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

Détails

ID Serval
serval:BIB_4DC5C860E150
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Hyperlactatémie et acidose lactique chez le patient critique [Hyperlactatemia and lactic acidosis in the critically ill patient].
Périodique
Revue Médicale Suisse
Auteur⸱e⸱s
Ben-Hamouda N., Haesler L., Liaudet L.
ISSN
1660-9379 (Print)
ISSN-L
1660-9379
Statut éditorial
Publié
Date de publication
2013
Volume
9
Numéro
410
Pages
2335-2340
Langue
français
Notes
Publication types: English Abstract ; Journal Article ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
Résumé
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.
Mots-clé
Acidosis, Lactic/blood, Acidosis, Lactic/complications, Critical Illness, Humans, Lactates/blood, Lactates/metabolism
Pubmed
Création de la notice
06/03/2014 14:45
Dernière modification de la notice
20/08/2019 14:02
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