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Sepsis Metabolic Acidosis Anion Gap

Lactate And Anion Gap In Sepsis

Lactate And Anion Gap In Sepsis

Summarized from Berkman M, Ufberg J, Nathanson L, Shapiro N. Anion gap as a screening tool for elevated lactate in patients with increased risk of developing sepsis in the room. J of Emerg Med 2009; 36: 391-94. As a global marker of tissue oxygenation serum lactate measurement has proven its usefulness in monitoring the critically ill. It has also proved useful as a screening tool for sepsis in the emergency room. However, lactate measurement is not always readily available. Increased lactate is a common cause of raised anion gap, a much more readily available parameter derived by calculation from serum electrolyte results, and this has led to the suggestion that anion gap could serve as a surrogate measure of lactate concentration. This suggestion is tested in a recent study whose precise aim was to determine if anion gap could be used as a surrogate marker for abnormal lactate in patients admitted to the emergency room who are at risk of sepsis. During a 9-month period, 1419 adult patients admitted to the emergency department of a Boston hospital were recruited to the study. All patients had signs and symptoms suggestive of possible infection, i.e. they were at risk of sepsis. All had blood sampled on admission for lactate and electrolyte estimation, the latter allowing calculation of anion gap. Mean lactate of the study population was 2.1 mmol/L (SD 1.3) and mean AG was 11.8 (SD 3.6). For the purposes of the study lactate >4.0 mmol/L and anion gap >12 were defined as abnormal. Of the 1419 patients studied, 108 had an abnormal lactate (>4.0 mmol/L). Anion gap was abnormal (>12) in 86 of these patients. Thus raised anion gap was found to have a sensitivity of 80 % for predicting raised lactate. Of the remaining 1311 patients whose lactate was normal (<4.0 mmol/L), 900 Continue reading >>

Unaccounted For Anion In Metabolic Acidosis During Severe Sepsis In Humans.

Unaccounted For Anion In Metabolic Acidosis During Severe Sepsis In Humans.

Unaccounted for anion in metabolic acidosis during severe sepsis in humans. Department of Medicine, University of Health Sciences/Chicago Medical School, IL. To quantitate the contribution of lactate, phosphate, urate, total serum proteins, and unidentified anions to the anion gap in patients with severe sepsis. Thirty critically ill patients with evidence of severe sepsis and systemic hypoperfusion were prospectively studied. The anion gap was calculated as [Na+] + [K+] - [Cl-] - [HCO3]. A corrected anion gap was calculated as the anion gap minus the anionic contribution of lactate, phosphate, urate, and total serum proteins. The corrected anion gap is a marker of unmeasured anion less unmeasured cation concentration. The mean anion gap was 21.8 +/- 1.4 mmol/L and the corrected anion gap was 3.7 +/- 0.8 mmol/L. The mean arterial blood lactate concentration was 5.9 +/- 0.8 mmol/L. The magnitude of the lactate concentration correlated linearly with the anion gap (r2 = .61, lactate = 0.4 anion gap - 3.9, n = 30, p less than .01). The corrected anion gap was greater than 0 in 24 (80%) of 30 patients. The magnitude of the corrected anion gap correlated linearly with the anion gap (r2 = .66, corrected anion gap = 0.5 anion gap - 6.3, n = 30, p less than .01). Since the slope of the regression line for estimating corrected anion gap from anion gap was 0.5, the contribution of unmeasured anions was as important as lactate in determining the anion gap. These data indicate that lactic acidosis does not entirely account for the metabolic acidosis during severe sepsis. Furthermore, the increased corrected anion gap suggests the presence of an unidentified anion (or anions) that is (or are) responsible, in large part, for the development of metabolic acidosis in patients with seps Continue reading >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acid–base disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide might be less frequent than in high anion gap metabolic acidosis because of better tissue perfusion and the ability to eliminate carbon dioxide. Further basic and clinical research is needed to facilitate development of evidence-based guidelines for therapy of this important and increasingly common acid–base disorder. Introduction Acute metabolic acidosis (defined temporally as lasting minutes to a few days) has traditionally been divided into two major categories based on the level Continue reading >>

