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Lactic Acidosis Ddx

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 >>

Lactate And Lactic Acidosis

Lactate And Lactic Acidosis

The integrity and function of all cells depend on an adequate supply of oxygen. Severe acute illness is frequently associated with inadequate tissue perfusion and/or reduced amount of oxygen in blood (hypoxemia) leading to tissue hypoxia. If not reversed, tissue hypoxia can rapidly progress to multiorgan failure and death. For this reason a major imperative of critical care is to monitor tissue oxygenation so that timely intervention directed at restoring an adequate supply of oxygen can be implemented. Measurement of blood lactate concentration has traditionally been used to monitor tissue oxygenation, a utility based on the wisdom gleaned over 50 years ago that cells deprived of adequate oxygen produce excessive quantities of lactate. The real-time monitoring of blood lactate concentration necessary in a critical care setting was only made possible by the development of electrode-based lactate biosensors around a decade ago. These biosensors are now incorporated into modern blood gas analyzers and other point-of-care analytical instruments, allowing lactate measurement by non-laboratory staff on a drop (100 L) of blood within a minute or two. Whilst blood lactate concentration is invariably raised in those with significant tissue hypoxia, it can also be raised in a number of conditions not associated with tissue hypoxia. Very often patients with raised blood lactate concentration (hyperlactatemia) also have a reduced blood pH (acidosis). The combination of hyperlactatemia and acidosis is called lactic acidosis. This is the most common cause of metabolic acidosis. The focus of this article is the causes and clinical significance of hyperlactatemia and lactic acidosis. The article begins with a brief overview of normal lactate metabolism. Normal lactate production and Continue reading >>

Etiology And Therapeutic Approach To Elevated Lactate

Etiology And Therapeutic Approach To Elevated Lactate

Etiology and therapeutic approach to elevated lactate aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States Corresponding author: Michael W. Donnino Beth Israel Deaconess Medical Center One Deaconess Road, W/CC 2 Boston, Boston, MA 02215 Phone: 617-754-2450 Fax: 617-754-2350 [email protected] The publisher's final edited version of this article is available at Mayo Clin Proc See other articles in PMC that cite the published article. Lactate levels are commonly evaluated in acutely ill patients. Although most commonly used in the context of evaluating shock, lactate can be elevated for many reasons. While tissue hypoperfusion is probably the most common cause of elevation Continue reading >>

Renal Fellow Network: Differential Diagnosis: Lactic Acidosis

Renal Fellow Network: Differential Diagnosis: Lactic Acidosis

As discussed in a recent post describing the success of early goal-directed therapy for sepsis, the test for serum lactate has enjoyed a rise in prominence in recent years. However, all that is lactic acid is not necessarily sepsis! Here's a differential diagnosis for lactic acidosis: 1. Shock--especially cardiogenic and septic shock, which is indicative of an inability of the circulatory system to match the metabolic demands of tissue. 2. Bowel Ischemia--mesenteric ischemia, necrotic bowel, etc.--the necrosis of cells in the intestine will release free lactate into the bloodstream. 3. Cirrhosis/Liver Failure--since lactate is metabolized to bicarbonate by the liver, patients with end-stage liver disease often have elevated lactate levels, which is NOT necessarily indicative of shock/hypoperfusion (although this group of patients often represents a conundrum in that they are precisely the type of patient who can get septic & die rapidly.) 4. Grand-mal Seizures: can lead to a transient increase in serum lactate which typically reverses on its own pretty quickly. 5. Thiamine Deficiency: thiamine is a cofactor for enzymes in the glycolytic pathway; its absence prevents adequate cellular metabolism and lactate can build up. 6. Citrate Toxicity in patients on CVVH given citrate-based replacement solution--this is heralded by an increased total calcium concentration along with a decreased ionized calcium concentration. 7. D-lactic acidosis: this atypical form of lactic acidosis occurs when bacterial overgrowth (as might occur in patients with GI bypass surgery) results in the metabolic synthesis of the D-isoform of lactic acidosis, which is not metabolizable to bicarbonate endogenously as is the naturally-occurring L-isoform of lactate. 8. Severe alkalosis: an increase in la 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 >>

