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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 >>

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 >>

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

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 >>

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 >>

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 >>

Hiv & Aids Information :: Factsheet Lactic Acidosis

Hiv & Aids Information :: Factsheet Lactic Acidosis

Please enter the email address. Separate multiple addresses with a comma. Lactic acidosis refers to a build-up of lactic acid in the blood. It is a rare but dangerous side-effect of some anti-HIV drugs most of these are no longer in regular use. Your HIV clinic will use blood tests to check your levels of lactic acid. Lacticacidosis is very rare. Nevertheless, it is an important subject to understandbecause people who develop the condition can become dangerously ill. Lacticacidosis is a serious side-effect of the nucleosidereverse transcriptaseinhibitor (NRTI)class of anti-HIV drugs. This class includes abacavir (Ziagen),didanosine (ddI, Videx), lamivudine (3TC, Epivir), stavudine (d4T,Zerit), tenofovir (Viread) andzidovudine (AZT, Retrovir). The drugsmost linked with lactic acidosis are stavudine and didanosine. However, neitherof these drugs is now used if any other treatment options are available, mainlybecause of the side-effects they can cause. Lactic acidosis is also apotential, but rare, side-effect of other drugs, including the commonlyprescribed diabetes drug, metformin. The term lactic acidosis is used to describehigh levels of a substance called lactate in the blood. Lactate is a by-productof the processing of sugar within the body. Lacticacidosis is one of several conditions which are believed to be caused by damage to mitochondria . Mitochondriaare found in all human cells and are involved in the production of energy.Other possible side-effects ofNRTIs which may also be associated withdamage to mitochondria include peripheral neuropathy (numbness or pain in the feetand hands); bone marrow suppression; pancreatitis (inflammation of thepancreas); hepatic steatosis (accumulation of fat in the liver); and myopathy(muscle damage). "Lactic acidosis may occurat a 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 >>

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 >>

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 >>

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 >>

Lactic Acidosis

Lactic Acidosis

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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: 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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