Severe hyperlactatemia with normal base excess: a quantitative analysis using conventional and Stewart approaches

Graciela Tuhay , María Carolina Pein , Fabio Daniel Masevicius , Daniela Olmos Kutscherauer and Arnaldo Dubin

Servicio de Terapia Intensiva, Sanatorio Otamendi y Miroli, Buenos Aires, Argentina

author email corresponding author email

Critical Care 2008, 12:R66doi:10.1186/cc6896


Published:	8 May 2008

Abstract

Introduction

Critically ill patients might present complex acid–base disorders, even when the pH, PCO₂, [HCO₃^-], and base excess ([BE]) levels are normal. Our hypothesis was that the acidifying effect of severe hyperlactatemia is frequently masked by alkalinizing processes that normalize the [BE]. The goal of the present study was therefore to quantify these disorders using both Stewart and conventional approaches.

Methods

A total of 1,592 consecutive patients were prospectively evaluated on intensive care unit admission. Patients with severe hyperlactatemia (lactate level ≥ 4.0 mmol/l) were grouped according to low or normal [BE] values (<-3 mmol/l or >-3 mmol/l).

Results

Severe hyperlactatemia was present in 168 of the patients (11%). One hundred and thirty-four (80%) patients had low [BE] levels while 34 (20%) patients did not. Shock was more frequently present in the low [BE] group (46% versus 24%, P = 0.02) and chronic obstructive pulmonary disease in the normal [BE] group (38% versus 4%, P < 0.0001). Levels of lactate were slightly higher in patients with low [BE] (6.4 ± 2.4 mmol/l versus 5.6 ± 2.1 mmol/l, P = 0.08). According to our study design, the pH, [HCO₃^-], and strong-ion difference values were lower in patients with low [BE]. Patients with normal [BE] had lower plasma [Cl^-] (100 ± 6 mmol/l versus 107 ± 5 mmol/l, P < 0.0001) and higher differences between the changes in anion gap and [HCO₃^-] (5 ± 6 mmol/l versus 1 ± 4 mmol/l, P < 0.0001).

Conclusion

Critically ill patients may present severe hyperlactatemia with normal values of pH, [HCO₃^-], and [BE] as a result of associated hypochloremic alkalosis.