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Chest Jan 2016Increased blood lactate concentration (hyperlactatemia) and lactic acidosis (hyperlactatemia and serum pH < 7.35) are common in patients with severe sepsis or septic... (Review)
Review
Increased blood lactate concentration (hyperlactatemia) and lactic acidosis (hyperlactatemia and serum pH < 7.35) are common in patients with severe sepsis or septic shock and are associated with significant morbidity and mortality. In some patients, most of the lactate that is produced in shock states is due to inadequate oxygen delivery resulting in tissue hypoxia and causing anaerobic glycolysis. However, lactate formation during sepsis is not entirely related to tissue hypoxia or reversible by increasing oxygen delivery. In this review, we initially outline the metabolism of lactate and etiology of lactic acidosis; we then address the pathophysiology of lactic acidosis in sepsis. We discuss the clinical implications of serum lactate measurement in diagnosis, monitoring, and prognostication in acute and intensive care settings. Finally, we explore treatment of lactic acidosis and its impact on clinical outcome.
Topics: Acidosis, Lactic; Humans; Sepsis
PubMed: 26378980
DOI: 10.1378/chest.15-1703 -
The New England Journal of Medicine Dec 2014
Review
Topics: Acid-Base Equilibrium; Acidosis, Lactic; Fluid Therapy; Humans; Hyperlactatemia; Lactic Acid; Prognosis; Sodium Bicarbonate
PubMed: 25494270
DOI: 10.1056/NEJMra1309483 -
Chest Jan 2000Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause,... (Review)
Review
Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause, ensuring adequate oxygen delivery to tissues, reducing oxygen demand through sedation and mechanical ventilation, and (most controversially) attempting to alkalinize the blood with IV sodium bicarbonate. Here we review the literature to answer the following questions: Is a low pH bad? Can sodium bicarbonate raise the pH in vivo? Does increasing the blood pH with sodium bicarbonate have any salutary effects? Does sodium bicarbonate have negative side effects? We find that the oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly. Further, given the lack of evidence supporting its use, we cannot condone bicarbonate administration for patients with lactic acidosis, regardless of the degree of acidemia.
Topics: Acidosis, Lactic; Animals; Humans; Hydrogen-Ion Concentration; Infusions, Intravenous; Sodium Bicarbonate; Treatment Outcome
PubMed: 10631227
DOI: 10.1378/chest.117.1.260 -
PLoS Pathogens Jan 2021Lactic acidosis and hyperlactatemia are common metabolic disturbances in patients with severe malaria. Lactic acidosis causes physiological adverse effects, which can... (Review)
Review
Lactic acidosis and hyperlactatemia are common metabolic disturbances in patients with severe malaria. Lactic acidosis causes physiological adverse effects, which can aggravate the outcome of malaria. Despite its clear association with mortality in malaria patients, the etiology of lactic acidosis is not completely understood. In this review, the possible contributors to lactic acidosis and hyperlactatemia in patients with malaria are discussed. Both increased lactate production and impaired lactate clearance may play a role in the pathogenesis of lactic acidosis. The increased lactate production is caused by several factors, including the metabolism of intraerythrocytic Plasmodium parasites, aerobic glycolysis by activated immune cells, and an increase in anaerobic glycolysis in hypoxic cells and tissues as a consequence of parasite sequestration and anemia. Impaired hepatic and renal lactate clearance, caused by underlying liver and kidney disease, might further aggravate hyperlactatemia. Multiple factors thus participate in the etiology of lactic acidosis in malaria, and further investigations are required to fully understand their relative contributions and the consequences of this major metabolic disturbance.
Topics: Acidosis, Lactic; Humans; Malaria; Plasmodium
PubMed: 33411818
DOI: 10.1371/journal.ppat.1009122 -
American Journal of Physiology.... Sep 2004The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the... (Review)
Review
The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P(i), a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD(+) needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.
