Skip to main content
main-content

01.10.2014 | Review | Ausgabe 5/2014 Open Access

Critical Care 5/2014

Sepsis-associated hyperlactatemia

Zeitschrift:
Critical Care > Ausgabe 5/2014
Autoren:
Mercedes Garcia-Alvarez, Paul Marik, Rinaldo Bellomo
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​s13054-014-0503-3) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Abstract

There is overwhelming evidence that sepsis and septic shock are associated with hyperlactatemia (sepsis-associated hyperlactatemia (SAHL)). SAHL is a strong independent predictor of mortality and its presence and progression are widely appreciated by clinicians to define a very high-risk population. Until recently, the dominant paradigm has been that SAHL is a marker of tissue hypoxia. Accordingly, SAHL has been interpreted to indicate the presence of an `oxygen debt’ or `hypoperfusion’, which leads to increased lactate generation via anaerobic glycolysis. In light of such interpretation of the meaning of SAHL, maneuvers to increase oxygen delivery have been proposed as its treatment. Moreover, lactate levels have been proposed as a method to evaluate the adequacy of resuscitation and the nature of the response to the initial treatment for sepsis. However, a large body of evidence has accumulated that strongly challenges such notions. Much evidence now supports the view that SAHL is not due only to tissue hypoxia or anaerobic glycolysis. Experimental and human studies all consistently support the view that SAHL is more logically explained by increased aerobic glycolysis secondary to activation of the stress response (adrenergic stimulation). More importantly, new evidence suggests that SAHL may actually serve to facilitate bioenergetic efficiency through an increase in lactate oxidation. In this sense, the characteristics of lactate production best fit the notion of an adaptive survival response that grows in intensity as disease severity increases. Clinicians need to be aware of these developments in our understanding of SAHL in order to approach patient management according to biological principles and to interpret lactate concentrations during sepsis resuscitation according to current best knowledge.
Zusatzmaterial
Literatur
Über diesen Artikel

Weitere Artikel der Ausgabe 5/2014

Critical Care 5/2014 Zur Ausgabe

Neu im Fachgebiet AINS

Mail Icon II Newsletter

Bestellen Sie unseren kostenlosen Newsletter Update AINS und bleiben Sie gut informiert – ganz bequem per eMail.

Bildnachweise