Advertisment Fosfocin
Indian Journal of Critical Care Medicine
An open access publication of ISCCM™ 
Users online: 1711 
     Home | Login 
  About Current Issue Archive Search Instructions Online Submission Subscribe Etcetera Contact  
 » Next article
 » Previous article 
 » Table of Contents
 »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
 »  Article in PDF (72 KB)
 »  Citation Manager
 »  Access Statistics
 »  Reader Comments
 »  Email Alert *
 »  Add to My List *
* Registration required (free) 

  IN THIS Article
 »  Abstract
 »  Introduction
 »  Lactate Metabolism
 »  Classification
 »  Importance of La...
 »  References
 »  Article Figures
 »  Article Tables

 Article Access Statistics
    PDF Downloaded961    
    Comments [Add]    
    Cited by others 3    

Recommend this journal


Year : 2004  |  Volume : 8  |  Issue : 3  |  Page : 173-181

Role of lactate in critically ill children

Department of Pediatrics, Sir Ganga Ram Hospital, New Delhi - 110 060, India

Correspondence Address:
Anil Sachdev
63/12, Old Rajinder Nagar, New Delhi - 110 060
Login to access the Email id

Source of Support: None, Conflict of Interest: None

Rights and PermissionsRights and Permissions

 » Abstract 

Lactic acidosis is a common finding in critically ill patients. It has been used as a prognostic marker of the outcome in Pediatric Intensive Care Unit patients. Lactic acid is produced as a product of anaerobic glycolysis and is reversibly converted to pyruvate in the presence of favorable metabolic environment. All the body tissues can produce and consume lactate with few having predominant function of production and others of consumption. Liver is a major organ for lactate consumption and it is the liver, which metabolizes the increased lactic acid produced in regional tissue beds. The lactate levels can be done on arterial, venous, or mixed venous blood and can be measured by various methods. Serial lactate concentrations and the difference in arterial and mixed venous lactate levels or between the arterial and regional blood lactate levels like jugular venous lactate levels have been shown to have better correlation with the outcome. High initial blood lactate levels and persistently high lactate levels have been correlated with poor outcome. There are various causes of lactic acid overproduction, which may produce either hyperlactatemia or lactic acidosis. High blood lactate levels are found in critically ill patients with shock of any etiology and sepsis due to various reasons, which include increased catecholamine induced glucose flux apart from the tissue hypoperfusion and hypoxia. Various other illnesses can cause an increase in blood lactate levels like acute lung/liver injury, severe asthma, poisoning, post cardiac surgery etc. Treating the underlying disease leading to lactic acidosis is the best measure to control lactic acidosis. Some therapeutic choices are available to neutralize the effect of lactic acid on cell function, but none has stood the test of time and are tried only in desperate situations.

Keywords: Lactic acidosis, glycolysis, shock, sepsis, blood lactate levels

How to cite this article:
Agrawal S, Sachdev A, Gupta D, Chugh K. Role of lactate in critically ill children. Indian J Crit Care Med 2004;8:173-81

How to cite this URL:
Agrawal S, Sachdev A, Gupta D, Chugh K. Role of lactate in critically ill children. Indian J Crit Care Med [serial online] 2004 [cited 2018 Apr 19];8:173-81. Available from:

 » Introduction Top

Lactic acidosis was first described clinically by Clausen in 1925 and later classified biochemically by Huckabee.[1],[2] Lactic acidosis is a broad anion gap metabolic acidosis caused by either overproduction or underutilization of lactate. Overproduction of lactate (also called type A lactic acidosis) occurs when the body generates ATP without oxygen, i.e., tissue hypoxia.[2],[3] Underutilization involves decreased removal of lactic acid by oxidation or conversion to glucose.[2],[3]

As more research is being done on the lactate values and their correlation with prognosis, the parameter has become established as an important marker for the Intensive care units.

