sodium-bicarbonate and Acidosis--Lactic

The use of sodium bicarbonate to treat metabolic acidosis is intuitive, yet data suggest that not all patients benefit from this therapy.. In this narrative review, we describe the physiology behind commonly encountered nontoxicologic causes of metabolic acidosis, highlight potential harm from the indiscriminate administration of sodium bicarbonate in certain scenarios, and provide evidence-based recommendations to assist emergency physicians in the rational use of sodium bicarbonate.. Sodium bicarbonate can be administered as a hypertonic push, as a resuscitation fluid, or as an infusion. Lactic acidosis and cardiac arrest are two common scenarios where there is limited benefit to routine use of sodium bicarbonate, although certain circumstances, such as patients with concomitant acute kidney injury and lactic acidosis may benefit from sodium bicarbonate. Patients with cardiac arrest secondary to sodium channel blockade or hyperkalemia also benefit from sodium bicarbonate therapy. Recent data suggest that the use of sodium bicarbonate in diabetic ketoacidosis does not confer improved patient outcomes and may cause harm in pediatric patients. Available evidence suggests that alkalinization of urine in rhabdomyolysis does not improve patient-centered outcomes. Finally, patients with a nongap acidosis benefit from sodium bicarbonate supplementation.. Empiric use of sodium bicarbonate in patients with nontoxicologic causes of metabolic acidosis is not warranted and likely does not improve patient-centered outcomes, except in select scenarios. Emergency physicians should reserve use of this medication to conditions with clear benefit to patients.

Topics: Acidosis; Acidosis, Lactic; Bicarbonates; Child; Heart Arrest; Humans; Sodium Bicarbonate

Topics: Abdominal Pain; Acidosis, Lactic; Aged; Antigens, Neoplasm; Carcinoma; Diabetes Mellitus, Type 2; Drug Resistance; Fatal Outcome; Female; Humans; Hypertension; Ki-1 Antigen; Sodium Bicarbonate; Stomach Neoplasms

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Fluid Therapy; Humans; Hyperlactatemia; Lactic Acid; Prognosis; Sodium Bicarbonate

Lactic acidosis (LA) is common in hospitalized patients and is associated with poor clinical outcomes. There have been major recent advances in our understanding of lactate generation and physiology. However, treatment of LA is an area of controversy and uncertainty, and the use of agents to raise pH is not clearly beneficial.. We reviewed animal and human studies on the pathogenesis, impact, and treatment of LA, published in the English language and available through the PubMed/MEDLINE database. Our aim was to clarify the physiology of the generation of LA, its impact on outcomes, and the different treatment modalities available. We also examined relevant data regarding LA induced by medications commonly prescribed by hospitalists: biguanides, nucleoside analog reverse-transcriptase inhibitors (NRTIs), linezolid, and lorazepam.. Lactic acid is a marker of tissue ischemia but it also may accumulate without tissue hypoperfusion. In the latter circumstance, lactic acid accumulation may be an adaptive mechanism-a novel possibility quite in contrast to the traditional view of lactic acid as only a marker of tissue ischemia. Studies on the treatment of LA with sodium bicarbonate or other buffers fail to show consistent clinical benefit. Severe acidemia in the setting of LA is a particularly poorly studied area. In the settings of medication-induced LA, optimal treatment, apart from prompt cessation of the offending agent, is still unclear.

Topics: Acidosis, Lactic; Hospitalization; Humans; Sodium Bicarbonate; United States

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.

Topics: Acidosis, Lactic; Humans; Shock, Septic; Sodium Bicarbonate

To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies.. Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines.. There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies.. Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease and the mechanisms generating metabolic acidemia. Other promising treatment alternatives have been proposed; however, the side effects and absence of controlled studies with pediatric populations translate into lack of evidence to support the routine use of such treatments.

