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Sepsis Lactic Acidosis

Lactic Acidosis In Sepsis And Septic Shock - Deranged Physiology

Lactic Acidosis In Sepsis And Septic Shock - Deranged Physiology

Lactic Acidosis in Sepsis and Septic Shock Increased lactate production in malignancy Sepsis and septic shock increase lactate in a number of exciting ways, many of which have little to do with impaired tissue perfusion (though it does play a role). Sepsis undeniably results in lactic acidosis and this is not a matter for dispute. However, the origin of the extra lactate is still being disputed. There is no doubt a combination of things happening here. In summary, the features of sepsis which promote lactic acidosis are as follows: Microcirculatory shunting (oxygenated blood never reaches hypoxic tissues) Catecholamine-related increase in the rate of glycolysis, especially in the skeletal muscle Decreased mitochondrial pyruvate dehydrogenase activity, due to cytokine activity and bacterial endotoxin A diagrammatic representation of microvascular failure in septic shock Thats a confusing diagram, which teaches us nothing about the many sources of lactate in sepsis. Firstly, the slow circulation is to blame; this results in a delay in the delivery of oxygen to the tissues, as well as a delay in removing the metabolic byproducts, which has the tendency to concentrate the lactate. The evidence for this is strong; the term used to describe this is microvascular stasis where collecting post-capillary venules are so vasodilated that flow in them essentially halts. There is at least one excellent article which goes over the potential causes for this stasis, including the increased adhesion of blood cells to endothelia, decreased red cell deformability, microthrombi interfering with the flow, etc. etc. Another feature of sepsis is that in some tissues the circulatory beds are completely shut down, and there is microcirculatory shunting of oxygenated blood away from these tissue 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 >>

Nursing Blog | Lippincott Nursingcenter

Nursing Blog | Lippincott Nursingcenter

Elevated Lactate Not just a marker for sepsis and septic shock Mar 17 2017 by Lisa Bonsall, MSN, RN, CRNP As nurses working at the bedside, most of us are familiar with the common lab test, lactate. We know that when cells become hypoxic, lactate levels increase. While working in the intensive care unit, checking a lactate level was routine. Unfortunately, an elevated lactate level is typically a bad sign for the patient, often related to increased organ dysfunction and mortality. In recent years, the blood lactate level has gained wide acceptance as an important marker in the diagnosis of sepsis and septic shock and is useful in evaluating response to fluid resuscitation. An elevated lactate is not only a marker for sepsis and septic shock it may signal other important clinical conditions as well. So, what is lactate and what exactly does it tell us? Lactate is an organic molecule produced by most tissues in the human body, with the highest production found in muscle.1Heres a quick and basic review of how lactate is produced. The body normally produces energy by way of aerobic metabolism, which requires oxygen to break down carbohydrates, amino acids, and fats. Via glycolysis, glucose is converted into pyruvate, which enters the Krebs cycle to produce oxygen and adenosine triphosphate (ATP) or energy. If oxygen isnt available to body cells, anaerobic metabolism kicks in to produce energy. In this pathway, pyruvate is metabolized by the enzyme lactate dehydrogenase (LDH) into lactate.2 Lactate leaves the cells, enters the bloodstream, and transports to the liver, where it is oxidized back to pyruvate and then converted to glucose via the Cori cycle.1,2 Lactate is cleared from the blood, primarily by the liver and, to a lesser extent, by the kidneys and skeletal muscles Continue reading >>

Lactic Acidosis: What You Need To Know

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 >>

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 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 >>

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 >>

What Is A Lactic Acid Blood Test?

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 >>

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 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 >>

