0
Correspondence |

ResponseResponse FREE TO VIEW

Alan E. Jones, MD
Author and Funding Information

From the Department of Emergency Medicine, University of Mississippi Medical Center.

Correspondence to: Alan E. Jones, MD, Department of Emergency Medicine, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216; e-mail: aejones@umc.edu


Financial/nonfinancial disclosures: The author has reported to CHEST the following conflicts of interest: Dr Jones has received funding from the National Institutes of Health to study lactate clearance in sepsis resuscitation. Dr Jones has never been assigned patents, nor has he received patent royalties, honoraria, consulting fees, or other monetary or nonmonetary payments at any time related to the use of lactate or lactate clearance.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(5):1362-1363. doi:10.1378/chest.12-0355
Text Size: A A A
Published online

To the Editor:

I thank Dr Manthous for his interest in the recently published Point/Counterpoint Editorials.1,2 A large portion of his letter addresses concepts and critiques of the trial by Rivers et al,3 which I will leave to Dr Rivers to address. Dr Manthous does, however, raise the point that lactic acidosis is not a marker of tissue-level hypoxia. As stated in my Point Editorial,1 elevated lactate levels reflect the total picture of energy metabolism in the acutely stressed patient with sepsis. Both anaerobic and aerobic processes contribute to lactate production in sepsis. Thus, as opposed to central venous oxygen saturation, which is a rudimentary indicator of only the balance between oxygen supply and demand, lactate clearance biologically reflects more of the general homeostasis of the host and provides more meaningful data about the overall adequacy of the resuscitative processes. I take issue with Dr Manthous’s assertion that treating the macrocirculation using lactic acidosis as a marker of success is ill founded. Human and controlled animal studies alike have consistently shown that impaired oxygen transfer at any point from the lungs to the nicotinamide adenine dinucleotide oxidase enzyme will cause lactic acidosis, and clearing lactate levels almost always signifies improvement in host oxygen use. As such, lactate clearance as a choice of a resuscitative end point in sepsis is supported by high-quality human and animal data and can assist clinicians in their bedside care of this disease.

Jones AE. Point: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy?Yes. Chest. 2011;1406:1406-1408. [CrossRef] [PubMed]
 
Rivers EP, Elkin R, Cannon CM. Counterpoint: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy?No. Chest. 2011;1406:1408-1413. [CrossRef] [PubMed]
 
Rivers E, Nguyen B, Havstad S, et al. Early Goal-Directed Therapy Collaborative Group Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;34519:1368-1377. [CrossRef] [PubMed]
 

Figures

Tables

References

Jones AE. Point: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy?Yes. Chest. 2011;1406:1406-1408. [CrossRef] [PubMed]
 
Rivers EP, Elkin R, Cannon CM. Counterpoint: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy?No. Chest. 2011;1406:1408-1413. [CrossRef] [PubMed]
 
Rivers E, Nguyen B, Havstad S, et al. Early Goal-Directed Therapy Collaborative Group Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;34519:1368-1377. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543