While the initial studies showed an increased mortality associated with peak serum lactate levels,[4] further work on the same subject failed to correlate well with this finding and demonstrated the significance of serial lactate levels over single values.[5] Although arterial lactate values have been used as an indicator of severity and prognosis in patients with acute shock,[4] in particular and in critically ill patients in general,[6] recent studies demonstrate a good correlation of arterial lactate with lactate levels in venous blood and mixed venous (pulmonary artery) blood.[7] The prognosis has been shown to depend more on the decrease in the measured serum lactate overtime, whether achieved by decreased production, increased clearance or both, rather than to the peak levels.

Hyperlactatemia is a cardinal finding of sepsis and septic shock. It is said that the mechanism of hyperlactatemia for the two is different. While in sepsis, the increased lactate levels represent the increased glycolytic flux due to hypermetabolism, in septic shock; the increase in glycolytic flux is because of tissue hypoxia. This suggests that there are two varieties of lactate namely, the "stress lactate" and the "shock lactate".[8]

Off late, reports of patients with normal or mildly increased lactate values in the setting of hyperlactatemia have been published. Further scrutinization explains this phenomenon to be because of decreased lactate clearance rather than overproduction.[9],[10]

To understand the importance of these values and correlate them with various clinical settings, it becomes essential to understand the lactate metabolism in brief.

 » Lactate Metabolism Top

The normal blood lactate concentration in an unstressed patient is 1.0 + 0.5 mmol/L.[2] The concentration in arterial blood depends on the rate of production and conversion by various organs and is normally maintained below 2 mmol/L. The turnover in various studies has been reported to be as high as 1300 mmol per 24 hrs.[11]

Lactate is a byproduct of glycolysis. During glycolysis, by an anaerobic process taking place in the cytosol, 2 molecules of ATP are produced alongwith pyruvate per molecule of glucose hydrolyzed. Pyruvate produced can have two fates, if the tissue redox potential is favorable; it enters the Kreb's cycle for further metabolism and production of more ATP's, and if the redox potential is not favorable, it gets converted to lactate [Figure - 1].[12] Conversion to lactate is a reversible process catalyzed by enzyme lactate dehydrogenase (LDH).[13]

Lactate is either converted back to pyruvate, which may then enter the Kreb's cycle in the mitochondria for further metabolism or is used in neoglucogenesis.[13] The pyruvate is consumed in aerobic tissues by two oxidative processes: - conversion to Acetyl-CoA by pyruvate dehydrogenase enzyme (PDH) complex in the presence of NAD+ or by use in gluconeogenesis [Figure - 1].[12] Impaired metabolic function of the mitochondrion in hypoxic states leads to accumulation of lactate.[14] This occurs due to increased production of pyruvate and decreased clearance by the two pathways and essentially represents the toll organism has to pay for energy generation during anaerobic state.[14]

The most important step in lactate homeostasis is the reversible reaction of conversion of lactate to pyruvate and vice-versa (Equation 1).

This equation can be rearranged as follows (Equation 2), which determines the concentration of lactate in the body at a given point of time.

The equilibrium of the equation favors formation of lactate and in a normal individual lactate levels are 4-10 times higher than pyruvate levels.[3],[15] The equation signifies that three factors, namely, pyruvate concentration, NADH/NAD+ ratio (redox potential) and the intracellular hydrogen ion concentration determine the cytosolic lactate concentration. Pyruvate concentration is determined by the rate of glycolysis, which in turn is controlled by NAD+ concentration.[13],[15]

The NADH/NAD+ ratio is altered in states of hypoxia and mitochondrial dysfunction. This ratio i.e., reduced to oxidized NAD, determines the lactate: pyruvate ratio. Whenever the rate of glycolysis increases with a normal redox potential, the lactate: pyruvate ratio remains stable as both lactate and pyruvate levels increase in proportion to each other. But if the redox potential is not favorable, the lactate levels rise out of proportion to the pyruvate levels.[13],[15]

The intracellular H+ ion concentration should increase the accumulation of lactate according to the equation given above but the strong effect of pH on one of the rate-limiting enzyme of glycolysis, phosphofructokinase, overrides the effect. The enzyme is inhibited in presence of intracellular acidosis and is augmented in presence of intracellular alkalosis.[13],[15]