Topics: Acidosis; Acidosis, Lactic; Cardiopulmonary Resuscitation; Child; Diabetic Ketoacidosis; Humans; Randomized Controlled Trials as Topic; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Anti-Bacterial Agents; Confusion; Diet, Carbohydrate-Restricted; Female; Fluid Therapy; Gait Ataxia; Humans; Memory, Short-Term; Mental Processes; Middle Aged; Risk Factors; Short Bowel Syndrome; Sodium Bicarbonate

Topics: Acidosis, Lactic; Contraindications; Diabetic Ketoacidosis; Humans; Hypoglycemic Agents; Insulin; Lactic Acid; Phenformin; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Blood Gas Analysis; Consciousness Disorders; Diabetes Complications; Diagnosis, Differential; Glucose; Humans; Hypoglycemic Agents; Insulin; Lactic Acid; Metformin; Pyruvic Acid; Sodium Bicarbonate

Topics: Acidosis, Lactic; Acute Disease; Diabetes Complications; Dichloroacetic Acid; Glucose; Humans; Insulin; Peritoneal Dialysis; Sodium Bicarbonate

Despite the lack of evidence for its effectiveness in the treatment of acid-base disturbances in critically ill patients of all ages, and despite several lines of evidence that indicate it might be dangerous, bicarbonate therapy is used routinely in many neonatal intensive care units. The justification for the persistent use of this controversial therapy comes from a variety of sources, many based more in philosophy than in science. Clinicians contemplating the use of bicarbonate therapy should consider what they expect the intervention to accomplish and what evidence exists that their therapeutic objective will be met. Without rigorous scientific support for this therapy, it should be considered of unproven value and, therefore, experimental.

Topics: Acidosis, Lactic; Acidosis, Respiratory; Acute Disease; Cardiopulmonary Resuscitation; Clinical Competence; Evidence-Based Medicine; Humans; Infant, Newborn; Intensive Care Units, Neonatal; Respiratory Distress Syndrome, Newborn; Sodium Bicarbonate

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.

Topics: Acidosis, Lactic; Animals; Humans; Hydrogen-Ion Concentration; Infusions, Intravenous; Sodium Bicarbonate; Treatment Outcome

Topics: Acidosis, Lactic; Diabetic Ketoacidosis; Diagnosis, Differential; Humans; Hyperglycemic Hyperosmolar Nonketotic Coma; Insulin; Potassium; Prognosis; Sodium Bicarbonate; Sodium Chloride

Metabolic acidosis occurs frequently in small children. The most common causes are hypoxia, sepsis, gastroenteritis and hypovolaemia. Calculation of the anion gap is useful in establishing the cause. An increased anion gap represents unmeasured anions, e.g. lactate in lactic acidosis. Metabolic acidosis was diagnosed in two boys aged one year and six weeks respectively. The first patient had a normal, the second an increased anion gap in blood. By determining the pH and the anion gap in urine it is possible to distinguish between a proximal and a distal tubular disease. The first patient had distal renal tubular acidosis; he recovered after correction of the acidosis. The second patient had a defect in the mitochondrial respiratory chain; he died at the age of seven months.

Topics: Acid-Base Imbalance; Acidosis, Lactic; Acidosis, Renal Tubular; Diagnosis, Differential; Fatal Outcome; Humans; Infant; Male; Mitochondrial Myopathies; Osteomalacia; Sodium Bicarbonate

Lactate can be viewed as a metabolic dead end in that it can only be produced or utilized via pyruvate. Lactate production is determined primarily by pyruvate concentration and to a lesser extend by the redox state. Increased lactate production may result from tissue hypoxia, alkalosis, catecholamine and alanine transamination to pyruvate. Hyperlactatemia is observed in many pathological conditions. Current diagnostic criteria for lactic acidosis are a pH less than 7.35 and lactate concentration greater than 5 to 6 mmol/l. In our study series, malignancy was the most common underlying disease accompanied by lactic acidosis. Organ failure, cardiovascular disease and diabetes mellitus were also common. The prognosis of patients with these diseases were grave. In cases of lactic acidosis associated with diabetes mellitus, alcoholic liver disease, rhabdomyolysis and diabetic comas were noticeable as complications. Alcohol abuse was the most common cause of lactic acidosis associated with diabetes mellitus. In these cases, laboratory data showed prominent hyperlactatemia, hyperglycemia and acidemia and elevated anion gap. The mortality rate in these cases was 36% and higher in cases with organ failure. Treatment of lactic acidosis consists of alkalization by sodium bicarbonate with carbicarb, insulin-glucose-infusion, dichloroacetate therapy, tham administration, bicarbonate-buffered peritoneal dialysis and high bicarbonate-containing dialysis.

