Understanding Lactate In Sepsis & Using It To Our Advantage
You are here: Home / PULMCrit / Understanding lactate in sepsis & Using it to our advantage Understanding lactate in sepsis & Using it to our advantage Once upon a time a 60-year-old man was transferred from the oncology ward to the ICU for treatment of neutropenic septic shock. Over the course of the morning he started rigoring and dropped his blood pressure from 140/70 to 70/40 within a few hours, refractory to four liters of crystalloid. In the ICU his blood pressure didn't improve with vasopressin and norepinephrine titrated to 40 mcg/min. His MAP remained in the high 40s, he was mottled up to the knees, and he wasn't making any urine. Echocardiography suggested a moderately reduced left ventricle ejection fraction, not terrible but perhaps inadequate for his current condition. Dobutamine has usually been our choice of inotrope in septic shock. However, this patient was so unstable that we chose epinephrine instead. On an epinephrine infusion titrated to 10 mcg/min his blood pressure improved immediately, his mottling disappeared, and he started having excellent urine output. However, his lactate level began to rise. He was improving clinically, so we suspected that the lactate was due to the epinephrine infusion. We continued the epinephrine, he continued to improve, and his lactate continued to rise. His lactate level increased as high as 15 mM, at which point the epinephrine infusion was being titrated off anyway. Once the epinephrine was stopped his lactate rapidly normalized. He continued to improve briskly. By the next morning he was off vasopressors and ready for transfer back to the ward. This was eye-opening. It seemed that the epinephrine infusion was the pivotal intervention which helped him stabilize. However, while clinically improving him, the epineph Continue reading >>
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 >>
Lactate And Sepsis: 10 Things You Need To Know To Save Lives
Lactate and Sepsis: 10 things you need to know to save lives Lactate may be used to identify a common killer in the prehospital environment The following is paid content sponsored by Pulsara According to data from the Centers for Disease Control & Prevention (CDC), one million cases of sepsis occur in the US each year, with 258,000 Americans succumbing annually to this life-threatening systemic inflammatory response to infection. Early recognition is crucial to the recovery of the sepsis patient, and lactate plays an important role in the diagnosis of this killer. Here are ten things you need to know about using lactate to identify sepsis: Sepsis: 10 things you need to know to save lives Lactate is a chemical naturally produced by the body to fuel the cells during times of stress. Its presence in elevated quantities is commonly associated with sepsis and severe inflammatory response syndrome. Serum lactate is an important indicator of the septic patients prognosis. A level over 4 mmol/L is associated with a 27% mortality rate, with mortality dropping significantly as the lactate level decreases[1]. Lactate can be used as a guide for determining the severity of the septic patients illness, and the effectiveness of their treatment. 3. Know what type of lactate you are dealing with. There are two types of lactate which may be encountered. The form of lactate associated with sepsis is called L-lactate. The other form is called D-lactate, and is more commonly associated with short bowel syndrome[2]. The chemicals are stereoisomers of each other, meaning the molecules of both compounds contain the same atoms, but with the atoms arranged differently. 4. Lactate is different from lactic acid. While the two terms are often used interchangeably, lactate is different from lactic Continue reading >>
Lactic Acidosis: Clinical Implications And Management Strategies
Lactic acidosis: Clinical implications and management strategies Cleveland Clinic Journal of Medicine. 2015 September;82(9):615-624 Quality Officer, Medical Intensive Care Unit, Departments of Pulmonary Medicine and Critical Care Medicine, Respiratory Institute, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Department of Pharmacy, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Medical ICU Clinical Specialist, Department of Pharmacy, Cleveland Clinic Director, Medical Intensive Care Unit, Department of Critical Care Medicine, Respiratory Institute, Cleveland Clinic Address: Anita J. Reddy, MD, Department of Critical Care Medicine, Respiratory Institute, A90, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: [email protected] ABSTRACTIn hospitalized patients, elevated serum lactate levels are both a marker of risk and a target of therapy. The authors describe the mechanisms underlying lactate elevations, note the risks associated with lactic acidosis, and outline a strategy for its treatment. Serum lactate levels can become elevated by a variety of underlying processes, categorized as increased production in conditions of hypoperfusion and hypoxia (type A lactic acidosis), or as increased production or decreased clearance not due to hypoperfusion and hypoxia (type B). The higher the lactate level and the slower the rate of normalization (lactate clearance), the higher the risk of death. Treatments differ depending on the underlying mechanism of the lactate elevation. Thus, identifying the reason for hyperlactatemia and differentiating between type A and B lactic acidosis are of the utmo Continue reading >>
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 >>
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Lactic Acidosis: What You Need To Know
Lactic acidosis is a form of metabolic acidosis that begins in the kidneys. People with lactic acidosis have kidneys that are unable to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike. This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis. Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism. There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate. Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening. The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause. Several symptoms of lactic acidosis represent a medical emergency: fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis) confusion jaundice (yellowing of the skin or the whites of the eyes) trouble breathing or shallow, rapid breathing If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away. Other lactic acidosis symptoms include: exhaustion or extreme fatigue muscle cramps or pain body weakness overall feelings of physical discomfort abdominal pain or discomfort diarrhea decrease in appetite headache rapid heart rate Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoni Continue reading >>
What Is A Lactic Acid Blood Test?
