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Lactic Acidosis Guidelines

Sustained Low-efficiency Dialysis As A Treatment Modality In A Patient With Lymphoma-associated Lactic Acidosis

Sustained Low-efficiency Dialysis As A Treatment Modality In A Patient With Lymphoma-associated Lactic Acidosis

Sustained low-efficiency dialysis as a treatment modality in a patient with lymphoma-associated lactic acidosis Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Correspondence and offprint requests to: M. Prikis, Division of Nephrology, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA. Email: [email protected] Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works Continue reading >>

Lactic Acidosis: Clinical Implications And Management Strategies

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 >>

Should Dialysis Be Offered In All Cases Of Metformin-associated Lactic Acidosis?

Should Dialysis Be Offered In All Cases Of Metformin-associated Lactic Acidosis?

Should dialysis be offered in all cases of metformin-associated lactic acidosis? Metformin is commonly used in diabetes mellitus type 2, with lactic acidosis being a rare but potentially fatal complication of this therapy. The management of metformin-associated lactic acidosis (MALA) is controversial. Treatment may include supportive care, activated charcoal, bicarbonate infusion, hemodialysis, or continuous venovenous hemofiltration. In the previous issue of Critical Care, Peters and colleagues systematically evaluated outcomes in MALA patients admitted to their intensive care unit. The mortality rate of patients who received dialysis was similar to that of patients who were not dialyzed. However, it was the more acutely and chronically ill patients who actually received dialysis. This suggests that hemodialysis was beneficial in preventing a higher mortality rate in those who required renal replacement therapy. Diabetes Mellitus TypeMetforminRenal Replacement TherapyAcute Kidney InjuryActivate Charcoal The literature on the management of metformin-associated lactic acidosis (MALA) is sparse and consists of case reports and case series. In the previous issue of Critical Care, Peters and colleagues [ 1 ] presented a retrospective cohort study in patients with MALA. This study represents an important step forward in systematically evaluating outcomes in this rare but serious condition. Metformin is commonly used in type 2 diabetes mellitus and accounts for approximately one third of all prescriptions for oral hypoglycemic agents in the US [ 2 ]. The United Kingdom Prospective Diabetes Study demonstrated impressive reductions in diabetes-related endpoints and mortality in overweight patients with type 2 diabetes who used this drug [ 3 ]. A rare but extremely serious adve Continue reading >>

Lactic Acidosis

Lactic Acidosis

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Lactic Acidosis Treatment & Management

Lactic Acidosis Treatment & Management

Approach Considerations Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery. The former is addressed by various therapies, including administration of appropriate antibiotics, surgical drainage and debridement of a septic focus, chemotherapy of malignant disorders, discontinuation of causative drugs, and dietary modification in certain types of congenital lactate acidosis. Cardiovascular collapse secondary to hypovolemia or sepsis should be treated with fluid replacement. Both crystalloids and colloids can restore intravascular volume, but hydroxyethyl starch solutions should be avoided owing to increased mortality. [21] Excessive normal saline administration can cause a nongap metabolic acidosis due to hyperchloremia, which has been associated with increased acute kidney injury. [32] Balanced salt solutions such as Ringer lactate and Plasma-Lyte will not cause a nongap metabolic acidosis and may reduce the need for renal replacement therapy; however, these can cause a metabolic alkalosis. [33] No randomized, controlled trial has yet established the safest and most effective crystalloid. If a colloid is indicated, albumin should be used. Despite appropriate fluid management, vasopressors or inotropes may still be required to augment oxygen delivery. Acidemia decreases the response to catecholamines, and higher doses may be needed. Conversely, high doses may exacerbate ischemia in critical tissue beds. Careful dose titration is needed to maximize benefit and reduce harm. Lactic acidosis causes a compensatory increase in minute ventilation. Patients may be tachypneic initially, but respiratory muscle fatigue can ensue rapidly and mechanical ventilation may be necessary. Alkali therapy remains controversial Continue reading >>

Treatment Of Lactic Acidosis.

Treatment Of Lactic Acidosis.

Severe lactic acidosis is often associated with poor prognosis. Recognition and correction of the underlying process is the major step in the treatment of this serious condition. Intravenous administration of sodium bicarbonate has been the mainstay in the treatment of lactic acidosis. Aggressive use of this therapeutic modality, however, can lead to serious complications and should therefore be considered with caution. Peritoneal dialysis and hemodialysis provide large amounts of alkali without causing the hypernatremia or hypervolemia commonly associated with bicarbonate infusion. Peritoneal dialysis with bicarbonate-based dialysate, in particular, appears to be an ideal means of delivering physiologic buffer. Administration of methylene blue was initially thought to increase lactate metabolism by altering the cellular oxidative state. Its subsequent clinical use, however, showed little efficacy. Sodium nitroprusside has been advocated for the treatment of some forms of lactic acidosis as a method of alleviating regional hypoperfusion. Insulin therapy has been found to be quite useful in the treatment of phenformin-associated lactic acidosis and is recommended in this setting. Since dichloroacetate activates pyruvate dehydrogenase and enhances lactate metabolism, it may be a useful adjunct in the treatment of lactic acidosis. Continue reading >>