Topics: Acidosis, Lactic; Alcoholism; Cardiovascular Diseases; Diabetes Complications; Dichloroacetic Acid; Female; Humans; Insulin; Lactates; Male; Neoplasms; Sodium Bicarbonate; Tromethamine

Topics: Acidosis; Acidosis, Lactic; Acidosis, Respiratory; Animals; Dogs; Guidelines as Topic; Humans; Hyperkalemia; India; Infant, Newborn; Sodium Bicarbonate; Tromethamine

The metabolic acidosis resulting from poor tissue perfusion is considered to have several significant hemodynamic effects. Correction of the acidosis with sodium bicarbonate seems to be a rational approach to this problem. However, the current medical literature shows little clinical benefit to this tactic. In fact, indiscriminate bicarbonate administration may, itself, have deleterious effects. Concurring with the absence of a consistent therapeutic advantage to the use of sodium bicarbonate in the treatment of lactic acidosis due to inadequate tissue perfusion, the American Heart Association removed the routine use of sodium bicarbonate from the treatment of cardiac arrest in the algorithms of the Advanced Cardiac Life Support course. Although the debate continues, a detailed review of the medical literature does not support the use of sodium bicarbonate in this setting.

Topics: Acidosis, Lactic; Heart Arrest; Hemodynamics; Humans; Respiratory Transport; Sodium Bicarbonate

Topics: Acidosis, Lactic; Adenosine Triphosphate; Brain; Cardiac Output, Low; Humans; Hydrogen-Ion Concentration; Sodium Bicarbonate

To document a case of severe metabolic and lactic acidosis secondary to phenformin. This adverse effect has almost been forgotten as 15 years have passed since its withdrawal from the US market.. A 64-year-old man presented with a four-day history of left upper abdominal pain and a one-week history of constipation and diarrhea. His arterial blood gases were pH 6.7, pCO2 2.80 kPa, and pO2 12.00 kPa with 90% oxygen saturation on room air. Serum chemistries indicated an unmeasurable serum bicarbonate concentration, anion gap 52 mmol/L, lactate concentration 29.5 mmol/L, blood urea nitrogen 6.63 mmol/L, creatinine 229.84 mumol/L, and blood glucose 4.35 mmol/L. There were low levels of urine and serum ketones. In the emergency department, he required resuscitation for hypotension and bradycardia. His diagnosis was lactic and ketoacidosis secondary to phenformin. The patient was treated with NaCl 0.9%, sodium bicarbonate, insulin, and hemodialysis. Although he survived the initial insult of lactic and ketoacidosis, his hospital course was complicated and he died on hospital day 105.. Treatment of lactic acidosis is difficult and challenging. The continued availability of phenformin in neighboring countries, and the renewed interest in biguanide therapy for treating diabetes mellitus make it an important diagnosis of exclusion in diabetic patients who present with severe acidosis. Metformin, another biguanide under investigation for the treatment of diabetes mellitus, is associated with a much lower incidence of lactic acidosis than is phenformin.

Topics: Acidosis, Lactic; Diabetes Mellitus; Dichloroacetic Acid; Drug and Narcotic Control; Humans; Insulin; Male; Middle Aged; Phenformin; Renal Dialysis; Sodium Bicarbonate; Sodium Chloride

Bicarbonate administration during lactic acidosis seems logical in view of the myocardial depression associated with the decrease in intracellular pH. This treatment has been recently challenged on the basis of observations showing an increase in the veno-arterial gradient for CO2 during acute circulatory failure. The partial transformation of bicarbonate in CO2 carries the risk of aggravating the phenomenon and thereby decreasing intracellular pH. Alternatives to sodium bicarbonate--carbicarb, THAM and dichloroacetate--are discussed.

