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Which Medications Are Associated With Hyperlactemia And Lactic Acidosis?

Lactic Acidosis

Lactic Acidosis

Background 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 Presentation and Differentials.) The causes of lactic acidosis are listed in the chart below. Go to Acute Lactic Ac Continue reading >>

(pdf) Reported Survival With Severe Mixed Acidosis And Hyperlactemia After Toluene Poisoning

(pdf) Reported Survival With Severe Mixed Acidosis And Hyperlactemia After Toluene Poisoning

Lactic acidosis is a recognized complication of the inhalant abuse such as toluene, especially in patients with renal insufciency. We report a case of severe metabolic acidosis and hyperlactemia due to toluene snifng. The favorable outcome, despite extremely poor clinical symptoms, signs, laboratory and radiological ndings, was unexpected. Specic aspects of the clinical course are addressed. Toluene snifng should be considered in evaluating sever metabolic acidosis. Favorable outcome could be achieved with early diagnosis and proper interventions. Key words: Lactic acidosis, toluene, hyperlactemia Reported survival with severe mixed acidosis and unstable with sinus tachycardia (heart rate of 120 beats per minute) and hypotension (blood pressure was 90/45 mmHg) on inotropic medications norepinephrine started at 10 microgram/min. He required an FIO2 of 80% to maintain his oxygen saturation above 90%. He had bilateral coarse crepitations on chest auscultation. Abdominal examinations were unremarkable. Initial arterial blood gases interpretations showed severe mixed acidosis with pH 6.5 (7.35-7.45). His arterial lactate was 16 mmol/L, his CBC was normal, he had a serum creatinine of 211 mmol/L, urea was 50 mmol/L and cardiac enzymes were normal. Toxicology screen was negative for alcohol, salicylates and acetaminophen. Chest radiographs were obtained which showed diffuse bilateral inltrates [Figure 1]. Compute tomography (CT) of the abdomen and chest showed a small stone in the left kidney and bilateral consolidative changes of both lungs. ECG was normal except for sinus tachycardia. Left ventricular (LV) function was good on echocardiography and chamber sizes were of normal dimensions. Patient received supportive treatment with invasive hemodynamic monitoring, intravenous 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-induced Lactic Acidosis (mila): A Case Report And Review Of Current Diagnostic Paradigm

Metformin-induced Lactic Acidosis (mila): A Case Report And Review Of Current Diagnostic Paradigm

Get rights and content A new diagnostic paradigm has been proposed to better categorize causes of Metformin-Associated Lactic Acidosis (MALA). The diagnostic criteria defines a link between Metformin and lactic acidosis if lactate is >5mmol/L, Ph<7.35 and Metformin assay >5mg/L. Metformin assays are not readily available in emergency departments including nationwide Veterans Affairs Hospitals; thereby making this proposed classification tool difficult to use in todays clinical practice. We describe a case report of a 45-year-old male, who took twice the amount of Metformin prescribed and presented with Metformin-induced lactic acidosis. According to the new criterion, our case would be classified as Lactic Acidosis in Metformin-Treated Patients (LAMT). However, the term LAMT does not distinguish between a septic patient taking Metformin with lactic acidosis, and a patient who ingested toxic amounts of Metformin and has lactic acidosis (in absence of Metformin assay). Our case highlights the importance of medication reconciliation done on arrival to emergency department. Timing and dosing of Metformin in patients who present to the emergency department with lactic acidosis may cinch the diagnosis of Metformin-Induced Lactic Acidosis (MILA) in the absence of a Metformin assay but in the right clinical context. Choose an option to locate/access this article: Check if you have access through your login credentials or your institution. Continue reading >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

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

Lactic Acidosis Medical Blog

Lactic Acidosis Medical Blog

By the turn of the 20th century, it had become apparent 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, Huckabees 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. The normal blood lactate concentration in unstressed patients is 1-0.5 mmol/L. Patients with critical illness can be considered to have normal lactate concentrations of less than 2 mmol/L. Hyperlactatemia is defined as a mild-to-moderate (2-5 mmol/L) persistent increase in blood lactate concentration without metabolic acidosis, whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually > 5 mmol/L) in association with metabolic acidosis. Hyperlactatemia generally occurs in the settings of adequate tissue perfusion, intact buffering systems, and adequate tissue oxygenation. Lactic acidosis is associated with major metabolic dysregulation, tissue hypoperfusion, effects of certain drugs or toxins, or congenital abnormalities in carbohydrate metabolism. Cohen and Woods divided lactic acidosis into 2 categories, type A and type B. Type A is lactic acidosis occurring in association with clinical evidence of poor tissue perfusion or oxygenation of blood (eg, hypotension, cyanosis, cool and clammy extremities). Type B is lactic acidosis occurring when no clinical evidence of poor tissue perfusion or oxygenation exi Continue reading >>