Congenital Lactic Acidosis

Congenital Lactic Acidosis

Causes Most cases of congenital lactic acidosis are caused by one or more inherited mutations of genes within the DNA located within the nucleus (nDNA) or within the mitochondria (mtDNA) of cells. Genes carry the genetic instructions for cells. A mutation is a change in a gene located in nuclear or mitochondrial DNA that may cause disease. Mutations of nDNA, which occur in cellular chromosomes, can be inherited through different forms of transmission of the mutation, including autosomal recessive, autosomal dominant or X-linked recessive inheritance. Mutations affecting the genes for mitochondria (mtDNA) are inherited from the mother. MtDNA that is found in sperm cells is typically lost during fertilization. As a result, all human mtDNA comes from the mother. An affected mother will pass on the mutation to all her children, but only her daughters will pass on the mutation to their children. Mitochondria, which are found by the hundreds or thousands in the cells of the body, particularly in muscle and nerve tissue, carry the blueprints for regulating energy production. As cells divide, the number of normal mtDNA and mutated mtDNA are distributed in an unpredictable fashion among different tissues. Consequently, mutated mtDNA accumulates at different rates among different tissues in the same individual. Thus, family members who have the identical mutation in mtDNA may exhibit a variety of different symptoms and signs at different times and to varying degrees of severity. Pyruvate dehydrogenase complex (PDC) deficiency is a genetic mitochondrial disease of carbohydrate metabolism that is due to a mutation in nDNA. It is generally considered to be the most common cause of biochemically proven cases of congenital lactic acidosis. PDC deficiency can be inherited as an autosom 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 >>

Lactic Acidosis Update For Critical Care Clinicians

Lactic Acidosis Update For Critical Care Clinicians

Lactic Acidosis Update for Critical Care Clinicians Franz Volhard Clinic and Max Delbrck Center for Molecular Medicine, Medical Faculty of the Charit Humboldt University of Berlin, Berlin, Germany. Correspondence to Dr. Friedrich C. Luft, Wiltberg Strasse 50, 13125 Berlin, Germany. Phone: 49-30-9417-2202; Fax: 49-30-9417-2206; E-mail: luft/{at}fvk-berlin.de Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction. Drugs used to treat lactic acidosis can aggravate the condition. NaHCO3 increases lactate production. Treatment of type A lactic acidosis is particularly unsatisfactory. NaHCO3 is of little value. Carbicarb is a mixture of Na2CO3 and NaHCO3 that buffers similarly to NaHCO3 but without net generation of CO2. The results from animal stud Continue reading >>

Systematic Review Of Current Guidelines, And Their Evidence Base, On Risk Of Lactic Acidosis After Administration Of Contrast Medium For Patients Receiving Metformin

Systematic Review Of Current Guidelines, And Their Evidence Base, On Risk Of Lactic Acidosis After Administration Of Contrast Medium For Patients Receiving Metformin

Systematic Review of Current Guidelines, and Their Evidence Base, on Risk of Lactic Acidosis after Administration of Contrast Medium for Patients Receiving Metformin 1From the Department of Diagnostic Imaging, Southern Health, 246 Clayton Rd, Clayton, VIC 3168, Australia (S.K.G., G.C.); and Centre for Clinical Effectiveness, Monash Institute of Health Services Research, Monash University, Clayton, Victoria, Australia (G.R., C.H.). From the 2008 RSNA Annual Meeting. Address correspondence to S.K.G. (e-mail: [emailprotected] ). To systematically review evidence about the relationship between metformin administration and the use of iodinated contrast medium and risk of lactic acidosis (LA) and to assess the quality of five current guidelines for use of contrast medium in patients who are taking metformin. A search strategy was developed by using search termsrelated to metformin, contrast media, and LA. Searches were conducted in MEDLINE (Ovid), all Evidence-based Medicine Reviews (Ovid), EMBASE, and Cochrane library databases and were augmented with searches for evidence-based guidelines on radiology and evidence-based medicine Web sites by using the Google Internet search engine. Guidelines were appraised by two independent reviewers by using the Appraisal of Guidelines Research and Evaluation Collaboration Instrument. Other studies were appraised by using structured appraisal checklists. Five guidelines were identified and five empirical studies met inclusion criteria. All guidelines had poor scores on some Appraisal of Guidelines for Research and Evaluation (AGREE) Collaboration criteria; poorer scores tended to occur in relation to objective assessment of rigor of guideline development, editorial independence, and applicability of the guideline to clinical practice. L Continue reading >>

Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine

Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery. The former is addressed by various therapies, including administration of appropriate antibiotics, surgical drainage and debridement of a septic focus, chemotherapy of malignant disorders, discontinuation of causative drugs, and dietary modification in certain types of congenital lactate acidosis. Cardiovascular collapse secondary to hypovolemia or sepsis should be treated with fluid replacement. Both crystalloids and colloids can restore intravascular volume, but hydroxyethyl starch solutions should be avoided owing to increased mortality. [ 21 ] Excessive normal saline administration can cause a nongap metabolic acidosis due to hyperchloremia, which has been associated with increased acute kidney injury. [ 32 ] Balanced salt solutions such as Ringer lactate and Plasma-Lyte will not cause a nongap metabolic acidosis and may reduce the need for renal replacement therapy; however, these can cause a metabolic alkalosis. [ 33 ] No randomized, controlled trial has yet established the safest and most effective crystalloid. If a colloid is indicated, albumin should be used. Despite appropriate fluid management, vasopressors or inotropes may still be required to augment oxygen delivery. Acidemia decreases the response to catecholamines, and higher doses may be needed. Conversely, high doses may exacerbate ischemia in critical tissue beds. Careful dose titration is needed to maximize benefit and reduce harm. Lactic acidosis causes a compensatory increase in minute ventilation. Patients may be tachypneic initially, but respiratory muscle fatigue can ensue rapidly a 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 >>

Metformin And Fatal Lactic Acidosis

Metformin And Fatal Lactic Acidosis

Publications Published: July 1998 Information on this subject has been updated. Read the most recent information. Dr P Pillans,former Medical Assessor, Centre for Adverse Reactions Monitoring (CARM), Dunedin Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Significant renal and hepatic disease, alcoholism and conditions associated with hypoxia (eg. cardiac and pulmonary disease, surgery) are contraindications to the use of metformin. Other risk factors for metformin-induced lactic acidosis are sepsis, dehydration, high dosages and increasing age. Metformin remains a major reported cause of drug-associated mortality in New Zealand. Of the 12 cases of lactic acidosis associated with metformin reported to CARM since 1977, 2 occurred in the last year and 8 cases had a fatal outcome. Metformin useful but small risk of potentially fatal lactic acidosis Metformin is a useful therapeutic agent for obese non-insulin dependent diabetics and those whose glycaemia cannot be controlled by sulphonylurea monotherapy. Lactic acidosis is an uncommon but potentially fatal adverse effect. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors.1 Examples of metformin-induced lactic acidosis cases reported to CARM include: A 69-year-old man, with renal and cardiac disease, was prescribed metformin due to failing glycaemic control on glibenclamide monotherapy. He was well for six weeks, then developed lactic acidosis and died within 3 days. Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery. A 56-year-old woman, with no predisposing disease, died from lactic acidosis following major Continue reading >>

Sustained Low-efficiency Dialysis As A Treatment Modality In A Patient With Lymphoma-associated Lactic Acidosis

Sustained Low-efficiency Dialysis As A Treatment Modality In A Patient With Lymphoma-associated Lactic Acidosis

Sustained low-efficiency dialysis as a treatment modality in a patient with lymphoma-associated lactic acidosis Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Correspondence and offprint requests to: M. Prikis, Division of Nephrology, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA. Email: [email protected] Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works Continue reading >>

Hemodialysis For Lactic Acidosis

Hemodialysis For Lactic Acidosis

Department of Critical Care Medicine, Apollo First Med Hospital, Chennai, Tamil Nadu, India 1Department of Critical Care Medicine, Apollo Hospitals, Chennai, Tamil Nadu, India Address for correspondence: Dr. Ashwin K. Mani, Department of Critical Care Medicine, Apollo First Med Hospital, 154, PH Road, Chennai - 600 010, Tamil Nadu, India. E-mail: [email protected] Author information Copyright and License information Disclaimer Copyright : 2017 Indian Journal of Critical Care Medicine This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. Lactic acidosis (Type A) is common in critically ill patients and usually treated by correcting the underlying etiology. We present the case of a young female who presented with life-threatening lactic acidosis secondary to hematological malignancy. Timely initiation of hemodialysis was lifesaving. The case highlights the importance of considering Type B lactic acidosis (in this case secondary to a hematological malignancy) and also initiating renal replacement therapy when routine measures are ineffective. Keywords: Hematological malignancy, hemodialysis, hyperlactatemia, lactic acidosis, malignancy Lactic acidosis is very commonly encountered in the critical care units. Treatments are generally focused on improving oxygen delivery and restoring tissue perfusion. We present a patient with grossly elevated lactate levels associated with lymphoma which improved only after initiation of dialysis. A 21-year-old female patient was transferred from an outside hospital to our tertiary Crit Continue reading >>

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