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Epinephrine And Metabolic Acidosis

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 >>

Bench-to-bedside Review: Is There A Place For Epinephrine In Septic Shock?

Bench-to-bedside Review: Is There A Place For Epinephrine In Septic Shock?

Bench-to-bedside review: Is there a place for epinephrine in septic shock? The use of epinephrine in septic shock remains controversial. Nevertheless, epinephrine is widely used around the world and the reported morbidity and mortality rates with it are no different from those observed with other vasopressors. In volunteers, epinephrine increases heart rate, mean arterial pressure and cardiac output. Epinephrine also induces hyperglycemia and hyperlactatemia. In hyperkinetic septic shock, epinephrine consistently increases arterial pressure and cardiac output in a dose dependent manner. Epinephrine transiently increases lactate levels through an increase in aerobic glycolysis. Epinephrine has no effect on splanchnic circulation in dopamine-sensitive septic shock. On the other hand, in dopamine-resistant septic shock, epinephrine has no effect on tonometric parameters but decreases fractional splanchnic blood flow with an increase in the gradient of mixed venous oxygen saturation (SVO2) and hepatic venous oxygen saturation (SHO2). In conclusion, epinephrine has predictable effects on systemic hemodynamics and is as efficient as norepinephrine in correcting hemodynamic disturbances of septic shock. Moreover, epinephrine is cheaper than other commonly used catecholamine regimens in septic shock. The clinical impact of the transient hyperlactatemia and of the splanchnic effects are not established. EpinephrineSeptic ShockMean Arterial PressureDobutamineAerobic Glycolysis Early goal directed therapy [ 1 ] is now considered as a gold standard in the early phase of septic shock. Fluid therapy and vasoactive therapy may be immediately required in order to maintain acceptable blood pressure levels. Invasive or non-invasive assessment of hemodynamic status, although essential to Continue reading >>

The Role Of Catecholamines In Metabolic Acidosis

The Role Of Catecholamines In Metabolic Acidosis

The role of glucagon in regulating plasma lipid concentrations (nonesterified fatty acids, ketone bodies, and triglycerides) is reviewed. The effects of glucagon-induced insulin secretion upon this lipid regulation are discussed that may resolve conflicting reports in the literature are resolved. In addition, the unresolved problem concerning the pharmacologic versus physiologic effects of glucagon is stressed. Glucagon's role in stimulating lipolysis at the adipocyte serves two important functions. First, it provides plasma nonesterified fatty acids for energy metabolism and secondly, it ensures substrate for hepatic ketogenesis. In vitro, glucagon's lipolytic activity has been consistently observed, but in vivo, this activity has sometimes been obscured by the effects of glucagon-induced insulin secretion. Frequently, a biphasic response has been reported in which a direct lipolytic response is followed by a glucagon-induced insulin suppression of plasma nonesterified fatty acid concentration. When the glucagon-induced insulin secretion has been controlled by various in vivo techniques, glucagon's lipolytic activity in vivo has frequently been demonstrable. In the 1960s, in vitro liver perfusion experiments demonstrated that glucagon enhanced hepatic ketogenesis independent of glucagon's lipolytic activity. However, this direct effect of glucagon on the hepatocyte was not universally accepted because of conflicting reports in the literature. Failure to observe an in vitro ketogenic effect of the hormone in some studies may have been due to suboptimal experimental conditions. Certain factors are now known to influence the ketogenic response, such as the concentration of fatty acids in the media and the nutritional status of the animal. Under optimal in vitro condition Continue reading >>