The Riddle Of Hyperlactatemia

The Riddle Of Hyperlactatemia

A recent observational study in a large cohort of critically ill patients confirms the association between hyperlactatemia and mortality. The mechanisms regulating the rates of lactate production and clearance in critical illness remain poorly understood. During exercise, hyperlactatemia clearly results from an imbalance between oxygen delivery and energy requirements. In critically ill patients, the genesis of hyperlactatemia is significantly more complex. Possible mechanisms include regional hypoperfusion, an inflammation-induced upregulation of the glycolitic flux, alterations in lactate-clearing mechanisms, and increases in the work of breathing. Understanding how these complex processes interact to produce elevations in lactate continues to be an important area of research. LactateCritical IllnessBlood LactateLactate ProductionBlood Lactate Level The lack of a reliable indicator to assess cellular hypoxia and monitor the effectiveness of therapeutic interventions remains a major challenge in critical care medicine. In a study published in the previous issue of Critical Care, Khosravani and colleagues [ 1 ] further illustrated the independent association between mortality and blood lactate levels. They noted an independent association between mortality and blood lactate levels of above 2.0 mmol/L. Their study is important for several reasons. First, the authors cast a wide net by including all adult intensive care unit admissions (n = 13,932) occurring during a 3-year period in a well-defined patient population of 1.2 million. Over 12,000 patients had at least one lactate determination during their first 24 hours. Of these, 36% had a lactate concentration of greater than 2.0 mmol/L (the authors' definition of hyperlactatemia) and another 4% developed hyperlactatemi Continue reading >>

Sepsis-associated Hyperlactatemia

Sepsis-associated Hyperlactatemia

Garcia-Alvarez et al. licensee BioMed Central Ltd.2014 There is overwhelming evidence that sepsis and septic shock are associated with hyperlactatemia (sepsis-associated hyperlactatemia (SAHL)). SAHL is a strong independent predictor of mortality and its presence and progression are widely appreciated by clinicians to define a very high-risk population. Until recently, the dominant paradigm has been that SAHL is a marker of tissue hypoxia. Accordingly, SAHL has been interpreted to indicate the presence of an `oxygen debt or `hypoperfusion, which leads to increased lactate generation via anaerobic glycolysis. In light of such interpretation of the meaning of SAHL, maneuvers to increase oxygen delivery have been proposed as its treatment. Moreover, lactate levels have been proposed as a method to evaluate the adequacy of resuscitation and the nature of the response to the initial treatment for sepsis. However, a large body of evidence has accumulated that strongly challenges such notions. Much evidence now supports the view that SAHL is not due only to tissue hypoxia or anaerobic glycolysis. Experimental and human studies all consistently support the view that SAHL is more logically explained by increased aerobic glycolysis secondary to activation of the stress response (adrenergic stimulation). More importantly, new evidence suggests that SAHL may actually serve to facilitate bioenergetic efficiency through an increase in lactate oxidation. In this sense, the characteristics of lactate production best fit the notion of an adaptive survival response that grows in intensity as disease severity increases. Clinicians need to be aware of these developments in our understanding of SAHL in order to approach patient management according to biological principles and to interpret Continue reading >>

Hyperlactemia Can Predict The Prognosis Of Liver Resection

Hyperlactemia Can Predict The Prognosis Of Liver Resection

Background and AimsLactate levels predict outcomes after hepatectomy. We compared metabolic effects of lactated versus lactate free solutions in living donor hepatectomy.MethodsConsecutive right lobe donors (n = 53) were alternatively allotted to lactated Ringer's solution and normal saline (Group L-control) or acetated crystalloid (Sterofundin B Braun Group S -study group) in an observational prospective randomised study. The primary outcome measure was lactate level, and secondary outcomes were base excess, bicarbonate, glucose and chloride intra- and post-operatively. MannWhitney and Chi-square tests were used for analysis.ResultsThe intraoperative, post-operative lactate levels and the time for normalisation were comparable. Group L had significantly lower intraoperative bicarbonate levels (mmol/L) at 6 and 8 h (20.0 2.14 vs. 21.3 1.6, P = 0.0471; 18.68 2.04 vs. 20.39 17, P = 0.002), base excess at 4 and 6 h (mmol/L) (3.64 2.73 vs. 3.0 1.52, P = 0.031; 6.64 2.76 vs. 4.35 1.7 P = 0.006). The intraoperative chloride levels (mmol/L) were higher in group L at 4 and 8 h (108 5.9 vs. 105.99 2.76, P = 0.0471; 109.51 3.86 vs. 106.93 3.09, P = 0.002). Intraoperative glucose (mg/dL) at 6 h was higher in group L, 160.55 31.52 vs. 145.5 24.29, P = 0.043. The highest post-operative chloride (mmol/L) was higher in Group L (112.3 3.86 vs. 109.81 3.72, P = 0.034). Post-operative base excess and bicarbonate showed an improved profile in Group S (7.37 2.99 vs. 5.06 1.71 P = 0.001 and 17.79 2.23 vs. 19.68 1.51 P = 0.005).ConclusionAcetated fluids were associated with higher levels of bicarbonate, lesser base deficit, glucose and chloride but no difference in lactate levels in comparison with Ringer's lactate and normal saline in living donor hepatectomy. Postoperative pancreatic fist Continue reading >>

