Clinical utility of standard base excess in the diagnosis and interpretation of metabolic acidosis in critically ill patients

M Park,D.T Noritomi,A.B Libório,L.M Cruz-Neto,L.U Taniguchi,A.T Maciel

doi:10.1590/s0100-879x2006005000199

Abstract

The aims of this study were to determine whether standard base excess (SBE) is a useful diagnostic tool for metabolic acidosis, whether metabolic acidosis is clinically relevant in daily evaluation of critically ill patients, and to identify the most robust acid-base determinants of SBE. Thirty-one critically ill patients were enrolled. Arterial blood samples were drawn at admission and 24 h later. SBE, as calculated by Van Slyke's (SBE VS) or Wooten's (SBE W) equations, accurately diagnosed metabolic acidosis (AUC = 0.867, 95%CI = 0.690-1.043 and AUC = 0.817, 95%CI = 0.634-0.999, respectively). SBE VS was weakly correlated with total SOFA (r = -0.454, P < 0.001) and was similar to SBE W (r = -0.482, P < 0.001). All acid-base variables were categorized as SBE VS <-2 mEq/L or SBE VS <-5 mEq/L. SBE VS <-2 mEq/L was better able to identify strong ion gap acidosis than SBE VS <-5 mEq/L; there were no significant differences regarding other variables. To demonstrate unmeasured anions, anion gap (AG) corrected for albumin (AG A) was superior to AG corrected for albumin and phosphate (AG A+P) when strong ion gap was used as the standard method. Mathematical modeling showed that albumin level, apparent strong ion difference, AG A, and lactate concentration explained SBE VS variations with an R(2) = 0.954. SBE VS with a cut-off value of <-2 mEq/L was the best tool to diagnose clinically relevant metabolic acidosis. To analyze the components of SBE VS shifts at the bedside, AG A, apparent strong ion difference, albumin level, and lactate concentration are easily measurable variables that best represent the partitioning of acid-base derangements.

Highlights

Various contemporary studies of acid-base physiology that quantify previously described acid-base derangements have been published recently [1,2]
At the bedside of a critically ill patient, it is important to note that there appears to be a difference in physiologic variables and outcomes between patients with respiratory acidosis and those with metabolic acidosis, leading some investigators to hypothesize that it is the cause of acidosis, rather than the acidosis per se, that drives the association with clinical outcomes [6]
anion gap corrected for albumin (AGA) was superior to the AGA+P when the strong ion gap (SIG) was taken as the standard method

Summary

Introduction

Various contemporary studies of acid-base physiology that quantify previously described acid-base derangements have been published recently [1,2] These studies have refined our understanding of the basic mechanisms that control blood pH in health and disease, and have described the epidemiology and clinical significance of acidbase imbalances in more detail than was previously possible [3,4,5]. It has been established with mathematical calculation that the modern (quantitative) and traditional (descriptive) approaches are interchangeable at a fundamental level This interchange has resulted in clarification of the limitations of each approach and has revealed how a combinatorial approach can be used to achieve a more complete understanding of clinical acid-base physiology [3,6]. When taking metabolic acidosis into account, there are many possible mechanisms involved, and it seems that there is a different reflex on the www.bjournal.com.br outcome based on the mechanism, again suggesting the concept that the cause of acidosis is more important than the acidosis per se [7,8,9,10]

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