increased short-term mortality.

## Full-text entities

- **Diseases:** metabolic derangement (MESH:D008659), sepsis (MESH:D018805)
- **Chemicals:** lactate (MESH:D019344)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC13021659/full.md

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Source: https://tomesphere.com/paper/PMC13021659