All body tissues are equipped for glycolysis, but the rate is higher in brain, skeletal muscles, heart, and intestinal mucosa. All body cells and tissues can produce and consume lactate except for erythrocytes, which cannot utilize lactate. A small portion of lactate is produced in the liver by transamination and in the kidney during ammoniagenesis. But there are certain body tissues, which produce or consume more lactate than the rest. These are listed in [Table - 1] and [Table - 2].[13],[15]

The increased amount of lactate produced at the tissue level due to local injury/insult is carried via lactate shuttle to the liver where it is metabolized. This delays the rise in lactate levels in the arterial blood till the time metabolic capacity of liver is exceeded.[13]

Liver has a massive capacity to metabolize lactate, which increases manifold in hyperlactatemic states. With the lactate uptake and metabolism by the liver there is synthesis of glucose with regeneration of HCO[3]. The extraction of lactate by the liver is an important factor, increasing as the blood flow decreases till the blood flow is lower than 25% of normal. Liver itself becomes an important source of lactate production when its own blood decreases to about 75%. Similarly renal consumption of lactate increases in states of hyperlactatemia, which enters both the metabolic and oxidative pathways.[13],[15]

 » Classification Top

Increased lactate levels may occur with or without concomitant metabolic acidosis. Normal lactate levels are < 2 mmol/L. Hyperlactatemia is defined as a persistent increase in blood lactate concentration (2-5 mmol/L) without metabolic acidosis, while lactic acidosis is metabolic acidosis associated with persistently high lactate levels (>5 mmol/L).[2],[3]

Hyperlactatemia is usually seen in conditions with maintained tissue perfusion and adequate buffering systems, which compensate for the fall in pH. It is also seen in conditions associated with increased pyruvate concentration, like transamination, down-regulation of PDH and occurs as a consequence of the factors which increase the glycolytic flux of glucose as in catecholamine administration and alkalosis. It is usually seen in critically ill children with hypermetabolic states like sepsis, burns and trauma. But here, the body buffers are able to mitigate any fall in pH caused by increasing lactate.[2],[3]

Lactic acidosis (LA) in contrast is associated with major metabolic dysregulation in conditions of tissue hypoperfusion, drug effect or metabolic abnormality. Lactate accumulation in blood depends on rate of glycolysis, exchange of lactate across cell membranes, lactate washout by circulation and lactate consumption and clearance by tissues.[3]

Cohen and Wood classified LA as type A and B according to the cause for increase in lactate level. It was also classified later as type I and type II depending upon the relative proportions of lactate and pyruvate. In Type I, lactate/pyruvate ratio is maintained, indicating a proportional increase of lactate and pyruvate. Type II is defined by a relatively greater increase in lactate levels as compared to pyruvate levels. Though the classification as A and B has its shortcomings, the classification is still in use, as given in [Table - 3].[2],[3]

Laboratory Tests for lactate

Lactate levels can be measured in plasma, serum or whole blood. Off late, various studies have shown better results with whole blood lactate levels, which require less quantity, give rapid results, and can be done by new available hand held devices which can be used in a bed side laboratory.[16],[17],[18]

Due to unavailability of such devices in our set-up, the lactate levels are done by autoanalyzers on citrated blood, which should ideally be transported and analyzed immediately and should be kept on ice after withdrawing the sample. Some authors recommend use of sodium heparin for the sample collection.[19]

It is unusual to find a lactate level more than 4 mmol/L in normal individuals, though different series report different values.[19] The Harriet Lane handbook of Pediatric Formulary[20] gives the following values as normal [Table - 4].

Ideal values are obtained from arterial blood samples, but some series have taken mixed venous and arterial level difference and correlated it with the regional deficiency in oxygen delivery, while some other studies have reported an equal value of lactate in hemodynamically stable critically ill patients in arterial and mixed venous bloods.[21] Whole blood lactate concentration may be affected by the hematocrit values.[18]

Blood lactate levels are also affected by the use of lactated Ringer, especially if the sample is drawn from the same catheter in which the fluid is being infused.[21]


A monitoring variable with predictive value becomes more valuable if the treatment can be adjusted by the serial determination of the parameter. Various studies have tried multiple therapeutic maneuvers to decrease the blood lactate levels. The primary treatment of lactic acidosis is to correct the underlying cause and may include additional supportive management. The main management strategy for Type A lactic acidosis is hemodynamic optimization, which at times helps Type B lactic acidosis also, where there can be occult tissue hypoperfusion. This is achieved by volume support, judicious use of vasopressors and mechanical ventilation.[2],[22] The following therapeutic options are also available but have not shown very consistent results, so are not used routinely.