G382(p)mind The Gap! Elevated Anions Secondary To Paracetamol And Sepsis | Archives Of Disease In Childhood

G382(p)mind The Gap! Elevated Anions Secondary To Paracetamol And Sepsis | Archives Of Disease In Childhood

G382(P) Mind the gap! elevated anions secondary to paracetamol and sepsis British Paediatric Respiratory Society and Association for Paediatric Palliative Medicine and Paediatric Intensive Care Medicine G382(P) Mind the gap! elevated anions secondary to paracetamol and sepsis 1Metabolic Medicine, Sheffield Childrens Hospital, Sheffield, UK 2Paediatric Intensive Care, Sheffield Childrens Hospital, Sheffield, UK 3Clinical Chemistry, Sheffield Childrens Hospital, Sheffield, UK Aim Metabolic acidosis is a common finding in children presenting with sepsis. Hypovolaemia and hypoxia are the common causes for this derangement but sometimes there are other culprits. We aim to highlight the significance of correlating the anion gap with the biochemical picture and, when there are discrepancies, look for alterative diagnoses. An unusual case of transient pyroglutamic aciduria, presenting during an episode of severe sepsis and paracetamol use, will be used to outline the importance of examining the anion gap. Methods We illustrate the case of a 15 month old girl who presented with an 11 day history of diarrhoea and vomiting. She presented to the emergency department in a state of decreased consciousness. She was found to be hypotensive, hypoglycaemic and have a profound metabolic acidosis. She required mechanical ventilation and fluid resuscitation. Despite these interventions, she continued to have a profound metabolic acidosis with a very high anion gap (30.5). The levels of lactate and ketones were insufficient to explain the clinical picture. Results Metabolic investigations for the child were instigated. Whilst a majority of these were normal, examination of the patients organic acid profile revealed large peaks of pyroglutamic acid (5-oxoproline) and paracetamol. Termination Continue reading >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Metabolic Muddle Litfl Clinical Cases Staph Sepsis Acidosis

Metabolic Muddle Litfl Clinical Cases Staph Sepsis Acidosis

Given that the lactate and ketones are normal the most likely cause is: pyroglutamic acidemia (aka 5-oxoprolinemia) This can be confirmed by performing a metabolic screen for urinary organic acids. Blood levels may be required if the patient is anuric. An elevated level of pyroglutamic acid confirms the diagnosis. Skip this one if youre biochemically challenged 5-oxoproline (aka pyroglutamic acid) is produced from -glutamyl cysteine by the enzyme -glutamyl cyclotransferase. This enzymes activity increases when glutathione levels are low, due to a loss of feedback inhibition from glutathione. Thus the accumulation of pyroglutamic acid is thought to be due to depletion of the glutathione, particularly when glutathione synthetase is inhibited. Decreased activity of 5-oxoprolinase, which breaks down pyroglutamic acid, may also play a role. Check out the -glutamyl cycle to see how this all links up: Key: A = excess -glutamyl cysteine becomes a substrate for -glutamyl cyclotransferase, P = paracetamol, S = sepsis, F = flucloxacillin. From Dempsey et al, 2000. See also Q5. Continue reading >>

