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

Graciela Tuhay email, Maria C Pein email, Fabio Daniel Masevicius email, Daniela Olmos Kutscherauer email and Arnaldo Dubin email

Critical Care 2008, 12:R66doi:10.1186/cc6896

Published: 8 May 2008

Abstract (provisional)

Background

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

Methods

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

Results

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

Conclusions

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

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.


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