It’s a test that measures the amount of lactic acid (also called “lactate”) in your blood. This acid is made in muscle cells and red blood cells. It forms when your body turns food into energy. Your body relies on this energy when its oxygen levels are low. Oxygen levels might drop during an intense workout or when you have an infection or disease. Once you finish your workout or recover from the illness, your lactic acid level tends to go back to normal. But sometimes, it doesn't. Higher-than-normal lactic acid levels can lead to a condition called lactic acidosis. If it’s severe enough, it can upset your body’s pH balance, which indicates the level of acid in your blood. Lactic acidosis can lead to these symptoms: It’s a simple blood test. Your doctor will draw blood from a vein or artery using a needle. In rare cases, he may take a sample of cerebrospinal fluid from your spinal column during a procedure called a spinal tap. Normally, you don’t have to adjust your routine to prepare for the test. If your lactic acid level is normal, you don’t have lactic acidosis. Your cells are making enough oxygen. It also tells your doctor that something other than lactic acidosis is causing your symptoms. He’ll likely order other tests to find out what it is. If your lactic acid level is high, it could be caused by a number of things. Most often, it’s because you have a condition that makes it hard for you to breathe in enough oxygen. Some of these conditions could include: Severe lung disease or respiratory failure Fluid build-up in your lungs Very low red blood cell count (severe anemia) A higher-than-normal lactic acid level in your blood can also be a sign of problems with your metabolism. And, your body might need more oxygen than normal because you have o Continue reading >>
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 >>
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 >>
Causes Of Lactic Acidosis In Sepsis - Deranged Physiology
This topic is for some reason the subject of one frequently repeated question. Notable duplicates include the following: Question 6.4 from the first paper of 2013 (a detailed discussion is carried out here) Question 22.2 from the second paper of 2011 Question 6.4 from the first paper of 2011 Mechanisms responsible for lactic acidosis in sepsis Endogenous catecholamine release and use of catecholamine inotropes Circulatory failure due to hypoxia and hypotension Inhibition of pyruvate dehydrogenase (PDH) by endotoxin Slowed hepatic blood flow, impairing clearance So the lactate in sepsis is raised. What of it? The college seems to favour this concept as an exam topic. It has come up repeatedly in the past papers. It seems important for the trainees to understand that in septic shock the lactate elevation is not purely a feature of tissue hypoperfusion, but rather the outcome of complex metabolic changes. The mechanism of lactate elevation in sepsis is discussed in greater detail in a chapter dedicated to these metabolic changes . Instead of revisiting that elaborate explanation, I will instead produce some references, and this confusing flowchart diagram: Jones, Alan E., and Michael A. Puskarich. "Sepsis-induced tissue hypoperfusion." Critical care clinics25.4 (2009): 769. Continue reading >>
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 >>
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: Symptoms, Causes, And Treatment
Lactic acidosis occurs when the body produces too much lactic acid and cannot metabolize it quickly enough. The condition can be a medical emergency. The onset of lactic acidosis might be rapid and occur within minutes or hours, or gradual, happening over a period of days. The best way to treat lactic acidosis is to find out what has caused it. Untreated lactic acidosis can result in severe and life-threatening complications. In some instances, these can escalate rapidly. It is not necessarily a medical emergency when caused by over-exercising. The prognosis for lactic acidosis will depend on its underlying cause. A blood test is used to diagnose the condition. Lactic acidosis symptoms that may indicate a medical emergency include a rapid heart rate and disorientaiton. Typically, symptoms of lactic acidosis do not stand out as distinct on their own but can be indicative of a variety of health issues. However, some symptoms known to occur in lactic acidosis indicate a medical emergency. Lactic acidosis can occur in people whose kidneys are unable to get rid of excess acid. Even when not related to just a kidney condition, some people's bodies make too much lactic acid and are unable to balance it out. Diabetes increases the risk of developing lactic acidosis. Lactic acidosis may develop in people with type 1 and 2 diabetes mellitus , especially if their diabetes is not well controlled. There have been reports of lactic acidosis in people who take metformin, which is a standard non-insulin medication for treating type 2 diabetes mellitus. However, the incidence is low, with equal to or less than 10 cases per 100,000 patient-years of using the drug, according to a 2014 report in the journal Metabolism. The incidence of lactic acidosis is higher in people with diabetes who Continue reading >>
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 >>
Lactic Acidosis In Sepsis: It's Not All Anaerobic: Implications For Diagnosis Andmanagement.
1. Chest. 2016 Jan;149(1):252-61. doi: 10.1378/chest.15-1703. Epub 2016 Jan 6. Lactic Acidosis in Sepsis: It's Not All Anaerobic: Implications for Diagnosis andManagement. (1)Centre for Heart Lung Innovation, University of British Columbia, Vancouver, BC, Canada. (2)Centre for Heart Lung Innovation, University of British Columbia, Vancouver, BC, Canada. Electronic address: [email protected] Increased blood lactate concentration (hyperlactatemia) and lactic acidosis(hyperlactatemia and serum pH< 7.35) arecommon in patients with severe sepsisorseptic shock and are associated with significant morbidity and mortality. Insome patients, most of the lactate that is produced in shock states is due toinadequate oxygen delivery resulting in tissue hypoxia and causing anaerobicglycolysis. However, lactate formation during sepsis is not entirely related totissue hypoxia or reversible by increasing oxygen delivery. In this review,weinitially outline the metabolism of lactateand etiology of lactic acidosis;we thenaddress the pathophysiology of lacticacidosis in sepsis. We discuss the clinical implications of serum lactate measurement in diagnosis, monitoring, and prognostication in acute and intensive care settings. Finally, we exploretreatment of lactic acidosis and its impact on clinical outcome.Copyright 2016 American College of Chest Physicians. Published by Elsevier Inc.All rights reserved. Continue reading >>