Recoverable, Record-high Lactic Acidosis In A Patient With Glycogen Storage Disease Type 1: A Mixed Type A And Type B Lactate Disorder

Recoverable, Record-high Lactic Acidosis In A Patient With Glycogen Storage Disease Type 1: A Mixed Type A And Type B Lactate Disorder

Recoverable, Record-High Lactic Acidosis in a Patient with Glycogen Storage Disease Type 1: A Mixed Type A and Type B Lactate Disorder 1Department of Medicine, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem, Israel 2Department of Pediatrics, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem, Israel 3Department of Critical Care Unit, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem, Israel Received 25 September 2016; Accepted 2 November 2016 Copyright 2016 Yonatan Oster et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 17-year-old patient with GSD type 1a (von Gierke disease) was hospitalized with an extremely elevated serum lactate following an intercurrent infection and interruption of his frequent intake of carbohydrates. The patient developed shock, oliguric renal failure, and cardiorespiratory failure requiring mechanical ventilation and inotropes. At the peak of metabolic decompensation and clinical instability, serum lactate reached a level of 47.6 mmol/L which was accompanied by a severe anion gap metabolic acidosis with a pH of 6.8 and bicarbonate of 4 meq/L. The patient was stabilized with massive infusions of sodium bicarbonate (45 meq/h) and glucose and recovered without the need for dialysis. This patient illustrates pathophysiologic mechanisms involved in the development of extreme mixed type A and type B lactic acidemia, reflecting altered metabolic pathways in GSD type 1, combined with tissue hypoperfusion. The rationale for the specific interventions in this case is outlined. Lactic acidosis is an anion gap metabolic acidosis that results from lactate Continue reading >>

Haart-induced Lactic Acidosis

Haart-induced Lactic Acidosis

Nucleoside Reverse Transcriptase Inhibitors are associated with hyperlactemia and lactic acidosis NRTI also cause pancreatitis, myopathy, peripheral neuropathy, anemia, neutropenia, hepatic toxicity [1] Specifically didanosine (ddI) and stavudine (d4T) These medicines are no longer first-line agents in the US and Europe, but are in low-middle income countries Adverse effects of NRTI is by way of mitochondrial toxicity. NRTI inhibit human DNA polymerase gamma, a key enzyme for mitochondrial replication. Impaired electron transport chain, leading to leakage of electrons and increased production of reactive oxygen species. [2] Variable onset of mitochondrial toxicity, and not at any set point in NRTI use. [2] Use of stavudine and didanosine containing regimens Additional studies cite a CD4 count less than 500 as a risk factor. [4] Age, as the risk of hyperlactemia increases 50% with every 10 years of aging Associated with dyslipidemia and insulin resistance [5] Since the symptoms are non-specific, most patients present with advanced symptoms and the more serious lactic acidosis. [3] Creatinine clearance, as renal failure is a significant risk factor for the development of lactic acidosis from hyperlactemia. . [7] Liver Function Test, as hepatic dysfunction precludes oxidation of lactate, thus resulting in elevated lactate levels in the blood Anecdotal evidence to support Riboflavin (50mg/day), and/or thiamine (100mg BID) [8] Stop all anti-retrovirals until lactate normalization [2] Consider antioixidant supplementation to reduce oxidative stress and hyperlactemia [9] Lee WM, Dienstag JL. Lee W.M., Dienstag J.L. Lee, William M., and Jules L. Dienstag.Toxic and Drug-Induced Hepatitis. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. Kasper D, Fauci A, Hauser Continue reading >>

