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Lactic Acidosis Treatment With Sodium Bicarbonate

Treatment Of Metformin-associated Lactic Acidosis With Closed Recirculation Bicarbonate-buffered Hemodialysis

Treatment Of Metformin-associated Lactic Acidosis With Closed Recirculation Bicarbonate-buffered Hemodialysis

Treatment of Metformin-Associated Lactic Acidosis With Closed Recirculation Bicarbonate-Buffered Hemodialysis To the Editor. The use of massive amounts of intravenous (IV) sodium bicarbonate in the management of lactic acidosis seems necessary as soon as the acidosis becomes severe.1 However, some patients have an apparent resistance to this alkali therapy.2 In addition, intensive administration of sodium bicarbonate carries the combined risks of volume and sodium overload. Several authors tried hemodialysis (HD) or peritoneal dialysis (PD) but, most of the time, the precarious hemodynamic state of these patients limits the use of conventional HD.3,4 The new possibilities allowing the use of dialysate containing bicarbonate in HD have led us to try this method in the case of a metformin-treated diabetic with severe lactic acidosis.5 Report of a Case. A 64-year-old woman was admitted to the hospital in severe shock. Despite chronic renal failure (serum creatinine level of 300 moles/L, she was given 1,700 mg/day of metformin for six Continue reading >>

Treatment Of Acidosis: Sodium Bicarbonate And Other Drugs

Treatment Of Acidosis: Sodium Bicarbonate And Other Drugs

Treatment of Acidosis: Sodium Bicarbonate and Other Drugs Lactic acidosis, defined as a lactate level > 5 mmol/1 and a pH 7.35, is far and away the most-important acidosis during critical illness and most of this discussion of acidosis treatment will focus on treatment of lactic acidosis. Even in the face of maximal supportive therapy, lactic acidosis is associated with a mortality of 60-90% [ 1 , 2 , 3 , 4 ], so physicians have long relied on treatments to lower the [H+], such as sodium bicarbonate. Less common than lactic acidosis, and much more amenable to conventional treatments, are ketoacidoses and respiratory acidosis, but these too occasionally prompt consideration of alkalinizing therapies. Lowering the [H+] in blood depends on manipulating the strong ion difference ([SID]), total concentration of non-volatile weak acid buffer (ATOT), or arterial CO2 tension (PaCO2), or raising the total concentration of weak bases, BTOT (normally sufficiently small that it can be ignored). Therefore, potential treatments include: 1. Raise [SID]: a) add strong cations: bicarbonate, carbicarb, dialysis b) remove strong anions: dichloroacetate (DCA), dialysis, thiamine, riboflavin, vasoactive drugs? 2. Lower the paCO2: raise VE or lower VD/VT or VCO2 3. Reduce ATOT: remove albumin, but very limited effect Acute Lung InjurySodium BicarbonateAcute Respiratory Distress SyndromeLactic AcidosisDiabetic Ketoacidosis These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Weil MH, Afifi AA (1970) Experimental and clinical studies on lactate and pyruvate as indicators of th 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 >>

Bicarbonate Therapy In Severe Metabolic Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis

Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>

Therapy Of Lactic Acidosis: Alternatives To Sodium Bicarbonate

Therapy Of Lactic Acidosis: Alternatives To Sodium Bicarbonate

Therapy of Lactic Acidosis: Alternatives to Sodium Bicarbonate Part of the Clinical Physiology Series book series (CLINPHY) Lactic acidosis is the most common form of metabolic acidosis, and the current mortality from this condition is in excess of 50%. Because of its diverse pathophysiology, the clinical management of lactic acidosis is difficult. The mainstay of therapy has traditionally been the intravenous administration of sodium bicarbonate (NaHCO3), but recent clinical and experimental evidence strongly suggests that such therapy may in fact be detrimental. Lactic acidosis is generally defined as a metabolic acidosis due to the accumulation of lactic acid in the blood in excess of 5 mM, with an accompanying blood pH of less than 7.25. However, the mechanisms by which lactic acid accumulation occurs vary and include both the stimulation of lactate production and reductions of lactate metabolism. Clinically, the disorders of lactate metabolism are conveniently divided as either anaerobic (type A) or aerobic (type B) (16). The hallmark of type A lactic acidosis is tissue hypoxia, resulting in anaerobic lactic acid production. The most common causes of type A lactic acidosis are cardiopulmonary arrest and other states characterized by impaired cardiac performance, reduced tissue perfusion, and arterial hypoxemia. In these states, the hypoxia and circulatory insufficiency combine to reduce tissue oxygen availability, resulting in anaerobic metabolism and stimulation of lactic acid production. In type B lactic acidosis, on the other hand, tissue hypoxia appears not to be present, and lactic acid production is metabolically enhanced for other reasons in what is apparently an aerobic state. Examples of type B lactic acidosis include diabetes mellitus, certain malignanci Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m 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 >>

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Curr Opin Crit Care. 2008 Aug;14(4):379-83. doi: 10.1097/MCC.0b013e3283069d5c. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? University of British Columbia, Critical Care Research Laboratories, Vancouver, British Columbia, Canada. Bicarbonate therapy for severe lactic acidosis remains a controversial therapy. The most recent 2008 Surviving Sepsis guidelines strongly recommend against the use of bicarbonate in patients with pH at least 7.15, while deferring judgment in more severe acidemia. We review the mechanisms causing lactic acidosis in the critically ill and the scientific rationale behind treatment with bicarbonate. There is little rationale or evidence for the use of bicarbonate therapy for lactic acidosis due to shock. We agree with the Surviving Sepsis guidelines recommendation against the use of bicarbonate for lactic acidosis for pH at least 7.15 and we further recommend a lower target pH of 7.00 or less. If bicarbonate is used, consideration must be given to slow infusion and a plan for clearing the CO2 that is produced and measuring and correcting ionized calcium as the resultant 10% drop may decrease cardiac and vascular contractility and responsiveness to catecholamines. When continuous renal replacement therapy is used during severe acidosis, we recommend bicarbonate-based replacement fluid over citrate as citrate may increase the strong ion gap. Effective therapy of lactic acidosis due to shock is to reverse the cause. Continue reading >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany 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. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium bicarbonate in the critically Ill patient with metabolic acidosis Uso de bicarbonato de sdio na acidose metablica do paciente gravemente enfermo Lactic acidosis is an acid-base imbalance frequently found in critically ill patients. It is associated with a poor prognosis. Despite the substantial body of evidence that critical levels of acidemia have several adverse effects on cell function, the use of sodium bicarbonate to treat lactic acidosis in critically ill patients remains highly controversial. This article aimed at: 1) analyzing the main differences between hyperchloremic and organic acidoses, with high anion gap; 2) comparing the risks associated with critical levels of acidemia with those associated with the use of sodium bicarbonate; 3) critically analyzing the literature evidence about the use of sodium bicarbonate for the treatment of lactic acidosis in critically ill patients, with an emphasis on randomized control trials in human beings; and 4) providing a rationale for the judicious use of sodium bicarbonate in that situation. Descriptors: lactic acidosis, diabetic ketoacidosis, sodium bicarbonate, septic shock. A acidose ltica um distrbio do equilbrio cido-base muito frequente em pacientes internados em unidades de terapia intensiva e est associado a um mau prognstico. Embora exista um acmulo substancial de evidncias de que nveis crticos de acidemia provocam inmeros efeitos adversos sobre o funcionamento celular, a utilizao de bicarbonato de sdio para o tratamento da acidose ltica em pacientes gravemente enfermos permanece alvo de controvrsias. Neste artigo, pretendemos: 1) analisar as principais diferenas entre as acidoses hiperclormicas e as acidoses orgnicas, com nion gap (AG) elevado, visando embasar a discusso sobre os fundamentos da terapia Continue reading >>