Lactate

Lactate

To detect high levels of lactate in the blood, which may be an indication of lack of oxygen ( hypoxia ) or the presence of other conditions that cause excess production or insufficient clearing of lactate from the blood; this test is not meant to be used for screening for health status. When you have symptoms such as rapid breathing, nausea, and sweating that suggest a lack of oxygen or an abnormal blood pH (acid/base imbalance); when a health practitioner suspects that you may be experiencing sepsis , shock, heart attack , severe congestive heart failure , kidney failure , or inadequately treated (uncontrolled) diabetes ; when a health practitioner suspects that you have inherited a rare metabolic or mitochondrial disorder A blood sample drawn from a vein in your arm; sometimes a blood sample collected from an artery and, rarely, a sample of cerebrospinal fluid collected from the spine You may be told to rest prior to sample collection. Rarely, fasting may be required. You may be able to find your test results on your laboratory's website or patient portal. However, you are currently at Lab Tests Online. You may have been directed here by your lab's website in order to provide you with background information about the test(s) you had performed.You will need to return to your lab's website or portal, or contact your healthcare practitionerin order to obtainyour test results. Lab Tests Online is an award-winning patient education website offering information on laboratory tests. The content on the site, which has been reviewed by laboratory scientists and other medical professionals,provides general explanations of what results might mean for each test listed on the site, such as what a high or low value might suggest to your healthcare practitionerabout your health or Continue reading >>

Lactic Acidosis: Causes & Diagnoses | Symptoma.com

Lactic Acidosis: Causes & Diagnoses | Symptoma.com

Congenital lactic acidosis is a rare form of lactic acidosis. [webmd.com] Congenital lactic acidosis Mitochondrial dna mutations cause this condition [ edit on Wikidata ] Congenital lactic acidosis (CLA) is a rare disease caused by mutations in [en.wikipedia.org] Info Overview Lactic acidosis congenital infantile: A rare congenital condition where an infant has high levels of lactic acid in the blood causing metabolic acidosis. [checkorphan.org] Research Phenformin and lactic... Phenformin and lactic acidosis. [bmj.com] A recurrent drama (phenformin and lactic acidosis) A recurrent drama (phenformin and lactic acidosis) A 73-year-old man with diabetes presented with upper-abdominal pain and [care.diabetesjournals.org] Hyperamylasemia was not significantly more frequent in patients with phenformin-associated lactic acidosis than in patients with lactic acidosis who had not received phenformin [annals.org] Historically, this is a cause of lactic acidosis in the malnourished patient in who there is no other apparent cause of lactic acidosis. [derangedphysiology.com] Pathogenesis of Lactic Acidosis There are 2 categories of lactic acidosis. [pediatrics.aappublications.org] [] short-term memory loss and confabulation chronic and irreversible Wet Beri-Beri tachycardia vasodilation high cardiac output fluid overload cardiac failure INVESTIGATIONS lactic [lifeinthefastlane.com] [] and hypoxemia, are at an increased risk for lactic acidosis; the risk for lactic acidosis increases with the degree of renal dysfunction and the patients age Do not start [reference.medscape.com] Lactic acidosis occurs very rarely, only once in every 30,000 person-years of use. [diabetesnet.com] A more serious side effect is a rare but potentially fatal condition called lactic acidosis , in which dan 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 >>

