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Abstract

Introduction: Measurement of serum lactate remains pivotal in sepsis evaluation as it is closely related to tissue hypoxia and mortality.1, 2 Serum lactate, however, can be elevated due to a myriad of reasons beyond hypoperfusion.3 A proposed alternative to control for serum lactate’s inherent variability is to measure pyruvate concomitantly to calculate the lactate/pyruvate (L/P) ratio.4, 5 As pyruvate transforms into lactate in anaerobic conditions, its value decreases in serum, increasing the L/P ratio, hence indicating an actual tissue-perfusion mismatch.6 Despite its clinical utility, there is a paucity of evidence evaluating the role of the L/P ratio in patients with sepsis without evidence of shock.

Methods: Using an observational design, we evaluated the clinical utility of the L/P ratio in patients with sepsis. We included patients with sepsis, regardless of the etiology, that were hemodynamically stable. Lactate and pyruvate, and consequently the L/P ratio, were measured at baseline, 4 hours, and 8 hours. Our primary outcome was to determine the prognostic utility of the L/P ratio on mortality across time. Our secondary outcome was to compare the L/P ratio prognostic utility when adding standard risk calculators such as APACHE-II and SOFA scores. Model performance and accuracy were determined using the residual mean square error (RMSE), R2, C-statistic, accuracy, and a visual inspection of the receiver operating characteristic (ROC) curve. A non-parametric bootstrap regression was used for all models, given that we expect a non-linear relationship between variables and to allow for more model flexibility.

Results: We had a total of 80 patients, with 18 (22.5%) survivors and 62 (77.5%) non-survivors. Pneumonia was the most common source of infection (44/80; 55%) and gastrointestinal the least common (15/80; 19%) (Table 1). There were no differences at baseline except for the SOFA and APACHE-II scores (Table 1). For our primary outcome, the prognostic model, patients with a higher L/P ratio at 8 hours had an OR of 1.08 (95% CI 1.02 – 1.18), holding constant the rest of the variables and had better performance than the other two models (Figure 1). For our secondary outcome, we found that the prognostic model using the APACHE-II in addition to the L/P ratio and the L/P ratio alone had a very similar association to the mortality (OR 1.07, 95% CI 1.01 – 1.17 and OR 1.08, 95% CI 1.02 – 1.18) (Figure 2). However, there was a substantial difference in the model’s performance between all models (Figure 2).

Conclusions: While the L/P ratio appears to be an earlier predictor of mortality than hyperlactatemia alone, its comparability against other standard clinical risk scores is negligible or suboptimal. The L/P ratio’s clinical applicability seems to be more towards daily use to avoid misinterpretation of isolated hyperlactatemia.

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Prognostic Utility of the Lactate/Pyruvate Ratio for Mortality in Patients with Sepsis: An Observational Study

Introduction: Measurement of serum lactate remains pivotal in sepsis evaluation as it is closely related to tissue hypoxia and mortality.1, 2 Serum lactate, however, can be elevated due to a myriad of reasons beyond hypoperfusion.3 A proposed alternative to control for serum lactate’s inherent variability is to measure pyruvate concomitantly to calculate the lactate/pyruvate (L/P) ratio.4, 5 As pyruvate transforms into lactate in anaerobic conditions, its value decreases in serum, increasing the L/P ratio, hence indicating an actual tissue-perfusion mismatch.6 Despite its clinical utility, there is a paucity of evidence evaluating the role of the L/P ratio in patients with sepsis without evidence of shock.

Methods: Using an observational design, we evaluated the clinical utility of the L/P ratio in patients with sepsis. We included patients with sepsis, regardless of the etiology, that were hemodynamically stable. Lactate and pyruvate, and consequently the L/P ratio, were measured at baseline, 4 hours, and 8 hours. Our primary outcome was to determine the prognostic utility of the L/P ratio on mortality across time. Our secondary outcome was to compare the L/P ratio prognostic utility when adding standard risk calculators such as APACHE-II and SOFA scores. Model performance and accuracy were determined using the residual mean square error (RMSE), R2, C-statistic, accuracy, and a visual inspection of the receiver operating characteristic (ROC) curve. A non-parametric bootstrap regression was used for all models, given that we expect a non-linear relationship between variables and to allow for more model flexibility.

Results: We had a total of 80 patients, with 18 (22.5%) survivors and 62 (77.5%) non-survivors. Pneumonia was the most common source of infection (44/80; 55%) and gastrointestinal the least common (15/80; 19%) (Table 1). There were no differences at baseline except for the SOFA and APACHE-II scores (Table 1). For our primary outcome, the prognostic model, patients with a higher L/P ratio at 8 hours had an OR of 1.08 (95% CI 1.02 – 1.18), holding constant the rest of the variables and had better performance than the other two models (Figure 1). For our secondary outcome, we found that the prognostic model using the APACHE-II in addition to the L/P ratio and the L/P ratio alone had a very similar association to the mortality (OR 1.07, 95% CI 1.01 – 1.17 and OR 1.08, 95% CI 1.02 – 1.18) (Figure 2). However, there was a substantial difference in the model’s performance between all models (Figure 2).

Conclusions: While the L/P ratio appears to be an earlier predictor of mortality than hyperlactatemia alone, its comparability against other standard clinical risk scores is negligible or suboptimal. The L/P ratio’s clinical applicability seems to be more towards daily use to avoid misinterpretation of isolated hyperlactatemia.

 

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