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation of Risk Factors Affecting Lactate Levels in Japanese Patients Treated with Metformin Department of Pharmacy, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Volume 39 (2016) Issue 12 Pages 2022-2027 Released on J-STAGE: December 01, 2016 [Advance Publication] Released: - Received: June 27, 2016 Revised: - Accepted: October 02, 2016 Metformin is a biguanaide antidiabetic drug used worldwide, and its effectiveness and benefits have already been established. However, the safety of high doses of metformin in Japanese patients, especially in elderly patients with a decreased renal function, remains unclear. Among the side effects of metformin, lactate acidosis is the most problematic due to a high mortality rate. Therefore, we assessed plasma lactate levels in metformin-treated patients to identify independent risk factors for hyperlactemia. 290 outpatients receiving various doses of metformin at our hospital were enrolled between March and July 2014. Serum electrolytes, Cre (creatinine), BUN (blood urea nitrogen), UA (uric acid), HbA1c (hemoglobin A1c), and lactate levels were investigated. Lactate levels did not significantly differ between the elderly (75 years) and non-elderly (<75 years) groups. Patients in the elderly group had a significantly lower daily metformin dose and estimated glomerular filtration rate (eGFR), compared with the non-elderly group (both p<0.005). Between with and without hyperlactemia groups, no significant differences were observed in either Cre or age. On the other hand, patients with hyperlactemia had a significantly higher dose of metformin than those without hyperlactemia (p<0.05). In this study, we fou Continue reading >>

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation Of Risk Factors Affecting Lactate Levels In Japanese Patients Treated With Metformin

Investigation of Risk Factors Affecting Lactate Levels in Japanese Patients Treated with Metformin Department of Pharmacy, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Department of Diabetes, Mazda Hospital of Mazda Motor Corporation Volume 39 (2016) Issue 12 Pages 2022-2027 Released on J-STAGE: December 01, 2016 [Advance Publication] Released: - Received: June 27, 2016 Revised: - Accepted: October 02, 2016 Metformin is a biguanaide antidiabetic drug used worldwide, and its effectiveness and benefits have already been established. However, the safety of high doses of metformin in Japanese patients, especially in elderly patients with a decreased renal function, remains unclear. Among the side effects of metformin, lactate acidosis is the most problematic due to a high mortality rate. Therefore, we assessed plasma lactate levels in metformin-treated patients to identify independent risk factors for hyperlactemia. 290 outpatients receiving various doses of metformin at our hospital were enrolled between March and July 2014. Serum electrolytes, Cre (creatinine), BUN (blood urea nitrogen), UA (uric acid), HbA1c (hemoglobin A1c), and lactate levels were investigated. Lactate levels did not significantly differ between the elderly (75 years) and non-elderly (<75 years) groups. Patients in the elderly group had a significantly lower daily metformin dose and estimated glomerular filtration rate (eGFR), compared with the non-elderly group (both p<0.005). Between with and without hyperlactemia groups, no significant differences were observed in either Cre or age. On the other hand, patients with hyperlactemia had a significantly higher dose of metformin than those without hyperlactemia (p<0.05). In this study, we fou Continue reading >>

Fatal Type-b Lactic Acidosis In Association With Hiv Associated Lymphoma - A Case Report With Review Of Literature

Fatal Type-b Lactic Acidosis In Association With Hiv Associated Lymphoma - A Case Report With Review Of Literature

Fatal Type-B Lactic Acidosis in Association with HIV Associated Lymphoma - A Case Report with Review of Literature Asif Salim, Sara Chinthu, Shobhana Nayak Rao * and Pradeep Shenoy M Department of Nephrology, K.S. Hegde Medical Academy, Medical Sciences Complex, Derlakatte, Mangalore 575013, Karnataka, India Associate Professor and Head, Department of Nephrology, K.S. Hegde Medical Academy, Derlakatte, Mangalore 575013, Karnataka, India Received date: June 27, 2017; Accepted date: June 27, 2017; Published date: July 24, 2017 Citation: Salim A, Chinthu S, Rao SN, Shenoy PM (2017) Fatal Type-B Lactic Acidosis in Association with HIV Associated Lymphoma- A Case Report with Review of Literature. Jour Ren Med Vol.1. No.2: 8. Visit for more related articles at Journal of Renal Medicine Hyperlactemia is defined as whole blood lactate levels > 2 mmol/L. Type-B lactic acidosis refers to conditions wherein overproduction of lactate is not related to reduction in tissue oxygen. The occurrence of severe lactic acidosis in malignancies is a rare and often pre-terminal complication. We present two HIV positive patients with type-B lactic acidosis as a pre-terminal event after being diagnosed with non Hodgkins lymphoma. The first patient, a 45-year-old male, HIV positive since 2012 on therapy admitted with h/o of pedal edema, generalized weakness and decreased appetite 1 week duration. Abdominal ultrasound scan revealed bilateral moderate hydro-ureteronephrosis with large left pleural effusion, cytology revealed malignant serous lymphoma confirmed by supraclavicular lymph node biopsy. Before initiation of chemotherapy, his general condition rapidly worsened with onset of lactic acidosis (10 mmol/L) and he expired. The second patient, a 59-year-old male presented with acute hematemesi 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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