1. Dichloroacetate: Dichloroacetate has been shown to increase the activity of enzyme pyruvate dehydrogenase complex and has been found to lead to a small but significant reduction in lactate levels, though no survival benefit or hemodynamic improvement was observed in any of these studies. This has been found more beneficial in type B lactic acidosis.[3],[22]

2. Bicarbonate: In the recent times, bicarbonate has fallen in disfavor, because of various factors [Table - 5]. Though there is a known decrease in the cardiac contractility and decreased myocardial performance with a significant fall in pH, bicarbonate administration might not improve it.[23]

However, bicarbonate administration addresses two issues, correction of serum and correction of tissue pH. Thus, despite all the above mentioned side effects, bicarbonate is still recommended for severe acidosis, when the pH is below 7.2.[23],[24],[25],[26]

1. Others: Tromethamine is a non-sodium buffer with a pK nearer to the physiological pH than bicarbonate or other used bases. It buffers the carbonic acid by accepting a proton and generating bicarbonate. It has the advantage of not causing an increase in CO2 and the associated side effects, but has not been found more effective than bicarbonate. It also has known side effects. Various other buffers like carbicarb, tribonat have been tried, but have not been found very effective.[23],[26]

2. Dialysis: Peritoneal dialysis has not been found very effective because most of the dialysate solutions are lactate based and do not decrease the serum lactate concentrations. Citrate based dialysate solutions are not easily available. Most of the critically ill patients are not stable hemodynamically to tolerate hemodialysis and in continuous hemofiltration, there is again a problem of lactate based dialysate solutions.[23],[27]

 » Importance of Lactate in common pediatric critical illnesses Top

1. Shock: Circulatory shock is the commonest cause of hyperlactatemia and the presence of increased blood lactate in shock signifies a poor prognosis [Table - 6]. Border and Weil were the first to state that excess lactate concentration in the patients of circulatory shock indicates poor prognosis with only 11% of the patients with hyperlactatemia surviving in their series.[4] This was later confirmed by the findings of Vitek and Cowley.[28] Fowler observed that the patients who had persistently elevated levels of lactate had poorer prognosis.[29] Certain other researchers then made similar observations that higher lactate level and a persistently elevated level indicated poor prognosis.[15],[30]

Occasionally, underlying disease state of the patient also reflects in the lactate level apart from acute condition and may then fail to have the same prognostic value as otherwise. For example, as the production of lactate also depends on the substrate availability, the malnourished patients in shock have lower lactate level as compared to normal healthy children for the same level of hypoxia. In contrast, a patient with underlying chronic liver disease will mount lactate earlier than those patients who have normal liver function for the same level of hypoxia. Lactate has been found elevated in shock states of varied etiology and correlates with high mortality.[2]

2. Sepsis: In contrast to shock states, the hyperlactatemia seen in patients with sepsis is not a marker of tissue hypoperfusion, but indicates the severity of hypermetabolism. It is expected that even during shock, both hypoxia and hypermetabolism play a role in lactate production [Table - 7].[8]

These have been aptly described by the author as "stress lactate" and "shock lactate" and define the different etiologies for the rise and the severity in the two illnesses.[8]

Blood lactate levels have been found to be the earliest predictor of mortality in sepsis, and identify survivors from non-survivors as early as 12 hrs after admission. In one such study, blood lactate levels > 3 mmol/L at 12 hrs of admission had a positive predictive value for death of 56% and < 3 mmol/L has a positive predictive value for survival of 84%. The predictive value increases to 71% for mortality at 24 hrs, and 86% for survival at the same time.[42] In a recently published study by Levraut et al, the rate of clearance of lactate was found more closely associated with deranged lactate metabolism than the actual levels of lactate. Poor lactate clearance and low endogenous production of lactate is found to be associated with inadequate body response to septic injury.[10]