Sodium Bicarbonate Use

Sodium Bicarbonate Use

metabolic acidosis leads to adverse cardiovascular effects bicarbonate must be administered in a solution as sodium bicarbonate 8.4% solution contains 1mmol of HCO3-/mL and is very hypertonic (2,000mOsm/kg) goal of NaHCO3 administration in severe metabolic acidosis to counteract the negative cardiovascular effects of acidaemia alternatives to NaHCO3 include carbicarb, dichloroacetate, Tris/THAM Treatment of sodium channel blocker overdose (e.g. tricyclic overdose) Urinary alkalinisation (salicylate poisoning) Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses) Cardiac arrest (in prolonged resuscitation + documented severe metabolic acidosis) Diabetic ketoacidosis (very rarely, perhaps if shocked and pH < 6.8) Severe pulmonary hypertension with RVF to optimize RV function Severe ischemic heart disease where lactic acidosis is thought to be an arrhythmogenic risk hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) hyperosmolality (cause arterial vasodilation and hypotension) impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve removal of acidotic inhibition of glycolysis by increased activity of PFK hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) severe tissue necrosis if extravasation takes place bicarbonate increases lactate production by: increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues POINTS TO REMEMBER WHEN USING BICARBONATE it is generally better to correct underlying cause of acidosis and give supportive care than to give sodium bicarbonate ensure adequate ventilation to eliminate CO2 pro 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 >>

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

Volume2015(2015), Article ID605830, 7 pages The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate 1Internal Medicine Department, University Hospital of Patras, 26500 Rion, Greece 2University of Patras School of Medicine, 26500 Rion, Greece 3Intensive Care Department, Brugmann University Hospital, 1030 Brussels, Belgium 4Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA Received 22 March 2015; Revised 29 June 2015; Accepted 1 July 2015 Copyright 2015 Dimitrios Velissaris 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. Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option. Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years. Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gas . Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and Continue reading >>

Sodium Bicarbonate For The Treatment Of Lactic Acidosis - Sciencedirect

Sodium Bicarbonate For The Treatment Of Lactic Acidosis - Sciencedirect

Volume 117, Issue 1 , January 2000, Pages 260-267 Sodium Bicarbonate for the Treatment of Lactic Acidosis Author links open overlay panel Sean M.ForsytheMDa Gregory A.SchmidtMD, FCCPb Get rights and content Lactic acidosis often challenges the intensivist and is associatedwith a strikingly high mortality. Treatment involves discerning andcorrecting its underlying cause, ensuring adequate oxygen delivery totissues, reducing oxygen demand through sedation and mechanicalventilation, and (most controversially) attempting to alkalinize theblood with IV sodium bicarbonate. Here we review the literature toanswer the following questions: Is a low pH bad? Can sodium bicarbonateraise the pH in vivo? Does increasing the blood pH withsodium bicarbonate have any salutary effects? Does sodium bicarbonatehave negative side effects? We find that the oft-cited rationale forbicarbonate use, that it might ameliorate the hemodynamic depression ofmetabolic acidemia, has been disproved convincingly. Further, given thelack of evidence supporting its use, we cannot condone bicarbonateadministration for patients with lactic acidosis, regardless of thedegree of acidemia. Continue reading >>

Sodium Bicarbonate For The Treatment Of Lactic Acidosis.

Sodium Bicarbonate For The Treatment Of Lactic Acidosis.

Sodium bicarbonate for the treatment of lactic acidosis. Department of Medicine, University of Chicago School of Medicine, Chicago, IL, USA. Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause, ensuring adequate oxygen delivery to tissues, reducing oxygen demand through sedation and mechanical ventilation, and (most controversially) attempting to alkalinize the blood with IV sodium bicarbonate. Here we review the literature to answer the following questions: Is a low pH bad? Can sodium bicarbonate raise the pH in vivo? Does increasing the blood pH with sodium bicarbonate have any salutary effects? Does sodium bicarbonate have negative side effects? We find that the oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly. Further, given the lack of evidence supporting its use, we cannot condone bicarbonate administration for patients with lactic acidosis, regardless of the degree of acidemia. Continue reading >>

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