Topics: Acidosis, Lactic; Bicarbonates; Carbon Dioxide; Carbonates; Dichloroacetic Acid; Drug Combinations; Humans; Hydrogen-Ion Concentration; Sodium Bicarbonate; Tromethamine

Topics: Acidosis, Lactic; Bicarbonates; Clinical Protocols; Evaluation Studies as Topic; Heart Arrest; Humans; Infant, Newborn; Neonatology; Osmolar Concentration; Resuscitation; Sodium; Sodium Bicarbonate

Methanol intoxication can be a challenge, in part because it is relatively uncommon but also because of the pharmacokinetics involved. A patient may not experience symptoms and thus may not present for treatment for several hours, or even a day or two, after exposure to the toxic substance. Yet, the interval between ingestion and treatment is one of the most important factors in determining patient outcome. Typical symptoms of methanol intoxication include lethargy, vertigo, vomiting, blurred vision, and decreased visual acuity. Treatment focuses on prevention of methanol conversion to its toxic metabolites, correction of metabolic acidosis, and elimination of the toxic substances from the system. Ethanol and bicarbonate administration and hemodialysis have been effective.

Topics: Acidosis, Lactic; Bicarbonates; Ethanol; Humans; Metabolic Clearance Rate; Methanol; Poisoning; Prognosis; Renal Dialysis; Sodium; Sodium Bicarbonate

This article reviews the current body of knowledge regarding lactic acidosis in critically ill patients. The classification of disordered lactate metabolism and its pathogenesis are examined. The utility of lactate as a metabolic monitor of shock is examined and current therapeutic strategies in the treatment of patients suffering from lactic acidosis are extensively reviewed. The paper is designed to integrate basic concepts with a current approach to lactate in critical illness that the clinician can use at the bedside.. Comprehensive review of the available, basic science, medical, surgical, and critical care literature.. The severity of lactic acidosis in critically ill patients correlates with overall oxygen debt and survival. Lactate determinations may be useful as an ongoing monitor of perfusion as resuscitation proceeds. Therapy of critically ill patients with lactic acidosis is designed to maximize oxygen delivery in order to reduce tissue hypoxia by increasing cardiac index, while maintaining hemoglobin concentration. Buffering agents have not been shown to materially affect outcome from lactic acidosis caused by shock. The benefits of other specific therapies designed to reduce the severity of lactic acidosis remain unproven.

Topics: Acidosis, Lactic; Bicarbonates; Blood Gas Analysis; Carbonates; Citric Acid Cycle; Critical Illness; Drug Combinations; Fluid Therapy; Glycolysis; Hemodynamics; Humans; Lactates; Lactic Acid; Metabolic Clearance Rate; Monitoring, Physiologic; Oxygen Consumption; Predictive Value of Tests; Severity of Illness Index; Shock; Sodium; Sodium Bicarbonate; Survival Rate

Topics: Acidosis; Acidosis, Lactic; Alkalies; Animals; Bicarbonates; Carbonates; Diabetic Ketoacidosis; Dichloroacetic Acid; Dogs; Drug Combinations; Humans; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Acute Disease; Animals; Bicarbonates; Carbon Dioxide; Cardiac Output, Low; Humans; Hypoxia; Resuscitation; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Bicarbonates; Diabetes Complications; Diabetes Mellitus; Humans; Metformin; Renal Dialysis; Sodium; Sodium Bicarbonate

The rare congenital lactic acidosis is a consequence of enzyme defects. The acquired form is relatively common in critically ill patients. The altered metabolism of pyruvate and the imbalance between lactate production and utilization have a central role in the pathogenesis of this disease. The physiologic compensating mechanisms are generally not sufficient for complete correction of acidosis. In most of the cases the basic disease is the one that should be treated. The correction of the acidosis must be careful, because overtreatment may worsen acidosis, or may cause severe post-treatment alkalosis.

Topics: Acidosis, Lactic; Alkalosis; Bicarbonates; Dose-Response Relationship, Drug; Humans; Insulin; Nitroprusside; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Bicarbonates; Biguanides; Humans; Sodium; Sodium Bicarbonate

