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Lactic Acidosis Guidelines

Lactic Acidosis

Lactic Acidosis

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Lactic Acidosis - Cancer Therapy Advisor

Lactic Acidosis - Cancer Therapy Advisor

Hyperlactatemia, anion gap metabolic acidosis, strong ion gap metabolic acidosis Tissue hypoperfusion, ischemia, anaerobic metabolism, shock, acid-base disorders Lactic acidosis associated with critical illness is commonly a byproduct of a much larger problem. In 1976 Cohen and Woods classified lactic acidosis based on etiology. Type A is due to clinical evidence of tissue hypoperfusion. Type B occurs in the absence of clinical evidence of tissue hypoperfusion. Type B is further divided into subgroups B1 - underlying disease/physiologic state; B2 - medication or toxin; and B3 - inborn errors of metabolism. In critically ill patients, lactic acidosis is typically associated with increased lactate production (hypoperfusion, mitochondrial dysfunction), and/or decreased metabolism/clearance. Approximately 1400 mmol of lactic acid is produced daily. The kidneys metabolize up to 30% with no significant elimination. The liver is very efficient in lactate metabolism and elimination and serum lactate levels should remain in the normal range until about 75% of hepatic function is lost. The clinical features of lactic acidosis are similar to other forms of metabolic acidoses. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Other clinical features are related to the underlying cause of lactic acidosis, such as signs of hypoperfusion. Hyperventilaton (rapid shallow or Kussmaul respirations). Seizure (generalized seizures can cause a transient lactic acidosis). Signs of hypovolemia (dry mucous membranes, decreased capillary refill, skin tenting, oliguria). Abdominal pain (especially with mesenteric ischemia). There may only be subtle clinical findings, therefore one needs to have a high suspicion in clinically relevent situations (e.g. i 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 >>

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 >>

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 >>

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 >>

Glyburide And Metformin (oral Route)

Glyburide And Metformin (oral Route)

Precautions Drug information provided by: Micromedex It is very important that your doctor check your progress at regular visits to make sure this medicine is working properly. Blood tests may be needed to check for unwanted effects. Under certain conditions, too much metformin can cause lactic acidosis. The symptoms of lactic acidosis are severe and quick to appear. They usually occur when other health problems not related to the medicine are present and very severe, such as a heart attack or kidney failure. The symptoms of lactic acidosis include abdominal or stomach discomfort; decreased appetite; diarrhea; fast, shallow breathing; a general feeling of discomfort; muscle pain or cramping; and unusual sleepiness, tiredness, or weakness. If you have any symptoms of lactic acidosis, get emergency medical help right away. It is very important to carefully follow any instructions from your health care team about: Alcohol—Drinking alcohol may cause severe low blood sugar. Discuss this with your health care team. Other medicines—Do not take other medicines unless they have been discussed with your doctor. This especially includes nonprescription medicines such as aspirin, and medicines for appetite control, asthma, colds, cough, hay fever, or sinus problems. Counseling—Other family members need to learn how to prevent side effects or help with side effects if they occur. Also, patients with diabetes may need special counseling about diabetes medicine dosing changes that might occur because of lifestyle changes, such as changes in exercise and diet. Furthermore, counseling on contraception and pregnancy may be needed because of the problems that can occur in patients with diabetes during pregnancy. Travel—Keep your recent prescription and your medical history with yo 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 >>

Metformin-induced Lactic Acidosis: No One Left Behind

Metformin-induced Lactic Acidosis: No One Left Behind

Abstract Metformin is a safe drug when correctly used in properly selected patients. In real life, however, associated lactic acidosis has been repeatedly, although rarely, reported. The term metformin-induced lactic acidosis refers to cases that cannot be explained by any major risk factor other than drug accumulation, usually due to renal failure. Treatment consists of vital function support and drug removal, mainly achieved by renal replacement therapy. Despite dramatic clinical presentation, the prognosis of metformin-induced lactic acidosis is usually surprisingly good. In the previous issue of Critical Care, Friesecke and colleagues demonstrate that the survival rate of patients with severe lactic acidosis due to metformin accumulation can be strikingly higher than expected based on the initial clinical evaluation [1]. Metformin is nowadays the first-line drug of choice for the treatment of adults with type 2 diabetes [2]. This drug is the sixth most frequently prescribed in the USA (> 50 million prescriptions in 2009) and is taken by almost 1.5% of the Italian population [3, 4]. Metformin is a safe drug when correctly used in properly selected patients. In particular, no cases of lactic acidosis (a relatively common side effect of other biguanide compounds) were reported in 347 trials with 70,490 patient-years of metformin use [5]. Real life can differ from research settings, however, and lactic acidosis has been repeatedly, although rarely, observed in patients treated with metformin. The number of inquiries to the Swedish Poison Information Centre for metformin intoxication has increased 10 times during the past decade, with 25 cases of severe lactic acidosis reported in 2007 and 2008 [6]. According to the American Association of Poison Control Centers, metform Continue reading >>

Can You Treat Lactic Acidosis By Dialysis?