Epinephrine Vs. Norepinephrine For Cardiogenic Shock

Epinephrine Vs. Norepinephrine For Cardiogenic Shock

Epinephrine vs. Norepinephrine for Cardiogenic Shock What is the efficacy and safety of epinephrine and norepinephrine in patients with cardiogenic shock (CS) after acute myocardial infarction (AMI)? The investigators conducted a prospective, double-blind, multicenter, randomized study to assess the efficacy and safety of epinephrine and norepinephrine in patients with CS after AMI. The primary efficacy outcome was cardiac index evolution, and the primary safety outcome was the occurrence of refractory CS. Refractory CS was defined as CS with sustained hypotension, end-organ hypoperfusion and hyperlactatemia, and high inotrope and vasopressor doses. Associations between treatment group and adverse events were assessed by using logistic regression model. Odds ratios are presented with their 95% confidence intervals using the norepinephrine group as reference. Fifty-seven patients were randomized into two study arms, epinephrine and norepinephrine. For the primary efficacy endpoint, cardiac index evolution was similar between the two groups (p = 0.43) from baseline (H0) to H72. For the main safety endpoint, the observed higher incidence of refractory shock in the epinephrine group (10 of 27 [37%] vs. norepinephrine 2 of 30 [7%]; p = 0.008) led to early termination of the study. Heart rate increased significantly with epinephrine from H2 to H24, while remaining unchanged with norepinephrine (p < 0.0001). Several metabolic changes were unfavorable to epinephrine compared with norepinephrine, including an increase in cardiac double product (p = 0.0002) and lactic acidosis from H2 to H24 (p < 0.0001). The authors concluded that in patients with CS secondary to AMI, the use of epinephrine compared with norepinephrine was associated with similar effects on arterial pressure an Continue reading >>

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild metabolic acidosis impairs the -adrenergic response in isolated human failing myocardium Schotola et al.; licensee BioMed Central Ltd.2012 Pronounced extracellular acidosis reduces both cardiac contractility and the -adrenergic response. In the past, this was shown in some studies using animal models. However, few data exist regarding how the human end-stage failing myocardium, in which compensatory mechanisms are exhausted, reacts to acute mild metabolic acidosis. The aim of this study was to investigate the effect of mild metabolic acidosis on contractility and the -adrenergic response of isolated trabeculae from human end-stage failing hearts. Intact isometrically twitching trabeculae isolated from patients with end-stage heart failure were exposed to mild metabolic acidosis (pH 7.20). Trabeculae were stimulated at increasing frequencies and finally exposed to increasing concentrations of isoproterenol (0 to 1 10-6 M). A mild metabolic acidosis caused a depression in twitch-force amplitude of 26% (12.1 1.9 to 9.0 1.5 mN/mm2; n = 12; P < 0.01) as compared with pH 7.40. Force-frequency relation measurements yielded no further significant differences of twitch force. At the maximal isoproterenol concentration, the force amplitude was comparable in each of the two groups (pH 7.40 versus pH 7.20). However, the half-maximal effective concentration (EC50) was significantly increased in the acidosis group, with an EC50 of 5.834 10-8 M (confidence interval (CI), 3.48 10-8 to 9.779 10-8; n = 9), compared with the control group, which had an EC50 of 1.056 10-8 M (CI, 2.626 10-9 to 4.243 10-8; n = 10; P < 0.05), indicating an impaired -adrenergic force response. Our data show that mild metabolic acidosis reduces cardiac contractility and significantly impairs the -adrenerg Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

(pdf) Epinephrine-induced Lactic Acidosis In The Setting Of Status Asthmaticus

(pdf) Epinephrine-induced Lactic Acidosis In The Setting Of Status Asthmaticus

Lactic acidosis is frequently encountered in the intensive care unit. It occurs when there is an imbalance between production and clearance of lactate. Although lactic acidosis is often associated with a high anion gap and is generally defined as a lactate level >5 mmol/L and a serum pH <7.35, the presence of hypoalbuminemia may mask the anion gap and concomitant alkalosis may raise the pH. The causes of lactic acidosis are traditionally divided into impaired tissue oxygenation (Type A) and disorders in which tissue oxygenation is maintained (Type B). Lactate level is often used as a prognostic indicator and may be predictive of a favorable outcome if it normalizes within 48 hours. The routine measurement of serum lactate, however, should not determine therapeutic interventions. Unfortunately, treatment options remain limited and should be aimed at discontinuation of any offending drugs, treatment of the underlying pathology, and maintenance of organ perfusion. The mainstay of therapy of lactic acidosis remains prevention. Hyperlactatemia and lactic acidosis are two syndromes that are associated with morbidity and mortality. Medicationinduced hyperlactatemia and lactic acidosis are diagnoses of exclusion and have the potential to be overlooked. The purpose of this systematic review is to identify published reports of medicationinduced lactate level elevations to aid clinicians in diagnosing and comprehending the underlying mechanism of this rare adverse drug effect, and to provide management strategies. The PubMed database was searched for case reports, case series, retrospective studies, and prospective studies describing cases of medicationinduced lactate level elevation, including lactic acidosis and hyperlactatemia, published between January 1950 and June 2017. A s 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 >>