Initial lactate level, lactate clearance, C-reactive protein, and procalcitonin in critically ill patients with sepsis are associated with hospital mortality. However, no study has yet discovered which factor is most important for mortality in severe sepsis patients with lactic acidosis. We sought to clarify this issue in patients with lactic acidosis who were supplementing with sodium bicarbonate.. Data were collected from a single center between May 2011 and April 2014. One hundred nine patients with severe sepsis and lactic acidosis who were supplementing with sodium bicarbonate were included.. The 7-day mortality rate was 71.6%. The survivors had higher albumin levels and lower SOFA, APACHE II scores, vasopressor use, and follow-up lactate levels at an elapsed time after their initial lactate levels were checked. In particular, a decrement in lactate clearance of at least 10% for the first 6 hours, 24 hours, and 48 hours of treatment was more dominant among survivors than non-survivors. Although the patients who were treated with broad-spectrum antibiotics showed higher illness severity than those who received conventional antibiotics, there was no significant mortality difference. 6-hour, 24-hour, and 48-hour lactate clearance (HR: 4.000, 95% CI: 1.309-12.219, P = 0.015) and vasopressor use (HR: 4.156, 95% CI: 1.461-11.824, P = 0.008) were significantly associated with mortality after adjusting for confounding variables.. Lactate clearance at a discrete time point seems to be a more reliable prognostic index than initial lactate value in severe sepsis patients with lactic acidosis who were supplementing with sodium bicarbonate. Careful consideration of vasopressor use and the initial application of broad-spectrum antibiotics within the first 48 hours may be helpful for improving survival, and further study is warranted.

Topics: Acidosis, Lactic; Aged; C-Reactive Protein; Female; Hospital Mortality; Humans; Lactic Acid; Male; Middle Aged; Retrospective Studies; Sepsis; Sodium Bicarbonate

To explore the use of sodium bicarbonate in stages in treating hypoperfusion induced lactic acidemia due to septic shock.. In this prospective randomized, double-blind, controlled clinical trial, a total of 65 patients of hypoperfusion induced lactic acidemia due to septic shock admitted between April 2006 and April 2010 were assigned to two groups. Thirty-five patients of "stage" group sodium bicarbonate was used in two stages: in first stage sodium bicarbonate was given by venous drip until pH≥7.15, and in second stage sodium bicarbonate was given by intravenous drip till pH≥7.25 after 6 hours. Thirty patients in control group intravenous drip of sodium bicarbonate was used till pH≥7.15. Early goal-directed therapy(EGDT) was used in the first 6 hours of fluid resuscitation. The number of dysfunction organ, time of mechanical ventilation, maximum sequential organ failure assessment (SOFA) score, delta SOFA score, durations of stay in intensive care unit (ICU) and in hospital, and mortality were recorded in two groups. Blood gas analysis and index of hemodynamics were monitored at 0 hour and 8 hours in both groups.. Compared with control group, "stage" group was associated with a lower number of dysfunction organ, time of mechanical ventilation, maximum SOFA score, delta SOFA score, durations of stay in ICU and in hospital, and mortality (number of dysfunction organ: 2.68±0.79 vs. 3.28±0.80, time of mechanical ventilation: 10.32±2.26 days vs. 13.80±2.56 days, maximum SOFA score: 11.01±2.26 vs. 13.11±2.26, delta SOFA score: 1.71±1.25 vs. 3.43±1.27, duration of stay in ICU: 14.0±3.6 days vs. 20.0±3.7 days, duration of stay in hospital: 28.3±12.9 days vs. 41.9±13.2 days, mortality: 34.28% vs. 60.00%, P<0.05 or P<0.01). There were no significant differences in blood gas analysis and index of hemodynamics at 0 hour, and they were improved at 8 hours. Compared with control group, in "stage" group, lactic acid (Lac) was significantly lowered (1.50±1.08 mmol/L vs. 2.93±1.09 mmol/L), and pH, mixed venous oxygen saturation (SvO2), oxygen extraction ratio (O2ER), cardiac index (CI), oxygen delivery (DO2) were significantly increased (pH:7.29±0.05 vs. 7.20±0.05, SvO2: 0.75±0.18 vs. 0.66±0.17, O2ER: 0.32±0.06 vs. 0.25±0.06, CI: 113.36±13.34 ml×s(-1)×m(-2) vs. 83.35±13.34 ml×s(-1)×m(-2), DO2: 840±170 ml×min(-1)×m(-2) vs. 630±171 ml×min(-1)×m(-2), all P<0.01).. The use of sodium bicarbonate in stages in treating hypoperfusion induced lactic acidemia as a result of septic shock can lower the occurrence rate of multiple organ dysfunction syndrome, time of mechanical ventilation, durations of stay in ICU and in hospital, and mortality.