Serum Anion Gap: Its Uses And Limitations In Clinical Medicine

Serum Anion Gap: Its Uses And Limitations In Clinical Medicine

Abstract The serum anion gap, calculated from the electrolytes measured in the chemical laboratory, is defined as the sum of serum chloride and bicarbonate concentrations subtracted from the serum sodium concentration. This entity is used in the detection and analysis of acid-base disorders, assessment of quality control in the chemical laboratory, and detection of such disorders as multiple myeloma, bromide intoxication, and lithium intoxication. The normal value can vary widely, reflecting both differences in the methods that are used to measure its constituents and substantial interindividual variability. Low values most commonly indicate laboratory error or hypoalbuminemia but can denote the presence of a paraproteinemia or intoxication with lithium, bromide, or iodide. Elevated values most commonly indicate metabolic acidosis but can reflect laboratory error, metabolic alkalosis, hyperphosphatemia, or paraproteinemia. Metabolic acidosis can be divided into high anion and normal anion gap varieties, which can be present alone or concurrently. A presumed 1:1 stoichiometry between change in the serum anion gap (ΔAG) and change in the serum bicarbonate concentration (ΔHCO3−) has been used to uncover the concurrence of mixed metabolic acid-base disorders in patients with high anion gap acidosis. However, recent studies indicate variability in the ΔAG/ΔHCO3− in this disorder. This observation undercuts the ability to use this ratio alone to detect complex acid-base disorders, thus emphasizing the need to consider additional information to obtain the appropriate diagnosis. Despite these caveats, calculation of the serum anion gap remains an inexpensive and effective tool that aids detection of various acid-base disorders, hematologic malignancies, and intoxication Continue reading >>

Anion Gap (elevated) Differential Diagnosis

Anion Gap (elevated) Differential Diagnosis

Acetaminophen Alcoholic Ketoacidosis Diabetic Ketoacidosis Ethylene Glycol Iron Isoniazid Lactic Acidosis Metformin Methanol Paraldehyde Salicylates Related Content Editors & Reviewers Normal Anion Gap: 8 - 12 +/- 2 Associations: Glucose levels > 250 mg/dL +/- abdominal pain +/- nausea & vomiting + ketones in the urine + serum bicarbonate < 18 Pathophysiology: Insufficient presence of insulin that results in the abnormal breakdown of fatty acids that generate ketoacids. Associations: History of tuberculosis (latent or active) Pathophysiology: Due to functional deficiencies in pyridoxine (vitamin B6) that can serve as a co-factor in metabolic reactions. This leads to a metabolic acidosis. Associations: Numerous medical conditions or drugs containing propylene glycol (lorazepam; phenytoin) Pathophysiology: Lactic acid formation is a byproduct of another underlying problem that prevents its metabolism or prevent pyruvate from entering the Krebs cycle. Associations: Reports of ingestion/Suicide Attempt (or) elderly patient on chronic aspirin +/- mixed acid/base disorder Pathophysiology: Initially stimulates the medullary center in the brain and causes increased respirations leading to respiratory alkalosis. Then shifts to a metabolic acidosis and uncoupling of cellular respiration. Continue reading >>

Lactic Acidosis

Lactic Acidosis

hyperlactaemia: a level from 2 to 5 mmol/L normal production is 20 mmols/kg/day, enters the circulation and undergoes hepatic and renal metabolism (Cori cycle) all tissues can produce lactate under anaerobic conditions lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH (i.e. it is a strong ion) during heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate during pregnancy, the placenta is an important producer of lactate (can pass to fetus as well) major source in sepsis and ARDS is the lung lactate is metabolised predominantly in the liver (60%) and kidney (30%) the heart can also use lactate for ATP production 50% is converted into glucose (gluconeogenesis) and 50% into CO2 and water (citric acid cycle) this results in no net acid accumulation but requires aerobic metabolism the small amount of lactate that is renally filtered (180mmol/day) is fully reabsorbed (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery once documented the cause must be found and treated appropriately D lactate is isomer of lactate produced by intestinal bacterial and not by humans it is not detected on standard lactate assays a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia venous samples are equivalent to arterial in clinical practice do not need to take off tourniq Continue reading >>

