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SPCI - Sociedade Portuguesa de Cuidados Intensivos

Revista Brasileira de Terapia Intensiva

AMIB - Associação de Medicina Intensiva Brasileira

OFFICIAL JOURNAL OF THE ASSOCIAÇÃO BRASILEIRA DE MEDICINA INTENSIVA AND THE SOCIEDADE PORTUGUESA DE CUIDADOS INTENSIVOS

ISSN: 0103-507X
Online ISSN: 1982-4335

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Noritomi DT, Sanga RR, Amaral ACK, Park M. O metabolismo ácido-básico em pacientes críticos: é o excesso de bases padronizado correlacionado com o nível sérico de lactato?. Rev Bras Ter Intensiva. 2006;18(1):22-26

 

 

2006;18(1):22-26
Original Article

http://dx.doi.org/10.1590/S0103-507X2006000100005

Metabolic acid-base status in critically ill patients: is standard base excess correlated with serum lactate level?

O metabolismo ácido-básico em pacientes críticos: é o excesso de bases padronizado correlacionado com o nível sérico de lactato?

Danilo Teixeira Noritomi, Ricardo Reis Sanga, André Carlos Kajdaksi-Balla Amaral, Marcelo Park

Medical Intensive Care Unit - Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo - São Paulo - Brazil

Apresentado em 25 de novembro de 2005
Aceito para publicação em 02 de janeiro de 2006

Corresponding author:

Danilo Teixeira Noritomi, MD
Av Dom Pedro I, 198/42
06083-908, Osasco-SP Brazil
Phone: 55-11-36810666
Fax: 55-11-37721568
Email: [email protected]

 

Abstract

BACKGROUND AND OBJECTIVES: To correlate standard base excess (SBE) with serum lactate level and demonstrate the independent prognostic significance of each one.
METHODS: In a retrospective study, we retrieved data from 333 patients of our prospectively collected database of 7-bed medical intensive care unit of a 1800-bed university hospital.
RESULTS: The results have shown a poor correlation between SBE and lactate, r = - 0.358, p < 0.001, and an independent prognostic significance of each one when analyzed concomitantly, odds ratio (95% Confidence interval) = 0.996 (0.992 - 0.999) to standard base excess and 1.000 (1.000 - 1.002) to lactate at entrance; and odds ratio (95% Confidence interval ) = 0.990 (0.985 - 0.994) to standard base excess and 1.003 (1.001 - 1.005) to lactate after 24 hours. The accuracy of standard base excess was close to lactate to determine in-intensive care unit death.
CONCLUSIONS: The lactic component of the metabolic acidosis is not the major determinant of standard base excess. Serum lactate and SBE are independent outcome predictors in critically ill patients.

Keywords: Acid-base equilibrium, acidosis, critical illness, lactic acid, prognosis

 

 

INTRODUCTION

Metabolic acidosis is common in critically ill patients and denotes great physiopathologic, clinical and prognostic features1,2. Traditionally, the acute metabolic acidosis in this context has been attributed to the presence of lactic acid, which is frequently seen in these patients3. However, recent studies in experimental and clinical field have stated that other several anions have an important role, sometimes even more important than lactate in the genesis and maintenance of this type of acid-base disturbance4-6. Regarding the outcome prediction capacity of acid-base variables, some controversies still persist. Hyperlactatemia has been accepted for a long time as an important outcome prediction tool in several critical situations7,8. Nevertheless, it is not clear if its value persists independently of the degree of metabolic acidosis7,9.

The aim of this study was to correlate acute metabolic acidosis measured by base excess and hyperlactatemia in a medical intensive care unit population. For this purpose we have tested the mathematical correlation between standard base excess (SBE) and lactate, and also the independent prognostic significance of each one.

 

METHODS

We retrospectively retrieved our prospectively-collected data base from February 2000 to January 2001, and analyzed biochemical and clinical data collected on admission and after 24 hours from unselected consecutive patients admitted to a 7-bed medical intensive care unit of a tertiary level university hospital. Laboratorial information was routinely obtained from an arterial blood sample gained immediately after the insertion of an arterial catheter on admission to the intensive care unit, and after 24 hours. SBE and lactate were analysed in a blood gas analyser OMNI AVL (Roche Medical Instruments, Indianapolis, Indiana). The Van Slyke methodology is currently used to calculate SBE in this gas analyser10. No additional blood sampling was required. According to our ethic committee, informed consent was waived.

Data are shown as median and interquartile range. Spearman's test was used to study correlations between variables. Univariate analyses were used to correlate tested variables and intensive care unit mortality. Multivariate analysis was performed using a binary logistic regression model to test SBE and lactate concomitantly as an intensive care unit death predictor. The areas under the receiver operating characteristic (ROC) curves for the death prediction accuracy of SBE and lactate were calculated. It was used the commercially available statistical package SPSS 10.0 (SPSS Inc., Chicago, Illinois) to statistical analysis. The significance level considered was p < 0.05.