Topics: Acidosis, Lactic; Adult; Aged; Double-Blind Method; Female; Humans; Male; Middle Aged; Multiple Organ Failure; Prospective Studies; Shock, Septic; Sodium Bicarbonate

To determine concentrations of electrolytes, total bilirubin, urea, creatinine, and hemoglobin; activities of some enzymes; and Hct and number of leukocytes and erythrocytes of newborn calves in relation to the degree of acidosis and treatment with a hypertonic sodium bicarbonate (NaHCO(3)) solution.. 20 acidotic newborn calves with a blood pH < 7.2 and 22 newborn control calves with a blood pH > or = 7.2.. Approximately 10 minutes after birth, acidotic calves were treated by IV administration of 5% NaHCO(3) solution. The amount of hypertonic solution infused was dependent on the severity of the acidosis.. Treatment resulted in a significant increase in the mean +/- SEM base excess from -8.4 +/- 1.2 mmol/L immediately after birth to 0.3 +/- 1.1 mmol/L 120 minutes later. During the same period, sodium concentration significantly increased from 145.3 +/- 0.8 mmol/L to 147.8 +/- 0.7 mmol/L. Mean chloride concentration before NaHCO(3) administration was significantly lower in the acidotic calves (99.6 +/- 1.1 mmol/L) than in the control calves (104.1 +/- 0.9 mmol/L). Calcium concentration in acidotic calves decreased significantly from before to after treatment. Concentrations of potassium, magnesium, and inorganic phosphorus were not affected by treatment.. Administration of hypertonic NaHCO(3) solution to acidotic neonatal calves did not have any adverse effects on plasma concentrations of several commonly measured electrolytes or enzyme activities. The treatment volume used was smaller, compared with that for an isotonic solution, which makes it more practical for use in field settings.

Topics: Acidosis, Lactic; Acidosis, Respiratory; Animals; Animals, Newborn; Cattle; Cattle Diseases; Electrolytes; Female; Male; Osmolar Concentration; Sodium Bicarbonate; Time Factors

Sodium bicarbonate (NaHCO3) ingestion may prevent exercise-induced perturbations in acid-base balance, thus resulting in performance enhancement. This study aimed to determine whether different levels of NaHCO3 intake influences acid-base balance and performance during high-intensity exercise after 5 d of supplementation.. Twenty-four men (22 +/- 1.7 yr) were randomly assigned to one of three groups (eight subjects per group): control (C, placebo), moderate NaHCO3 intake (MI, 0.3 g x kg(-1) x d(-1)), and high NaHCO3 intake (HI, 0.5 g x kg(-1) x d(-1)). Arterial pH, HCO3(-), PO2, PCO2, K+, Na, base excess (BE), lactate, and mean power (MP) were measured before and after a Wingate test pre- and postsupplementation.. HCO3(-) increased proportionately to the dosage level. No differences were detected in C. Supplementation increased MP (W x kg(-)) in MI (7.36 +/- 0.7 vs 6.73 +/- 1.0) and HI (7.72 +/- 0.9 vs 6.69 +/- 0.6), with HI being more effective than MI. NaHCO3 ingestion resulted postexercise in increased lactate (mmol x L(-1)) (12.3 +/- 1.8 vs 10.3 +/- 1.9 and 12.4 +/- 1.2 vs 10.4 +/- 1.5 in MI and HI, respectively), reduced exercise-induced drop of pH (7.305 +/- 0.04 vs 7.198 +/- 0.02 and 7.343 +/- 0.05 vs 7.2 +/- 0.01 in MI and HI, respectively) and HCO3(-) (mmol x L(-1)) (13.1 +/- 2.4 vs 17.5 +/- 2.8 and 13.2 +/- 2.7 vs 19.8 +/- 3.2 for HCO3 in MI and HI, respectively), and reduced K (3.875 +/- 0.2 vs 3.625 +/- 0.3 mmol x L(-1) in MI and HI, respectively).. NaHCO3 administration for 5 d may prevent acid-base balance disturbances and improve performance during anaerobic exercise in a dose-dependent manner.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Adult; Alkalosis; Dietary Supplements; Exercise; Humans; Male; Oxygen Consumption; Sodium Bicarbonate; Surveys and Questionnaires; Time Factors

