Hyperlactatémie et acidose lactique chez le patient critique [Hyperlactatemia and lactic acidosis in the critically ill patient].

Details

Serval ID
serval:BIB_4DC5C860E150
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Hyperlactatémie et acidose lactique chez le patient critique [Hyperlactatemia and lactic acidosis in the critically ill patient].
Journal
Revue Médicale Suisse
Author(s)
Ben-Hamouda N., Haesler L., Liaudet L.
ISSN
1660-9379 (Print)
ISSN-L
1660-9379
Publication state
Published
Issued date
2013
Volume
9
Number
410
Pages
2335-2340
Language
french
Notes
Publication types: English Abstract ; Journal Article ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
Abstract
Hyperlactatemia is associated with an ominous prognosis in critical illness and must be rapidly detected. Lactate is produced by glycolysis through reduction of pyruvate, itself oxidized in the mitochondria. It is transported to the liver and converted to glucose through gluconeogenesis (Cori's cycle). Hyperlactatemia can result from excessive production or reduced clearance. Excess production can occur in aerobic conditions, following an increase in pyruvate generation, or in anaerobic conditions, due to impaired pyruvate oxidation. Reduced lactate clearance occurs as a result of liver hypoperfusion or hepatic failure. Lactate/pyruvate ratio, as well as the concomitant existence of metabolic acidosis (lactic acidosis), help distinguish the different mechanisms leading to hyperlactatemia, which are reviewed in detail in this article.
Keywords
Acidosis, Lactic/blood, Acidosis, Lactic/complications, Critical Illness, Humans, Lactates/blood, Lactates/metabolism
Pubmed
Create date
06/03/2014 15:45
Last modification date
20/08/2019 15:02
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