Résumé
L’existence d’une acidose lactique est généralement synonyme chez un patient en réanimation d’une situation clinique grave. Les étiologies de l’acidose lactique sont multiples, classées en type A liées à l’hypoxie tissulaire et type B regroupant les causes liées à des maladies primitives sousjacentes, aux intoxications et iatrogénies ou à des maladies congénitales du métabolisme. L’état de choc est sans conteste la situation la plus typique d’acidose lactique en réanimation, mais elle ne sera pas abordée dans cette revue. L’hyperlactatémie résulte de l’apparition d’un déséquilibre entre la production (stimulation de la glycolyse anaérobie ou dysfonction de la chaîne respiratoire mitochondriale) et la clairance des lactates. Les expositions toxiques sont l’une des causes principales d’acidose lactique, avec notamment la metformine, le cyanure, l’acide valproïque, les inhibiteurs nucléosidiques/nucléotidiques de la réverse transcriptase et les substances adrénergiques. Lorsqu’une acidose lactique apparaît chez un patient déjà hospitalisé en réanimation, il faut savoir évoquer une hypothèse iatrogène comme un syndrome de perfusion du propofol, une intoxication au propylène glycol ou un effet secondaire d’une perfusion d’une catécholamine béta-adrénergique ou d’une prescription de linézolide. D’autres étiologies, souvent évidentes d’emblée mais parfois plus complexes à établir, sont associées à la survenue d’une acidose lactique, comme les convulsions ou état de mal convulsif notamment tonicoclonique ou l’insuffisance hépatocellulaire. Plus rarement, une acidose lactique inexpliquée peut orienter vers la découverte d’une néoplasie ou d’une hémopathie sous-jacente. Enfin, il faut savoir évoquer, chez certains patients à risque, un déficit en thiamine, en biotine ou une erreur innée du métabolisme des hydrates de carbone. Dans tous les cas et en l’absence d’un traitement spécifique de l’hyperlactatémie, la prise en charge d’une acidose lactique fait appel au traitement étiologique qu’il faut savoir instaurer en urgence, après avoir suspecté ou établi l’étiologie potentielle, en raison du mauvais pronostic généralement associé à la persistance ou à l’aggravation de l’hyperlactatémie et de l’acidose.
Abstract
The development of lactic acidosis in a patient admitted in the intensive care unit (ICU) usually indicates a severe clinical situation. Etiologies of lactic acidosis are multiple and classified as A-type in relation to tissue hypoxia and B-type including all cases related to underlying primary diseases, poisonings and iatrogenic events as well as inborn errors of metabolism. Circulatory failure is clearly the most typical situation associated with lactic acidosis in the ICU; however, this cause will not be discussed in this review. Increase in blood lactate concentrations results from an unbalance between lactate production (stimulation of anaerobic glycolysis or dysfunction of mitochondria respiratory chain) and clearance. Toxic exposures represent a major cause of lactic acidosis, including intoxications with metformin, cyanide, valproic acid, nucleoside/tide reverse transcriptase inhibitors, and adrenergic stimulants. In the presence of ICU-acquired lactic acidosis, iatrogenic hypotheses should be suggested like propofol infusion syndrome, propylene glycol intoxication, as well as beta-adrenergic catecholamine- and linezolid-related side-effect. Other etiologies, sometimes obvious and sometimes more difficult to assess, include liver insufficiency and seizures or status epilepticus especially if tonic or clonic. More rarely, lactic acidosis leads to the identification of an underlying solid cancer or blood malignancy. Finally, in selected patients at risk, vitamin deficiencies like thiamine and biotin as well as inborn errors of sugar metabolism should be suspected. In all lactic acid cases as no specific treatment of increased blood lactate exist, patient management should rely on the treatment of the underlying etiology and be prompt once the diagnosis is assessed, since this severe condition is usually associated with a bad final outcome.
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Cet article correspond à la conférence faite par l’auteur au congrès de la SRLF 2013 dans la session: Des maladies qu’il faut connaître.
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Mégarbane, B. Acidoses lactiques graves en dehors des états de choc. Réanimation 22 (Suppl 2), 435–445 (2013). https://doi.org/10.1007/s13546-013-0654-2
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DOI: https://doi.org/10.1007/s13546-013-0654-2
Mots clés
- Lactate
- Acidose métabolique
- Intoxication
- Metformine
- Cyanure
- Acide valproïque
- Convulsion
- Insuffisance hépatocellulaire