Topics: Acidosis; Acidosis, Lactic; Animals; Buffers; Exercise; History, 18th Century; History, 20th Century; Humans; Lactic Acid; Models, Biological; Protons
PubMed: 15308499
DOI: 10.1152/ajpregu.00114.2004 -
Minerva Anestesiologica Apr 2003The detection of tissue hypoxia and its correction is one of the aim of the hemodynamic monitoring. Classical hemodynamic variable often fail to achieve this goal.... (Review)
Review
The detection of tissue hypoxia and its correction is one of the aim of the hemodynamic monitoring. Classical hemodynamic variable often fail to achieve this goal. Lactate measurements may be a good indicator of tissue hypoxia. Selected review of the articles on lactate in critically ill patients. Tissue hypoxia is associated with an increase in blood lactate levels. However lactate can also be produced in aerobic conditions, in inflammated tissues, and lactate clearance is often decreased in critically ill patients. Whatever its origin, blood lactate levels have a strong predictive value. The interpretation of blood lactate levels is difficult. Nevertheless, monitoring blood lactate levels can be useful to detect tissue hypoxia and to monitor the effects of therapy.
Topics: Acidosis, Lactic; Aerobiosis; Anaerobiosis; Humans; Lactates; Prognosis; Sepsis
PubMed: 12766720
DOI: No ID Found -
Endocrinology and Metabolism Clinics of... Jun 1993Lactic acidosis is the most common metabolic acidosis. At clinical presentation, several causes usually can be identified. The liver is a major site of removal of... (Review)
Review
Lactic acidosis is the most common metabolic acidosis. At clinical presentation, several causes usually can be identified. The liver is a major site of removal of lactate and hydrogen ions, and abnormalities in the aerobic metabolism of lactate by mitochondria in hepatocytes and other cells may contribute to many clinical conditions in which overproduction and underuse of lactate occur. To date, no therapy specifically designed to lower arterial blood lactate levels has reduced mortality significantly. Prompt recognition and treatment of the underlying causes of lactic acidosis remain the cornerstone of treatment.
Topics: Acidosis, Lactic; Humans
PubMed: 8325284
DOI: No ID Found -
Nutrition in Clinical Practice :... Dec 2005D-lactic acidosis, also referred to as D-lactate encephalopathy, is a rare neurologic syndrome that occurs in individuals with short bowel syndrome or following... (Review)
Review
D-lactic acidosis, also referred to as D-lactate encephalopathy, is a rare neurologic syndrome that occurs in individuals with short bowel syndrome or following jejuno-ileal bypass surgery. Symptoms typically present after the ingestion of high-carbohydrate feedings. Neurologic symptoms include altered mental status, slurred speech, and ataxia, with patients often appearing drunk. Onset of neurologic symptoms is accompanied by metabolic acidosis and elevation of plasma D-lactate concentration. In these patients, malabsorbed carbohydrate is fermented by an abnormal bacterial flora in the colon, which produces excessive amounts of D-lactate. High amounts of D-lactate are absorbed into the circulation, resulting in an elevated concentration of D-lactate in the blood. Development of neurologic symptoms has been attributed to D-lactate, but it is unclear if this is the cause or whether other factors are responsible. This review examines the pathophysiology of the production and accumulation of D-lactate while exploring the potential factors contributing to the development of neurologic manifestations. Methods of diagnosis and treatment are reviewed. Areas requiring further investigation are identified.
Topics: Acidosis, Lactic; Humans
PubMed: 16306301
DOI: 10.1177/0115426505020006634 -
American Journal of Therapeutics Jul 2022
Topics: Acidosis, Lactic; Anti-HIV Agents; Humans; Lamivudine; Reverse Transcriptase Inhibitors
PubMed: 35622009
DOI: 10.1097/MJT.0000000000000922 -
Clinical Medicine (London, England) Nov 2023Lactic acidosis is commonly associated with tissue hypoperfusion and gives rise to concern regarding hypoxia or underlying hypotension. In the cancer patient, especially...
Lactic acidosis is commonly associated with tissue hypoperfusion and gives rise to concern regarding hypoxia or underlying hypotension. In the cancer patient, especially one undergoing chemotherapy, there is always concern for sepsis; however, in the otherwise clincially stable patient with cancer, type B lactic acidosis can also be related to their underlying malignancy. It is considered a haematological emergency given its high mortality rate. However, despite the urgency to treat type B lactic acidosis in these circumstances, treatment options beyond treatment of the malignancy are limited, and its presence portends a poor prognosis. This case highlights our current understanding of type B lactic acidosis and an approach to lactic acidosis evaluation in the cancer patient.
Topics: Humans; Acidosis, Lactic; Neoplasms; Sepsis
PubMed: 38065594
DOI: 10.7861/clinmed.2023-0391