 

RESULTS

During 1-year period, 333 patients had complete data recorded available for retrieval. The general characteristics of patients are shown in table 1. The correlation between SBE and lactate is expressed individually on the admission and after 24 hours in graphic 1. For the prediction of intensive care unit death, we tested the following variables: age, APACHE II score, SBE and lactate (both on admission and after 24 hours). In the univariate analysis, besides the APACHE II score, SBE and lactate both on admission and after 24 were significantly associated with the intensive care unit mortality (Table 2). In the multivariate analysis, only SBE and lactate were concomitantly analyzed, and both still remained as independent death predictors when analyzed on admission, and when analyzed independently after 24 hours (Table 3). The ROC curves, on admission and after 24 hours, to SBE and lactate are shown in figure 2.

 

DISCUSSION

Our results have shown a poor correlation between SBE and lactate, r = - 0.358, p < 0.001 (Figure 1), and an independent prognostic significance of each one when analyzed concomitantly, odds ratio (Confidence interval) = 0.996 (0.992 - 0.999) to SBE and 1.001 (1.000 - 1.002) to lactate on admission; and odds ratio (Confidence interval) = 0.990 (0.985 - 0.994) to SBE and 1.003 (1.001 - 1.005) to lactate after 24 hours (Table 3). The accuracy to predict death of SBE was close to the lactate (Figure 2).

The existence of several potential mechanisms has been proposed to justify the complexity of acid-base disequilibrium frequently seen in critically ill patients. Hyperchloremia induced by volume expansion with routinely used solutions4,11 or differential shifts of chloride ion to and from the plasma4 seem to be an important cause of metabolic acidosis in several contexts. Renal failure and reduced acid clearance as a part of multiple organ dysfunction can result in decreased SBE by several reasons, increased levels of phosphate and unmeasureable anions probably are the most important ones12. Lactate and unmeasurable anions production by ischemic or inflamed tissues can represent another important cause of reduction in SBE in shock states (1;3). Hypoalbuminemia is an almost universal finding in ICU patients and its alkalinising effect has been shown to be quite significant according to the quantitative approach13. The relative weight of each disturbance in different clinical situations is far from being completely elucidated14.

The SBE offers an overview of acid basic metabolism independently of its complexity. The SBE does not disclose all metabolic acidosis15 but it is suggested that it may reflect the gastric mucosal intracellular pH 16. According to what was mentioned above, hyperlactatemia is only one possibility among several others to justify the SBE alteration seen in our population and the lack of association between the two variables is not completely unexpected. Applying the Stewart's acid-base methodology, it can be clearly demonstrated that lactate quantitative contribution to SBE alteration is quite small considering the range of values seen in clinical practice17,18.

From the mechanistic point-of-view, hyperlactatemia is also a partially explained finding. It is no longer considered a perfect marker of tissue hypoxia and several other conditions have been associated with it3. Nevertheless, lactate serum level is one of the most traditional laboratorial monitoring tools, and it is still used with success in diverse forms of critical diseases3,19.

In terms of outcome prediction capacity, some points are still under debate. SBE reflects a sum of several acid-base disturbances occurring concomitantly in each patient. Probably, each of these physiopathological processes carries different clinical meanings, for instance, it is suggested that predominantly hyperchloremic acidosis brings a better prognosis than lactic acidosis20. Despite this fact, can SBE still be used as an outcome prediction tool? Or should we focus our attention on more specific values, such as lactate or unmeasureable anions levels? Our results reaffirm that SBE still keeps a lactate-independent prognostic capacity. This goes in accordance with Smith et al.7 who have shown that prognostic information given by SBE is complementary to the lactate level prognostic prediction.

In a clinical scenario, Balasubramanyan et al.8 have shown that diminished SBE and base excess corrected to unmeasured anions are good death predictors in a pediatric intensive care unit. Smith et al.7 have found that the association of SBE and lactate levels can be especially useful in the outcome prediction. Hatherill et al.21 have shown in a paediatric critically ill population that the magnitude of metabolic acidosis measured by the SBE is not associated with mortality and that the lactate levels were more likely to predict outcome. Ultimately, Rocktaeschel et al.9 have shown that base excess is able to mark hyperlactatemia but not able to predict in-hospital death. This controversy has specially motivated our present study.

Limitations to our study include its retrospective nature and the lack of a complete quantitative analysis that could disclose the whole scenario of the acid-base disorder in our population, mainly characterizing the chloride and unmeasurable anions contributions.

In conclusion, the lactic component of the metabolic acidosis is not the major determinant of SBE. Serum lactate level and SBE are independent outcome predictors in critically ill patients.

 

LIST OF ABBREVIATIONS USED

SBE: standard base excess

ROC: receiver operating characteristic

 

REFERENCES

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19. Bakker J, Coffernils M, Leon M et al - Blood lactate levels are superior to oxygen-derived variables in predicting outcome in human septic shock. Chest, 1991;99:956-962.

20. Brill SA, Stewart TR, Brundage SI et al - Base deficit does not predict mortality when secondary to hyperchloremic acidosis. Shock, 2002;17:459-462

21. Hatherill M, Waggie Z, Purves L et al - Mortality and the nature of metabolic acidosis in children with shock. Intensive Care Med, 2003;29:286-291.

 

 

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