Open Access

Is lactate clearance impaired in septic shock?

  • Thiago Domingos Corrêa1, 2,
  • Jukka Takala2 and
  • Stephan Matthias Jakob2Email author
Critical Care201519:306

https://doi.org/10.1186/s13054-015-1039-x

Published: 10 September 2015

In a recent article in Critical Care, Tapia and colleagues evaluated the relationship between exogenous lactate clearance and liver perfusion in a short-term model of endotoxemic shock [1]. The authors concluded that the very low portal-hepatic vein lactate gradient was indicative of the inability of the liver to metabolize the increased lactate load. Although we believe that the authors addressed an important issue, we have some concerns regarding their methodology.

The portal-hepatic vein lactate gradient as a surrogate of liver lactate metabolism may be misleading, since systemic hyperlactatemia increases hepatic arterial lactate delivery and may result in net mesenteric lactate uptake [2]. Given a contribution of 15 % of the hepatic artery to total hepatic blood flow [3], hepatic lactate uptake in endotoxemic animals in the study by Tapia and colleagues (portal vein plus hepatic artery lactate delivery minus hepatic vein lactate efflux) would have roughly doubled during their experiment. At the same time, the net mesenteric lactate uptake (estimated from the product of portal vein flow and portal vein-arterial lactate gradient) increased more than sevenfold. Given the increased mesenteric and hepatic lactate uptake in the study by Tapia and colleagues, we wonder how it is possible that exogenous lactate clearance decreased by a factor of more than 20 during their experiment [1]. Finally, the authors took only six arterial lactate samples until 20 min after completion of L-lactate infusion as opposed to 20 samples with an extension up to 60 min after completion of L-lactate infusion in the original literature [4, 5] and did not present the results, although this was their main finding.

Notes

Declarations

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Intensive Care Unit, Hospital Israelita Albert Einstein
(2)
Department of Intensive Care Medicine, Inselspital, Bern University Hospital and University of Bern

References

  1. Tapia P, Soto D, Bruhn A, Alegria L, Jarufe N, Luengo C, et al. Impairment of exogenous lactate clearance in experimental hyperdynamic septic shock is not related to total liver hypoperfusion. Crit Care. 2015;19:188.PubMed CentralView ArticlePubMedGoogle Scholar
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  4. Connor H, Woods HF, Ledingham JG, Murray JD. A model of L(+)-lactate metabolism in normal man. Ann Nutr Metab. 1982;26:254–63.View ArticlePubMedGoogle Scholar
  5. Levraut J, Ciebiera JP, Chave S, Rabary O, Jambou P, Carles M, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J Respir Crit Care Med. 1998;157:1021–6.View ArticlePubMedGoogle Scholar

Copyright

© Corrêa et al. 2015

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