Metformin-associated Lactic Acidosis

Metformin-associated Lactic Acidosis

Please donate! Funds go solely to hosting and development costs that allow medical practitioners around the globe to freely access WikEM. Acute and chronic use of metformin can lead to rare complication of Metformin-associate lactic acidosis (MALA) Excreted (unmetabolized) in proximal tubules Stimulates anaerobic glucose metabolism in splanchnic bed increased lactate production Inhibits mitochondrial respiratory chain decreased gluconeogenesis from lactate lactate accumulation Associated with overdose, renal failure, liver disease, and septicemia [1] Acidosis onset several hours after acute ingestion Lactate only predictive of mortality in overdose patients, not in incidental metformin accumulation Elevated PT associated with increased mortality pH >6.9, lactate >25 portends a poor prognosis [3] Lactate utilization secondary to hepatic dysfunction NAD+/NADH ratio leads to conversion of pyruvate to lactate Mainly due to D-lactate production, though hypovolemia contributes Adrenergic receptor agonism; viz., albuterol, epinephrine, etc episodes of encephalopathy and metabolic acidosis typically following high carbohydrate meals in patients with short bowel syndrome metabolic acidosis and high serum anion gap, normal lactate level, short bowel syn or other forms of malabsorption, and characteristic neurologic findings Type D lactate is not detected with standard lactate levels NaMonofluoroacetate (Coyote Poison give Etoh as antidote) If intubated, maintain minute ventilation so as to not remove respiratory compensation for acidosis Activated charcoal if peri-ingestion/mental status appropriate Metformin should not cause hypoglycemia and, if present, should lead to work up of cause No evidence to support its use in MALA patients [5] Metformin can be cleared with hemodialysi Continue reading >>

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

1 A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2 The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a β- hydroxybutyrate dominated ketoacidosis. 3 Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4 The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5 The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6 The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7 It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recom mended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication. Continue reading >>

Acid-base Differential Diagnosis

Acid-base Differential Diagnosis

This patient's elevated blood pH and decrease in PaCO2 is consistent with acute respiratory alkalosis. Respiratory acid-base disorders are caused by primary changes in PaCO2, whereas metabolic acid-base disorders are due to primary changes in the concentration of HCO3-. A primary rise in PaCO2 or a fall in plasma HCO3- reduces the pH (acidemia), whereas the opposite increase the pH (alkalemia). Patients suffering from pneumonia can have tachypnea due to hypoxia. Increased minute ventilation reduces arterial CO2, an acid, resulting in alkalosis. A slight decrease in bicarbonate level may be seen due to early renal compensation. Answer 1: Normal pH range is 7.35-7.45. This patient's pH is outside this range, which indicates an acid-base disturbance. Answer 2: A decreased pH and an decrease in HCO3- would be consistent with metabolic acidosis. Answer 3: An elevated pH and an increase in HCO3- would be consistent with metabolic alkalosis. Answer 4: Respiratory acidosis results from decreased alveolar ventilation, which causes increased arterial CO2 levels. Continue reading >>

Normal Anion Gap Acidosis

Normal Anion Gap Acidosis

Terry W. Hensle, Erica H. Lambert, in Pediatric Urology , 2010 Nonanion gap acidosis occurs in situations in which HCO3 is lost from the kidney or the gastrointestinal tract or both. When this occurs, Cl (along with Na+) is reabsorbed to replace the HCO3; this leads to the hyperchloremia, which leaves the anion gap in normal range.10 Diarrhea causes a hyperchloremic, hypokalemic metabolic acidosis. Treatment depends on the severity of the acidosis incurred. In mild to moderate acidosis (pH >7.2), fluid and electrolyte replacement is often all that is required. Once adequate renal perfusion is restored, excess H+ can be excreted efficiently, restoring the pH to normal. In severe acidosis (pH <7.2), the addition of intravenous bicarbonate may be needed to correct the metabolic deficit. Before bicarbonate is administered, a serum potassium level should be obtained. The addition of bicarbonate can worsen hypokalemia, leading to neuromuscular complications. Hyperchloremic acidosis also occurs with renal insufficiency and renal tubular acidosis.9,20 Katherine Ahn Jin, in Comprehensive Pediatric Hospital Medicine , 2007 As in any condition, the first priority in management is stabilizing the ABCs, as necessary. Management of metabolic acidosis is directed toward treating the underlying cause. In general, treating the causes of anion gap acidosis can regenerate bicarbonate within hours; however, nonanion gap acidosis can take days to resolve and may require exogenous bicarbonate therapy. Insulin, hydration, and electrolyte repletion will correct the acidosis in diabetic ketoacidosis. In addition to treating the underlying condition, lactic acidosis can be resolved by increasing tissue oxygenation using crystalloid, blood products, afterload reduction, inotropic agents (e.g., d Continue reading >>

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