During heavy-intensity exercise, the mechanisms responsible for the continued slow decline in phosphocreatine concentration ([PCr]) (PCr slow component) have not been established. In this study, we tested the hypothesis that a reduced intracellular acidosis would result in a greater oxidative flux and, consequently, a reduced magnitude of the PCr slow component. Subjects (n = 10) performed isotonic wrist flexion in a control trial and in an induced alkalosis (Alk) trial (0.3g/kg oral dose of NaHCO3, 90 min before testing). Wrist flexion, at a contraction rate of 0.5 Hz, was performed for 9 min at moderate- (75% of onset of acidosis; intracellular pH threshold) and heavy-intensity (125% intracellular pH threshold) exercise. 31P-magnetic resonance spectroscopy was used to measure intracellular [H+], [PCr], [Pi], and [ATP]. The initial recovery data were used to estimate the rate of ATP synthesis and oxidative flux at the end of heavy-intensity exercise. In repeated trials, venous blood sampling was used to measure plasma [H+], [HCO3-], and [Lac-]. Throughout rest and exercise, plasma [H+] was lower (P < 0.05) and [HCO3-] was elevated (P < 0.05) in Alk compared with control. During the final 3 min of heavy-intensity exercise, Alk caused a lower (P < 0.05) intracellular [H+] [246 (SD 117) vs. 291 nmol/l (SD 129)], a greater (P < 0.05) [PCr] [12.7 (SD 7.0) vs. 9.9 mmol/l (SD 6.0)], and a reduced accumulation of [ADP] [0.065 (SD 0.031) vs. 0.098 mmol/l (SD 0.059)]. Oxidative flux was similar (P > 0.05) in the conditions at the end of heavy-intensity exercise. In conclusion, our results are consistent with a reduced intracellular acidosis, causing a decrease in the magnitude of the PCr slow component. The decreased PCr slow component in Alk did not appear to be due to an elevated oxidative flux.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Adenosine Diphosphate; Adenosine Triphosphate; Adult; Alkalosis; Exercise; Forearm; Humans; Lactic Acid; Male; Muscle, Skeletal; Oxidative Phosphorylation; Phosphocreatine; Protons; Sodium Bicarbonate

Marked lactic acidosis occurs during orthotopic liver transplantation (OLT), especially during the anhepatic phase. Current standard therapy is NaHCO3, although it may exacerbate intracellular acidosis, increase plasma lactate, and contribute to hypernatremia. Alternatively, dichloroacetate (DCA) stimulates pyruvate oxidation in vivo, reduces plasma lactate, and moderates intracellular acidosis. The aims of this study were to test the efficacy of DCA to control lactic acidosis, reduce the NaHCO3 requirement and incidence of hypernatremia, and stabilize perioperative acid-base homeostasis. Others aims were to examine the DCA pharmacokinetic profile during OLT and the role of lactate metabolism in OLT-associated hyperglycemia.. Patients (n = 66) for OLT were divided into two equal groups to receive or not receive DCA during OLT. DCA 40 mg.kg-1 was infused over 60 min after induction of anesthesia and 4 h later. Plasma DCA concentration was measured by gas chromatography-mass spectroscopy, and pharmacokinetics were assessed by a one-compartment model. Serial arterial blood gases, lactate, Na+, glucose, and hemodynamic measurements were compared, as were intraoperative utilization of blood products, CaCl2, and NaHCO3.. Plasma DCA concentration was maintained between 0.28 and 1.18 mM during OLT, with peak concentrations of 0.73 +/- 0.06 (mean +/- SE) and 1.18 +/- 0.09 mM, respectively after the first and second doses. In control patients, plasma lactate was 1.07 +/- 0.04 at baseline and 1.20 +/- 0.06 before incision and reached a peak of 7.30 +/- 0.41 mM after graft reperfusion. In DCA-treated patients, the respective values were 1.07 +/- 0.06 (difference not significant), 0.63 +/- 0.05 (P < 0.001), and 3.39 +/- 0.20 (P < 0.001) mM. Intraoperative changes in arterial blood pH, HCO3(-1), and base excess were comparable though less marked in DCA-treated patients, whose NaHCO3 requirement was reduced (0.59 +/- 0.36 vs. 2.83 +/- 0.53 mEq.kg-1 in control patients, P < 0.001). There was no difference between groups in requirements for CaCl2 or blood products, in intraoperative hemodynamics, in duration of the surgical stages, or in graft ischemia times. Twelve control and 4 DCA-treated patients exhibited a plasma Na+ concentration > 145 mEq/1 at completion of surgery (P < 0.05). Hyperglycemia was not attenuated by DCA despite decreased plasma lactate concentration. Sixteen and 28 h after graft reperfusion, when plasma DCA had been eliminated, plasma lactate and degree of metabolic alkalosis did not differ between groups.. DCA safely and effectively attenuated lactic acid accumulation and moderated acidosis during OLT. DCA decreased the requirement for NaHCO3 therapy and the incidence of hypernatremia. OLT-associated hyperglycemia did not result from lactate-induced stimulation of hepatic gluconeogenesis. Postoperative metabolic alkalosis was not substantially influenced by lactate metabolism.