Can You Treat Lactic Acidosis By Dialysis?

Can you treat lactic acidosis by dialysis? 10 Comments on Can you treat lactic acidosis by dialysis? Managing patients with lactic acidosis, especially the type A variety, is really hard! Usually they have multiple problems, are septic, hypotensive, often on multiple machines and the lactate keeps going up. The choices are between giving soda bicarb, carbicarb or dichloroacetate. The main purpose is to avoid some of complications of severe acidosis such arrhythmias, decreased response to cathechloamines, or reduced contractility. Bicarbonate therapy is a double-edged sword, however, because of the several side-effects such as decreased cardiac output, reduced ionized cardiac output, increased CO2 generation, volume overload and increased lactate generation. Paradoxically, it can also worsen intracellular acidosis. Staff managing these patients think that it would be great to simply clear it out using an extracorporeal therapy, such as hemodialysis or CRRT. Unfortunately it usually does not work. Lactate clearance by dialysis is only 3% of the overall clearance, most of which is in the tissue. In one study, they evaluated the utility of continuous venovenous hemofiltration with dialysis, to calculate lactate clearance by the hemofilter in 10 critically ill patients with acute renal failure and stable blood lactate concentrations. They found that the median blood lactate concentration increased despite renal replacement therapy. The median total plasma lactate clearance was 1379 ml/min (range, 754 to 1881 ml/min), and the median filter lactate clearance was 24 ml/min (range, 7 to 36 ml/min). The authors concluded that continuous venovenous hemofiltration with dialysis cannot meet lactate overproduction. Moreover, the generation of lactic acid is at least order of magnitu 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 >>

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 >>

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Abstract Although metformin has become a drug of choice for the treatment of type 2 diabetes mellitus, some patients may not receive it owing to the risk of lactic acidosis. Metformin, along with other drugs in the biguanide class, increases plasma lactate levels in a plasma concentration-dependent manner by inhibiting mitochondrial respiration predominantly in the liver. Elevated plasma metformin concentrations (as occur in individuals with renal impairment) and a secondary event or condition that further disrupts lactate production or clearance (e.g., cirrhosis, sepsis, or hypoperfusion), are typically necessary to cause metformin-associated lactic acidosis (MALA). As these secondary events may be unpredictable and the mortality rate for MALA approaches 50%, metformin has been contraindicated in moderate and severe renal impairment since its FDA approval in patients with normal renal function or mild renal insufficiency to minimize the potential for toxic metformin levels and MALA. However, the reported incidence of lactic acidosis in clinical practice has proved to be very low (< 10 cases per 100,000 patient-years). Several groups have suggested that current renal function cutoffs for metformin are too conservative, thus depriving a substantial number of type 2 diabetes patients from the potential benefit of metformin therapy. On the other hand, the success of metformin as the first-line diabetes therapy may be a direct consequence of conservative labeling, the absence of which could have led to excess patient risk and eventual withdrawal from the market, as happened with earlier biguanide therapies. An investigational delayed-release metformin currently under development could potentially provide a treatment option for patients with renal impairment pending the resu Continue reading >>

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Open Access funded by Sociedad Colombiana de Anestesiologa y Reanimacin Lactic acidosis is defined as the presence of pH <7.35, blood lactate >2.0mmol/L and PaCO2 <42mmHg. However, the definition of severe lactic acidosis is controversial. The primary cause of severe lactic acidosis is shock. Although rare, metformin-related lactic acidosis is associated with a mortality as high as 50%. The treatment for metabolic acidosis, including lactic acidosis, may be specific or general, using sodium bicarbonate, trihydroxyaminomethane, carbicarb or continuous haemodiafiltration. The successful treatment of lactic acidosis depends on the control of the aetiological source. Intermittent or continuous renal replacement therapy is perfectly justified, shock being the argument for deciding which modality to use. We report a case of a male patient presenting with metformin poisoning as a result of attempted suicide, who developed lactic acidosis and multiple organ failure. The critical success factor was treatment with continuous haemodiafiltration. Definimos acidosis lctica en presencia de pH <7.35, lactato en sangre >2.0mmol/L y PaCO2 <42mmHg. Por otro lado, la definicin de acidosis lctica grave es controvertida. La causa principal de acidosis lctica grave es el estado de choque. La acidosis lctica por metformina es rara pero alcanza mortalidad del 50%. La acidosis metablica incluyendo a la acidosis lctica puede recibir tratamiento especfico o tratamiento general con bicarbonato de sodio, trihidroxiaminometano, carbicarb o hemodiafiltracin continua. El xito del tratamiento de la acidosis lctica yace en el control de la fuente etiolgica; la terapia de reemplazo renal intermitente o continua est perfectamente justificada, donde el argumento para decidir cul utilizar ser el estado de 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 >>

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