Understanding Lactate In Sepsis & Using It To Our Advantage

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 >>

The Pathogenesis Of Lactic Acidosis In Sepsis

The Pathogenesis Of Lactic Acidosis In Sepsis

The pathogenesis of lactic acidosis in sepsis Bellomo, Rinaldo MBBS (Hons), MD, FRACP, FACCP*; Ronco, Claudio MD Lactic acidosis is a common finding in critically ill patients during severe sepsis/septic shock, and a powerful predictor of mortality. Because of the knowledge that lactate is the end product of anaerobic glycolysis, the presence of hyperlactatemia in sepsis has been taken to indicate the development of anaerobic glycolysis within tissues. Such anaerobic glycolysis is understood to result from oxygen debt at cellular level. The metabolic acidosis frequently associated with hyperlactatemia has thus been ascribed to hydrogen ions released from adenosine triphosphate hydrolysis. This simplistic view of the pathogenesis and meaning of hyperlactatemia, however, is not supported by available data. Systemic oxygen transport is usually increased rather than decreased in septic patients. Whenever studied, tissue oxygenation is either preserved or increased in septic animals and humans. In addition, lactate levels may fluctuate in response to inotropic drugs and do not consistently decrease when tissue oxygen delivery is increased. Furthermore, there is strong evidence that large amounts of lactate can be produced and released under aerobic conditions and that the pathogenesis of hyperlactatemia in septic states is complex. Such pathogenesis may involve accelerated glycolytic fluxes, the inhibition of pyruvate dehydrogenase activity, and changes in intermediary metabolism. It may also involve the need to modulate the rate and efficiency of glycolytic flux by controlling the redox state of cytoplasm and mitochondria through lactate accumulation. Furthermore, recent investigations have attempted to establish which organs are responsible for lactate production in septi Continue reading >>

Lactic Acidosis In Sepsis: Its Not All Anaerobic: Implications For Diagnosis And Management - Sciencedirect

Lactic Acidosis In Sepsis: Its Not All Anaerobic: Implications For Diagnosis And Management - Sciencedirect

Volume 149, Issue 1 , January 2016, Pages 252-261 Contemporary Reviews in Critical Care Medicine Lactic Acidosis in Sepsis: Its Not All Anaerobic: Implications for Diagnosis and Management Author links open overlay panel BandarnSuetrongMD Keith R.WalleyMD Get rights and content Increased blood lactate concentration (hyperlactatemia) and lactic acidosis (hyperlactatemia and serum pH< 7.35) arecommon in patients with severe sepsis orseptic shock and are associated with significant morbidity and mortality. In some patients, most of the lactate that is produced in shock states is due to inadequate oxygen delivery resulting in tissue hypoxia and causing anaerobic glycolysis. However, lactate formation during sepsis is not entirely related to tissue hypoxia or reversible by increasing oxygen delivery. In this review, 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 explore treatment of lactic acidosis and its impact on clinical outcome. Continue reading >>

New Clinical Criteria For Septic Shock: Serum Lactate Level As New Emerging Vital Sign

New Clinical Criteria For Septic Shock: Serum Lactate Level As New Emerging Vital Sign

New clinical criteria for septic shock: serum lactate level as new emerging vital sign Department of Internal Medicine, Dong-A University, Busan, Korea Correspondence to: Won Suk An. Department of Internal Medicine, Dong-A University, 3Ga-1, Dongdaesin-Dong, Seo-Gu, Busan 602-715, Korea. Email: [email protected] . Received 2016 Apr 10; Accepted 2016 Apr 18. Copyright 2016 Journal of Thoracic Disease. All rights reserved. See the article " Developing a New Definition and Assessing New Clinical Criteria for Septic Shock " in JAMA, volume 315 onpage775. Sepsis is leading cause of acute hospital mortality and commonly results in multi-organ dysfunction secondary to culture-positive or negative infection. Septic shock is defined as unrecovered hypotension despite adequate fluid replacement in the Surviving Sepsis Campaign (SSC) Guidelines ( 1 ). Sepsis-induced arterial hypotension is defined as a systolic blood pressure (SBP) <90 mmHg or mean arterial pressure (MAP) <70 mmHg or a SBP decrease >40 mmHg or less than two standard deviations below normal for age in the absence of other causes of hypotension ( 1 ). Until recently, septic shock was considered to be composed of three components, including systemic arterial hypotension, tissue hypoperfusion associated with organ dysfunction, and hyperlactatemia ( 2 ). According to the new definition of this issue ( 3 ), septic shock can be diagnosed under two conditions. The first condition is persistent hypotension after fluid resuscitation and requiring vasopressors to maintain MAP >65 mmHg. The second condition is serum lactate level >2 mmol/L. Since heart rate, respiration rate, and other laboratory data are not included, the diagnosis and recognition of septic shock have become simplified. This very new definition implies that in 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 >>

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 >>

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