3. Cardiac Surgery: Survivors have lower lactate values than non-survivors after cardiopulmonary bypass. High lactate levels are also associated with increased number of extra cardiac organs involved and correlated positively with total bypass time and circulatory arrest time.[43] In another series by Duke et al, blood lactate was found the most consistent predictor of major post-operative adverse event.[42] Though it was found to be a marker of stormy post-operative course, it was found to have poor sensitivity.[43]

4. Neonatal Intensive Care: It has again been found to be an early predictor of sepsis and necrotizing enterocolitis in preterm neonates.[44]

5. Bronchial asthma: Use of beta agonist may at times lead to increase in blood lactate level which is associated with hypokalemia and is probably because of associated respiratory alkalosis.[45] Though seen infrequently in pediatric age group, hyperlactatemia has been shown to decrease the bronchodilator response, produce dyselectrolytemia and affect the cardiovascular system.[45]

6. Traumatic brain injury: Arterial to venous blood lactate difference has been shown to correlate with the severity of the traumatic brain injury and can be used as a prognostic marker.[46],[47] Especially the lactate levels done on the jugular venous blood have been shown to have a direct correlation with the neurological outcome when compared with the simultaneous arterial blood lactate levels.[48],[49]

7. Acute Liver Failure: Lactate levels go up in patients with acute liver failure and have been found to come down after liver transplantation where the transplanted liver takes over the function of lactate utilization.[50],[51],[52] Apart from overproduction and underutilization, increased lactate production by the lungs also contributes to the rise in the lactate levels.[35]

8. Acute Lung Injury: in patients developing ARDS, lactate levels have been found high, especially the arterial to venous difference across the lungs. On the contrary, normal lactate levels have been found in other types of respiratory failures. The lactate level in the aforementioned state has been found to correlate with the degree of hypoxia and venous admixture.[34]

9. Acute Cyanide poisoning: during the course of cyanide poisoning, high lactate levels (> 8 mmol/L) are found to be sensitive (94%) and moderately specific (70%) for a toxic blood cyanide concentration. The specificity is further shown to increase in patients not receiving catecholamines.[53]

Overall mortality in patients with lactic acidosis is about 60-70%, and virtually 100% when there is associated hypotension due to inappropriate and inadequate treatment available. It is diagnosed on an average in 1% of the hospital admissions.[54] Hyperlactatemia is common in emergency admission patients. Hyperlactatemia with elevated lactate pyruvate ratio and lactic acidosis is likely to be associated with inadequate tissue perfusion.[55] Hyperlactatemia persisting for > 6 hrs and simultaneous elevation of lactate pyruvate ratio are associated with increased mortality.[54] Admission lactate levels > 5 mmol/L has been shown to have maximum diagnostic efficacy for mortality.[47],[56] Non survivors may be distinguished by the peak lactate level, or by persistent hyperlactatemia after 24 hrs of treatment.[47] Therefore, serial lactate levels are more significant for predicting the patient outcome and effectiveness of the therapy. Judiciously used, blood lactate values can give a direction to the treating intensivist about the severity of initial insult, response to the therapy, and the expected outcome.