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting

A profile of metabolic acidosis in patients with sepsis in an Intensive Care Unit setting Department of Internal Medicine, Amrita Institute of Medical Sciences, Kochi, Kerala, India 1Department of Emergency Medicine, Amrita Institute of Medical Sciences, Kochi, Kerala, India Address for correspondence: Dr. Kartik Ganesh, Department of Nephrology, Amrita Institute of Medical Sciences, Kochi - 682 041, Kerala, India. E-mail: [email protected] Author information Copyright and License information Disclaimer Copyright : International Journal of Critical Illness and Injury Science This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. This article has been cited by other articles in PMC. Metabolic acidosis is frequently found in patients with severe sepsis. An understanding of types of acidosis in sepsis and their evolution over the course of treatment may give us insight into the behavior of acidbase balance in these patients. To describe at Intensive Care Unit (ICU) admission and over the first 5 days the composition of metabolic acidosis in patients with sepsis and to evaluate and compare acidosis patterns in survivors and nonsurvivors. A prospective study conducted at Amrita Institute of Medical Sciences, Kochi, Kerala, in the Department of Internal Medicine. Seventy-five consecutive patients admitted in the medical ICU with sepsis and metabolic acidosis were assessed. Arterial blood gas and serum electrolytes were measured during the first five days of admission or until death, renal replacement or discharge supervened. Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

Increased Anion Gap Metabolic Acidosis As A Result Of 5-oxoproline (pyroglutamic Acid): A Role For Acetaminophen

Increased Anion Gap Metabolic Acidosis As A Result Of 5-oxoproline (pyroglutamic Acid): A Role For Acetaminophen

Increased Anion Gap Metabolic Acidosis as a Result of 5-Oxoproline (Pyroglutamic Acid): A Role for Acetaminophen *Department of Internal Medicine; Metabolic Disease Center, BRI Baylor University Medical Center, Dallas, Texas Dr. Andrew Z. Fenves, Nephrology Division, Baylor University Medical Center, 3500 Gaston, Dallas, TX 75246. Phone: 214-820-2350; Fax: 214-820-7367; E-mail: fenvesa{at}dneph.com The endogenous organic acid metabolic acidoses that occur commonly in adults include lactic acidosis; ketoacidosis; acidosis that results from the ingestion of toxic substances such as methanol, ethylene glycol, or paraldehyde; and a component of the acidosis of kidney failure. Another rare but underdiagnosed cause of severe, high anion gap metabolic acidosis in adults is that due to accumulation of 5-oxoproline (pyroglutamic acid). Reported are four patients with this syndrome, and reviewed are 18 adult patients who were reported previously in the literature. Twenty-one patients had major exposure to acetaminophen (one only acute exposure). Eighteen (82%) of the 22 patients were women. Most of the patients were malnourished as a result of multiple medical comorbidities, and most had some degree of kidney dysfunction or overt failure. The chronic ingestion of acetaminophen, especially by malnourished women, may generate high anion gap metabolic acidosis. This undoubtedly is an underdiagnosed condition because measurements of serum and/or urinary 5-oxoproline levels are not readily available. The endogenous organic acid metabolic acidoses that occur most frequently in adults are lactic acidosis and ketoacidosis. Other organic acidoses that are encountered in adult patients are those that are caused by the metabolism of toxic substances such as methanol to formaldehyde or ethy Continue reading >>

Unmeasured Anions In Metabolic Acidosis: Unravelling The Mystery

Unmeasured Anions In Metabolic Acidosis: Unravelling The Mystery

Unmeasured anions in metabolic acidosis: unravelling the mystery In the critically ill, metabolic acidosis is a common observation and, in clinical practice, the cause of this derangement is often multi-factorial. Various measures are often employed to try and characterise the aetiology of metabolic acidosis, the most popular of which is the anion gap. The purpose of the anion gap can be perceived as a means by which the physician is alerted to the presence of unmeasured anions in plasma that contribute to the observed acidosis. In many cases, the causative ion may be easily identified, such as lactate, but often the causative ion(s) remain unidentified, even after exclusion of the 'classic' causes. We describe here the various attempts in the literature that have been made to address this observation and highlight recent studies that reveal potential sources of such hitherto unmeasured anions. Metabolic AcidosisIntensive Care Unit PatientLactic AcidosisKrebs CycleDiabetic Ketoacidosis Metabolic acidosis remains a common problem in acute medicine and is frequently encountered on the intensive care unit (ICU) [ 1 3 ]. Although many 'classic' causes of metabolic acidosis are known, including diabetic ketoacidosis, lactic acidosis and the ingestion of acid-generating poisons, the origin is often multifactorial and, indeed, often cannot be ascribed solely to such 'classic' causes or a single causative anion. In such cases, the source of the acidosis remains unidentified or unmeasured. For example, given that hydroxybutyrate is seldom measured, diabetic ketoacidosis is, strictly speaking, an example of acidosis associated with large quantities of an unmeasured anion, although in practice its concentration is regularly inferred. Similarly, it is only in the past 15 years or Continue reading >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Metabolic Acidosis And Strong Ion Gap In Critically Ill Patients With Acute Kidney Injury

