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Background and aims <p>The diagnosis and management of pediatric sepsis remain challenging and time-sensitive. Early biological markers that may identify patients at risk of progression to septic shock are needed. Base deficit (BD) has been associated with adverse outcomes in adult sepsis, while alactic base excess (ABE) reflects non-lactate metabolic acidosis. This study aimed to evaluate the performance of BD and ABE compared with lactate in pediatric sepsis and to assess their association with time to progression to septic shock.</p> Methods <p>This retrospective single-center cohort study included pediatric patients with sepsis between January 1, 2020, and September 1, 2024. Biomarkers were obtained at initial presentation prior to resuscitation. BD and ABE were categorized into normal, abnormal, and extremely abnormal groups based on distribution thresholds, while lactate was classified as normal (≤2.2 mmol/L) or abnormal (&gt;2.2 mmol/L). Diagnostic performance was assessed using ROC curve analysis. Time-to-event analyses were performed using Kaplan–Meier curves and multivariable Cox regression models adjusted for BMI, CRP, albumin, and Phoenix Sepsis Score.</p> Results <p>A total of 44 patients were included, of whom 30 (68.18%) developed septic shock. Lactate demonstrated lower discriminative performance (AUC 0.624, 95% CI 0.447–0.800) compared with BD (AUC 0.940, 95% CI 0.875–0.999) and ABE (AUC 0.905, 95% CI 0.813–0.997). Both BD and ABE showed higher sensitivity and specificity for identifying patients who progressed to septic shock. In adjusted analyses, abnormal and extremely abnormal ABE and BD were associated with an increased hazard of progression to septic shock. Median time to shock was shortest in patients with extremely abnormal BD and ABE (approximately 8–9 hours), followed by abnormal lactate (13 hours), abnormal ABE (17 hours), and abnormal BD (18 hours).</p> Conclusions <p>BD and ABE were associated with progression to septic shock in pediatric sepsis and may provide clinically relevant information for early risk stratification. In this cohort, these markers demonstrated stronger discriminative performance than lactate and may reflect metabolic disturbances present earlier in the disease course. However, these findings should be interpreted cautiously given the retrospective design and require prospective multicenter validation before clinical implementation.</p>

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Base deficit and alactic base excess are promising early biological markers in pediatric sepsis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月16日

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  • Amani Assaad,
  • Marianne Majdalani,
  • Ali Ismail,
  • Jihane Moukhaiber

摘要

Background and aims

The diagnosis and management of pediatric sepsis remain challenging and time-sensitive. Early biological markers that may identify patients at risk of progression to septic shock are needed. Base deficit (BD) has been associated with adverse outcomes in adult sepsis, while alactic base excess (ABE) reflects non-lactate metabolic acidosis. This study aimed to evaluate the performance of BD and ABE compared with lactate in pediatric sepsis and to assess their association with time to progression to septic shock.

Methods

This retrospective single-center cohort study included pediatric patients with sepsis between January 1, 2020, and September 1, 2024. Biomarkers were obtained at initial presentation prior to resuscitation. BD and ABE were categorized into normal, abnormal, and extremely abnormal groups based on distribution thresholds, while lactate was classified as normal (≤2.2 mmol/L) or abnormal (>2.2 mmol/L). Diagnostic performance was assessed using ROC curve analysis. Time-to-event analyses were performed using Kaplan–Meier curves and multivariable Cox regression models adjusted for BMI, CRP, albumin, and Phoenix Sepsis Score.

Results

A total of 44 patients were included, of whom 30 (68.18%) developed septic shock. Lactate demonstrated lower discriminative performance (AUC 0.624, 95% CI 0.447–0.800) compared with BD (AUC 0.940, 95% CI 0.875–0.999) and ABE (AUC 0.905, 95% CI 0.813–0.997). Both BD and ABE showed higher sensitivity and specificity for identifying patients who progressed to septic shock. In adjusted analyses, abnormal and extremely abnormal ABE and BD were associated with an increased hazard of progression to septic shock. Median time to shock was shortest in patients with extremely abnormal BD and ABE (approximately 8–9 hours), followed by abnormal lactate (13 hours), abnormal ABE (17 hours), and abnormal BD (18 hours).

Conclusions

BD and ABE were associated with progression to septic shock in pediatric sepsis and may provide clinically relevant information for early risk stratification. In this cohort, these markers demonstrated stronger discriminative performance than lactate and may reflect metabolic disturbances present earlier in the disease course. However, these findings should be interpreted cautiously given the retrospective design and require prospective multicenter validation before clinical implementation.