 » References Top

1.Nimmo GR, Grant IS, Mackenzie SJ. Lactate and acid-base changes in the critically ill. Postgrad Med J 1991;67:56-61.  Back to cited text no. 1    
2.Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med 1992;20:80-93.  Back to cited text no. 2  [PUBMED]  
3.Luft FC. Lactic Acidosis Update for Critical Care Clinicians. J Am Soc Nephrol 2001;12:15-9.  Back to cited text no. 3    
4.Broder G, Weil MH. Excess lactate: An index of reversibility of shock in human patients. Science 1964;143:1457-9.  Back to cited text no. 4  [PUBMED]  
5.Cowan BN, Burns HJG, Boyle P, et al. The relative prognostic value of lactate and hemodynamic measurements in early shock. Anesthesia 1985:39:750.  Back to cited text no. 5    
6.Cady LD, Weil HH, Afifi AA, et al. Quantitation of severity of critical illness with special reference to blood lactate. Crit Care Med 1973:1;73.  Back to cited text no. 6    
7.Weil MH, Michael S, Rackow EC. Comparison of blood lactate concentration in central vein, pulmonary artery and arterial blood. Crit Care Med 1987:15:489.  Back to cited text no. 7    
8.Mizock BA. The hepatosplanchnic area and hyperlactatemia: A tale of two lactates. Crit Care Med 2001;29:442-59.  Back to cited text no. 8    
9.Levraut J, Ciebiera JP, Chave S, Rabary O, Jambou P, Carles M, et al. Mild hyperlactatemia in stable septic patients is due to impaired lactate clearance rather than overproduction. Am J Respir Crit Care Med 1998;157:1021-6.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Levraut J, Ichai C, Petit I, Ciebierra JP, Perus O, Grimaud D. Low exogenous lactate clearance as an early predictor of mortality in normolactatemic critically ill septic patient. Crit Care Med 2003;31:705-10.  Back to cited text no. 10    
11.Stacpoole PW, Wright EC, Baumgartner TG, Bersin RM, Buchalter S, Curry SH, et al. Natural history and course of acquired lactic acidosis in adults. Am J Med 1994;97:47-54.  Back to cited text no. 11  [PUBMED]  
12.Gutierrez G, Wulf ME. Lactic acidosis in sepsis: A commentary. Intensive Care Med 1996:22;6-16.  Back to cited text no. 12    
13.Madias NE. Lactic Acidosis. Kidney Int 1986;29:752-74.  Back to cited text no. 13  [PUBMED]  
14.Duke T. Dysoxia and Lactate. Arch Dis Child 1999;81:343-50.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Laski ME, Wesson DE. Lactic Acidosis. In: Acid-Base and Electrolyte Disorders: A companion to Brenner and Rector's The Kidney. Dubose TD, Hamm LL, editors. Philadelphia: WB Saunders; 2000:83-107.  Back to cited text no. 15    
16.Slomovitz BM, Lavery RF, Tortella BJ, Siegel JH, Bachl BL, Ciccone A. Validation of hand held lactate device in determination of blood lactate in critically injured patients. Crit Care Med 1998;26:1523-8.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Aduen J, Bernstein WK, Khastgir T, Miller J, Kerzner R, Bhatiani A, et al. The use and clinical importance of a substrate specific electrode for rapid determination of blood lactate concentration. JAMA 1994;272:1678-85.  Back to cited text no. 17  [PUBMED]  
18.Toffaletti J, Hammes ME, Gray R, Lineberry B, Abrams B. Lactate measured in diluted and undiluted whole blood and plasma: Comparison of methods and effects of hematocrit. Clin Chem 1992;3B:2430-4.  Back to cited text no. 18    
19.Wiese J, Didwania A, Kernzer R, Chernow B. Use of different anticoagulants in test tubes for analysis of blood lactate concentrations. Crit Care Med 1997;25:1847-50.  Back to cited text no. 19    
20.Gunn VL, Nechyba C, editors. Missouri, Mosby: The Harriet Lane Handbook, 16th Ed.; 2002. p. 553.  Back to cited text no. 20    
21.Jackson EV, Wiese J, Sigal B, Miller J, Bernstein W, Kassel D, et al. Effects of crystalloid solutions on circulating lactate concentration. Crit Care Med 1997;25:1840-6.  Back to cited text no. 21    