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 >>

Lactic Acidosis In Pheochromocytoma

Lactic Acidosis In Pheochromocytoma

MICHAEL BORNEMANN, M.D.; SUSAN C. HILL, M.D.; GERALD S. KIDD II, M.D. Article, Author, and Disclosure Information Author, Article, and Disclosure Information Requests for reprints should be addressed to COL Michael Bornemann, MC; Box 700, Tripler Army Medical Center; Honolulu, HI 96859-5000. Lactic acidosis is not generally recognized as a complication of pheochromocytoma. We review three prior case reports of lactic acidosis in patients with pheochromocytoma and one report of lactic acidosis following epinephrine poisoning and describe an additional case report of a patient with lactic acidosis in whom an unsuspected pheochromocytoma was discovered at autopsy. The pathophysiology of lactic acidosis in pheochromocytoma is related to the effect of catecholamines on intermediary metabolism and the peripheral circulation. Although the possible development of lactic acidosis in persons with pheochromocytoma is underappreciated, the differential diagnosis of lactic acidosis should include this tumor. 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 >>

Influence Of Respiratory And Metabolic Acidosis On Epinephrine-inotropic Effect In Isolated Guinea Pig Atria

Influence Of Respiratory And Metabolic Acidosis On Epinephrine-inotropic Effect In Isolated Guinea Pig Atria

, Volume 347, Issue4 , pp 297307 | Cite as Influence of respiratory and metabolic acidosis on epinephrine-inotropic effect in isolated guinea pig atria The inotropic effect of calcium and of epinephrine was examined in an isolated guinea pig atrial preparation during a simulated respiratory and metabolic acidosis. Special care was taken to avoid alterations in ionized calcium which usually accompany most forms of acidosis. In acidosis the inotropic response to epinephrine is depressed to a greater extent than the response to calcium, independent of respiratory or metabolic origin. It is concluded that the overall depression of the inotropic response to epinephrine is produced by two mechanisms: firstly, by an unspecific depression of contractility caused by a direct action of hydrogen ions on the heart, and secondly, by a specific depression of the inotropic epinephrine-effector mechanism. The dose-ratios for production of identical epinephrine-specific responses as compared with those at pH 7.5 were calculated. At a pH of 6.9, the doseratio was 1.5 to 2.5; at a pH of 6.6, it was in the range of 4 to 4.6. In conclusion these observations are in accordance with a concept that acute acidosis affects myocardial function in intact animals bydirect andindirect effects in at least four ways: by a depression of contractility, by a diminished responsiveness of the epinephrineinotropic response mechanism, by an increase in the concentration of ionized calcium, and by a release of catecholamines. AcidosispHCardiac ContractilityEpinephrineCalcium This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Andersen, M. N., Border, J. R., Mouritzen, Ch. V.: Acidosis, catecholamines and cardiovascular dynamics: When does acidosi Continue reading >>

Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus Epinephrine raises plasma lactate concentrations when infused intravenously in normal subjects. We studied a patient with noninsulin-dependent diabetes mellitus who developed lactic acidosis and marked insulin resistance when treated with epinephrine after open heart surgery. Caruso M, Orszulak TA, Miles JM. Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus. Arch Intern Med. 1987;147(8):14221424. doi:10.1001/archinte.1987.00370080058013 New! JAMA Network Open is now accepting submissions. Learn more. Customize your JAMA Network experience by selecting one or more topics from the list below. Challenges in Clinical Electrocardiography Clinical Implications of Basic Neuroscience Health Care Economics, Insurance, Payment Scientific Discovery and the Future of Medicine United States Preventive Services Task Force JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Facial Plastic Surgery JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA OtolaryngologyHead & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) AMA Manual of Style Art and Images in Psychiatry Breast Cancer Screening Guidelines Colorectal Screening Guidelines Declaration of Helsinki Depression Screening Guidelines Evidence-Based Medicine: An Oral History Fishbein Fellowship Genomics and Precision Health Health Disparities Hypertension Guidelines JAMA Network Audio JAMA Network Conferences Med Men Medical Education Opioid Management Guidelines Peer Review Congress Research Ethics Sepsis and Septic Shock Continue reading >>

