Jean-Sebastien Rachoin1, Lawrence S Weisberg, Christopher B McFadden. 1. Division of Nephrology, Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Cooper University Hospital, Camden, New Jersey 08103, USA. Rachoin-Jean@CooperHealth.edu
Abstract
BACKGROUND: Lactic acidosis (LA) is common in hospitalized patients and is associated with poor clinical outcomes. There have been major recent advances in our understanding of lactate generation and physiology. However, treatment of LA is an area of controversy and uncertainty, and the use of agents to raise pH is not clearly beneficial. AIM AND METHODS: We reviewed animal and human studies on the pathogenesis, impact, and treatment of LA, published in the English language and available through the PubMed/MEDLINE database. Our aim was to clarify the physiology of the generation of LA, its impact on outcomes, and the different treatment modalities available. We also examined relevant data regarding LA induced by medications commonly prescribed by hospitalists: biguanides, nucleoside analog reverse-transcriptase inhibitors (NRTIs), linezolid, and lorazepam. RESULTS/ CONCLUSIONS: Lactic acid is a marker of tissue ischemia but it also may accumulate without tissue hypoperfusion. In the latter circumstance, lactic acid accumulation may be an adaptive mechanism-a novel possibility quite in contrast to the traditional view of lactic acid as only a marker of tissue ischemia. Studies on the treatment of LA with sodium bicarbonate or other buffers fail to show consistent clinical benefit. Severe acidemia in the setting of LA is a particularly poorly studied area. In the settings of medication-induced LA, optimal treatment, apart from prompt cessation of the offending agent, is still unclear. (c) 2010 Society of Hospital Medicine.
BACKGROUND:Lactic acidosis (LA) is common in hospitalized patients and is associated with poor clinical outcomes. There have been major recent advances in our understanding of lactate generation and physiology. However, treatment of LA is an area of controversy and uncertainty, and the use of agents to raise pH is not clearly beneficial. AIM AND METHODS: We reviewed animal and human studies on the pathogenesis, impact, and treatment of LA, published in the English language and available through the PubMed/MEDLINE database. Our aim was to clarify the physiology of the generation of LA, its impact on outcomes, and the different treatment modalities available. We also examined relevant data regarding LA induced by medications commonly prescribed by hospitalists: biguanides, nucleoside analog reverse-transcriptase inhibitors (NRTIs), linezolid, and lorazepam. RESULTS/ CONCLUSIONS:Lactic acid is a marker of tissue ischemia but it also may accumulate without tissue hypoperfusion. In the latter circumstance, lactic acid accumulation may be an adaptive mechanism-a novel possibility quite in contrast to the traditional view of lactic acid as only a marker of tissue ischemia. Studies on the treatment of LA with sodium bicarbonate or other buffers fail to show consistent clinical benefit. Severe acidemia in the setting of LA is a particularly poorly studied area. In the settings of medication-induced LA, optimal treatment, apart from prompt cessation of the offending agent, is still unclear. (c) 2010 Society of Hospital Medicine.
Authors: Garry M Steil; Olive S Eckstein; Julie Caplow; Michael S D Agus; Brian K Walsh; Jackson Wong Journal: J Clin Monit Comput Date: 2011-06-21 Impact factor: 2.502