22.Stacpoole PW, Wright WC, Baumgartner TG, Bersin RM, Buchalter S, Curry SH, et al. A controlled clinical trial of dichloroacetate for therapy of lactic acidosis in adults. N Engl J Med 1992;327:1564-9.  Back to cited text no. 22    
23.Stacpoole PW. Lactic Acidosis: The case against bicarbonate therapy. Ann Intern Med 1986;105:276-9.  Back to cited text no. 23  [PUBMED]  
24.Fraley DS, Adler S, Bruns FJ, Zett B. Stimulation of lactate production by administration of bicarbonate in a patient with a solid neoplasm and lactic acidosis. N Engl J Med 1980;303:1100-2.  Back to cited text no. 24  [PUBMED]  
25.Narins RG, Cohen JJ. Bicarbonate therapy for organic acidosis: The case for its continued use. Ann Intern Med 1987;106:615-8.  Back to cited text no. 25  [PUBMED]  
26.Bjemeroth G. Alkaline buffers for correction of metabolic acidosis during cardiopulmonary resuscitation with focus of tribonat. Resusc 1998;137:161-71.  Back to cited text no. 26    
27.Levraut J, Ciebierra JP, Jambou P, Ichai C, Labib Y, Grimaud D. Effect of continuous venovenous hemofiltration with dialysis on lactate clearance in critically ill patients. Crit Care Med 1997;25:58-62.  Back to cited text no. 27    
28.Vitek V, Cowley RA. Blood lactate in the prognosis of various forms of shock. Ann Surg 1971;41:989-1001.  Back to cited text no. 28    
29.Fowler AA, Hamman RF, Zerbe GO, Benson KN, Hyers TM. Adult Respiratory Distress Syndrome - Prognosis after onset. Am Rev Respir Dis 1985;132:472-8.  Back to cited text no. 29  [PUBMED]  
30.Maclean LD, Mulligan WG, Mclean APH, Duff JH. Patterns of septic shock in man - a detailed study of 56 patients. Ann Surg 1967;166:5-43.  Back to cited text no. 30    
31.DuBose TD. Acid Base Disorders. In: Brenner BM, editor. Brenner and Rector's The Kidney, 7th Ed. Philadelphia: WB Saunders; 2000. p. 925-97.  Back to cited text no. 31    
32.Mizock BA. Metabolic derangements in sepsis and septic shock. Crit Care Clin 2000;16:319-36.  Back to cited text no. 32  [PUBMED]  
33.Haji-Michael PG, Ladriere L, Sener A, Vincent JL, Malaisse WS. Leukocyte glycolysis and lactate output in animal sepsis and ex vivo human blood. Metabolism 1999;48:779-85.  Back to cited text no. 33    
34.Backer DD, Creteur J, Zhang H, Norrenberg M, Vincent JL. Lactate production by the lungs in acute lung injury. Am J Respir Crit Care Med 1997;156:1099-104.  Back to cited text no. 34    
35.Walsh TS, McLellan S, Mackenzie SJ, Lee A. Hyperlactatemia and pulmonary lactate production in patients with fulminant hepatic failure. Chest 1999;116:471-6.  Back to cited text no. 35  [PUBMED]  [FULLTEXT]
36.Brinkmann A, Calzia E, Trager K. Monitoring the hepato-splanchnic region in the critically ill patient. Intensive Care Med 1998;24:542-56.  Back to cited text no. 36    
37.De Baker D, Creuter J, Noordally O, Nadia S, Beatrice G, Vincent JL. Does hepatosplanchnic VO/ DO dependency exist in critically ill septic shock patients? Am J Respir Crit Care 1998;157:1219-25.  Back to cited text no. 37    
38.Bellomo R, Kellum JA, Pinsky MR. Transvisceral lactate fluxes during early endotoxemia. Chest 1996;110:198-204.  Back to cited text no. 38  [PUBMED]  [FULLTEXT]
39.Backer DD, Creuter J, Silva E, Vincent JL. The hepatosplanchnic area is not a common source of lactate in patients with severe sepsis. Crit Care Med 2001;29:256-61.  Back to cited text no. 39    
40.Curtis SE, Cain SM. Regional and systemic oxygen delivery/ uptake relations and lactate flux in hyperdynamic, endotoxin treated dogs. Am Rev Respir Dis 1992;145:348-54.  Back to cited text no. 40  [PUBMED]  
41.Douzinas EE, Tsiemiadou PD, Pitaridis MT, Andrinakis I, Bobota-Chloraki A, Katsouyami K, et al. The regional production of cytokines and lactate in sepsis-related multiple organ failure. Am J Respir Crit Care Med 1997;155:53-9.  Back to cited text no. 41    