Comparison Of Equipressor Doses Of Norepinephrine, Epinephrine, And Phenylephrine On Septic Myocardial Dysfunction | Anesthesiology | Asa Publications

Comparison Of Equipressor Doses Of Norepinephrine, Epinephrine, And Phenylephrine On Septic Myocardial Dysfunction | Anesthesiology | Asa Publications

Comparison of Equipressor Doses of Norepinephrine, Epinephrine, and Phenylephrine on Septic Myocardial Dysfunction *Doctoral Student, Groupe Choc Contrat Avenir Inserm, U961, Faculte de Medecine, Nancy Universite, Nancy, France; Service Ranimation Mdicale, CHU Nancy-Brabois, Vandoeuvre-les-Nancy, France. Masters Degree Student, Groupe Choc Contrat Avenir Inserm, U961, Faculte de Medecine, Nancy Universite. Researcher, Service Mdecine Nuclaire et Nancyclotep, CHU Nancy-Brabois. Professor, Service Mdecine Nuclaire et Nancyclotep, CHU Nancy-Brabois. Professor, Groupe Choc Contrat Avenir Inserm, U961, Faculte de Medecine, Nancy Universite; Service Ranimation Mdicale, CHU Nancy-Brabois. Critical Care Medicine / Cardiovascular Anesthesia / Critical Care / Gastrointestinal and Hepatic Systems / Technology / Equipment / Monitoring Comparison of Equipressor Doses of Norepinephrine, Epinephrine, and Phenylephrine on Septic Myocardial Dysfunction Anesthesiology 5 2012, Vol.116, 1083-1091. doi: Anesthesiology 5 2012, Vol.116, 1083-1091. doi: Comparison of Equipressor Doses of Norepinephrine, Epinephrine, and Phenylephrine on Septic Myocardial Dysfunction You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Myocardial dysfunction occurs during septic shock Norepinephrine and epinephrine improved global hemodynamics and myocardial function during experimental septic shock but epinephrine increased myocardial oxygen consumption, whereas phenylephrine decreased ventricular performance CARDIOVASCULAR dysfunction is a major contributor in septic shock-induced mortality. 1 Septic shock is characterized by both an alteration in vascular tone 2 and a systolic and diastolic biventricular dys Continue reading >>

Lactic Acidosis

Lactic 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. Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. Lactate is a byproduct of anaerobic respiration and is normally cleared from the blood by the liver, kidney and skeletal muscle. Lactic acidosis occurs when the body's buffering systems are overloaded and tends to cause a pH of ≤7.25 with plasma lactate ≥5 mmol/L. It is usually caused by a state of tissue hypoperfusion and/or hypoxia. This causes pyruvic acid to be preferentially converted to lactate during anaerobic respiration. Hyperlactataemia is defined as plasma lactate >2 mmol/L. Classification Cohen and Woods devised the following system in 1976 and it is still widely used:[1] Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia. Type B: lactic acidosis occurs without clinical evidence of tissue hypoperfusion or hypoxia. It is further subdivided into: Type B1: due to underlying disease. Type B2: due to effects of drugs or toxins. Type B3: due to inborn or acquired errors of metabolism. Epidemiology The prevalence is very difficult to estimate, as it occurs in critically ill patients, who are not often suitable subjects for research. It is certainly a common occurrence in patients in high-dependency areas of hospitals.[2] The incidence of symptomatic hyperlactataemia appears to be rising as a consequence of the use of antiretroviral therapy to treat HIV infection. It appears to increase in those taking stavudine (d4T) regimens.[3] Causes of lactic acid Continue reading >>

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