Metabolic Acidosis And Strong Ion Gap In Critically Ill Patients With Acute Kidney Injury

Copyright © 2014 Cai-Mei Zheng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Purpose. To determine the influence of physicochemical parameters on survival in metabolic acidosis (MA) and acute kidney injury (AKI) patients. Materials and Methods. Seventy-eight MA patients were collected and assigned to AKI or non-AKI group. We analyzed the physiochemical parameters on survival at 24 h, 72 h, 1 week, 1 month, and 3 months after AKI. Results. Mortality rate was higher in the AKI group. AKI group had higher anion gap (AG), strong ion gap (SIG), and apparent strong ion difference (SIDa) values than non-AKI group. SIG value was higher in the AKI survivors than nonsurvivors and this value was correlated serum creatinine, phosphate, albumin, and chloride levels. SIG and serum albumin are negatively correlated with Acute Physiology and Chronic Health Evaluation IV scores. AG was associated with mortality at 1 and 3 months post-AKI, whereas SIG value was associated with mortality at 24 h, 72 h, 1 week, 1 month, and 3 months post-AKI. Conclusions. Whether high or low SIG values correlate with mortality in MA patients with AKI depends on its correlation with serum creatinine, chloride, albumin, and phosphate (P) levels. AG predicts short-term mortality and SIG value predicts both short- and long-term mortality among MA patients with AKI. 1. Introduction Metabolic acidosis is an acid-base disorder of the blood and is an especially challenging condition among patients in intensive care units (ICUs). The acid-base status of a patient is most often determined based on standard base excess (SBE), serum bicarbonate Continue reading >>

Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine

Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine

Montagnani and Nardi: Lactic Acidosis, Hyperlactatemia and Sepsis Lactic Acidosis, Hyperlactatemia and Sepsis [1] Division of Internal Medicine, Misericordia Hospital, Grosseto [2] Division of Internal Medicine, Maggiore Hospital, Bologna, Italy Correspondence to: Ospedale Misericordia di Grosseto, via Senese, 58100 Grosseto, Italy. +39.0564.485330. [email protected] Among hospitalized patients, lactic acidosis represents the most common cause of metabolic acidosis. Lactate is not just a metabolic product of anaerobic glycolysis but is triggered by a variety of metabolites even before the onset of anaerobic metabolism as part of an adaptive response to a hypermetabolic state. On the basis of such considerations, lactic acidosis is divided into two classes: inadequate tissue oxygenation (type A) and absence of tissue hypoxia (type B). Lactic acidosis is characterized by non-specific symptoms but it should be suspected in all critical patients who show hypovolemic, hypoxic, in septic or cardiogenic shock or if in the presence of an unexplained high anion gap metabolic acidosis. Lactic acidosis in sepsis and septic shock has traditionally been explained as a result of tissue hypoxia when whole-body oxygen delivery fails to meet whole body oxygen requirements. In sepsis lactate levels correlate with increased mortality with a poor prognostic threshold of 4 mmol/L. In hemodynamically stable patients with sepsis, hyperlactatemia might be the result of impaired lactate clearance rather than overproduction. In critically ill patients the speed at which hyperlactatemia resolves with appropriate therapy may be considered a useful prognostic indicator. The measure of blood lactate should be performed within 3 h of presentation in acute care setting. The presence of lactic a Continue reading >>

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