42.Duke TD, Butt W, South M. Predictors of mortality and multiorgan failure in children with sepsis. Intensive Care Med 1997;33:684-92.  Back to cited text no. 42    
43.Hatherill M, Sajjanhar T, Tibby SM, Champion MP, Anderson D, Marsh DJ, et al. Serum lactate as a predictor of mortality after pediatric cardiac surgery. Arch Dis Child 1997;77:235-8.  Back to cited text no. 43    
44.Deshpande SA, Platt MPW. Association between blood lactate and acid base status and mortality in ventilated babies. Arch Dis Child 1997;76:15-20.  Back to cited text no. 44    
45.Yousef F, McGeady SJ. Lactic acidosis and status asthmaticus: How common in pediatrics. Ann Allergy Asthma Immunol 2002;89:585-8.  Back to cited text no. 45    
46.James JH, Luchette FA, McCarter FD, Fischer JE. Lactate as an unreliable indicator of tissue hypoxia in injury or sepsis. Lancet 1999;354:505-8.  Back to cited text no. 46  [PUBMED]  [FULLTEXT]
47.Hatherill M, McIntyre G, Walter M, Murdoch IA. Early hyperlactatemia in critically ill children. Intensive Care Med 2000;26:314-8.  Back to cited text no. 47    
48.Perez A, Minces SA, Ciraolo CA, Schnitzler EJ, Agosta GE, Portillo Medina SA. Jugular venous oxygen saturation or arteriovenous difference of lactate content and outcome in children with severe traumatic brain injury. Pediatr Crit Care Med 2003;4:33-8.  Back to cited text no. 48    
49.Cormio M, Valadka AB, Robertson CS. Elevated jugular venous oxygen saturation after severe head injury. J Neurosurg 1999;90:9-15.  Back to cited text no. 49  [PUBMED]  
50.Murphy ND, Kodakat SK, Wendon JA, Jooste CA, Muiesan P, Rela M. Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation. Crit Care Med 2001;29:2111-8.  Back to cited text no. 50    
51.Mizock BA. Hyperlactatemia in acute liver failure: Decreased clearance vs. increased lactate production. Crit Care Med 2001;29:2225-6.  Back to cited text no. 51  [PUBMED]  [FULLTEXT]
52.De Backer D, Creteur J, Zhang H, Norrenberg H, Vincent JL. Hyperlactatemia and pulmonary lactate production in patients with fulminant hepatic failure. Chest 1999;116:471-6.  Back to cited text no. 52    
53.Baud FJ, Borron SW, Megarbane B, Trout H, Tapostolle F, Vicant E, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med 2002;30:2044-50.  Back to cited text no. 53    
54.Suistomaa M, Buokonen E, Kari M, Takala J. Time pattern of lactate and lactate to pyruvate ratio in the first 24 hours of intensive care emergency admissions. Shock 2000;14:8-12.  Back to cited text no. 54    
55.Levy B, Sadoune LO, Gelot AM, Bollaert PE, Nabet P, Larcan A. Evolution of lactate/pyruvate and arterial ketone body ratios in the early course of catecholamine treated septic shock. Crit Care Med 2000;28:114-9.  Back to cited text no. 55  [PUBMED]  [FULLTEXT]
56.Hatherill M, Waggie Z, Perves L, Reynolds L, Argent A. Mortality and nature of metabolic acidosis in children with shock. Intensive Care Med 2000;26:314-8.  Back to cited text no. 56    


[Figure - 1]


[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7]

This article has been cited by
1 Acid-base disorders in critically ill neonates
Lekhwani, S., Shanker, V., Gathwala, G., Vaswani, N.D.
Indian Journal of Critical Care Medicine. 2010; 14(2): 65-69
2 Does lactate level in the first 12 hours of life predict mortality in extremely premature infants?
Hussain, F., Gilshenan, K., Gray, P.H.
Journal of Paediatrics and Child Health. 2009; 45(5): 263-267
3 Caecal ligation and puncture in the rat mimics the pathophysiological changes in human sepsis and causes multi-organ dysfunction
Brooks, H.F., Osabutey, C.K., Moss, R.F., Andrews, P.L.R., Davies, D.C.
Metabolic Brain Disease. 2007; 22(3-4): 353-373


Print this article  Email this article
Previous article Next article
Online since 7th April '04
Published by Wolters Kluwer - Medknow