Topics: Acidosis, Lactic; Adult; Blood Glucose; Dichloroacetic Acid; Female; Humans; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Liver Transplantation; Male; Middle Aged; Sodium Bicarbonate

Recent recommendations suggest that sodium bicarbonate may not be useful for the treatment of metabolic acidosis. However, these recommendations are based primarily on both clinical studies and animal models of metabolic acidosis with arterial hypoxemia (PaO2 of < 80 torr [< 10.7 kPa]). This study was designed to determine the safety and physiologic effects of low-dose sodium bicarbonate in humans who developed intraoperative metabolic acidosis in the absence of hypoxemia.. Prospective, double-blind, randomized trial.. Veterans Affairs Medical Center (a teaching hospital of the University of California, San Francisco).. We prospectively studied 40 patients with coronary artery disease who underwent major surgery and developed mild intraoperative metabolic acidosis (decrease of plasma bicarbonate by > 3 mM).. Patients were randomly assigned to receive either sodium bicarbonate (n = 20) or sodium chloride (n = 20) by intravenous bolus, up to a maximum dose of 88 mmol of sodium.. Bicarbonate treatment significantly increased the mean arterial pH from 7.36 to 7.39; the mean serum bicarbonate concentration from 21 to 25 mmol/L; and PCO2 from 41 to 44 torr (5.5 to 5.9 kPa). Total body oxygen consumption and lactate production did not change. Similarly, no adverse changes occurred in systemic or pulmonary arterial pressures or in cardiac ejection fraction. After bicarbonate administration, both the cardiac output and systemic oxygen consumption decreased by 8% to 11%, while both variables increased by 13% after sodium chloride administration; but, none of the changes was significant. One patient in the bicarbonate group developed myocardial ischemia, compared with three patients in the saline group.. Administration of sodium bicarbonate to well-oxygenated patients with mild metabolic acidosis resulted in a correction of the acidosis, without significant changes in cardiac output, total body oxygen use, or PaO2 (oxygen tension). These effects remain to be validated in patients with hypoxemia, more severe acidosis, or less stable circulation.

Topics: Acidosis, Lactic; Aged; Bicarbonates; Blood Gas Analysis; Blood Glucose; Calcium; Cardiac Output; Coronary Disease; Double-Blind Method; Drug Monitoring; Electrolytes; Humans; Injections, Intravenous; Intraoperative Complications; Lactates; Lactic Acid; Male; Middle Aged; Monitoring, Intraoperative; Myocardial Ischemia; Oxygen Consumption; Prospective Studies; Sodium; Sodium Bicarbonate; Stroke Volume

To analyze the cardiovascular effects of sodium bicarbonate in neonates with metabolic acidosis.. Prospective, open, non-randomized, before-after intervention study with hemodynamic measurements performed before and 1, 5, 10, 20, and 30 min after bicarbonate administration.. Neonatal intensive care unit, tertiary care center.. Sequential sample of 16 paralysed and mechanically ventilated newborn infants with a metabolic acidosis (pH < 7.25 in premature and < 7.30 in term infants, base deficit > -8).. An 8.4% sodium bicarbonate solution diluted 1:1 with water (final osmolality of 1000 mOsm/l) was administered in two equal portions at a rate of 0.5 mmol/min. The dose in mmol was calculated using the formula "base deficit x body weight (kg) x 1/3 x 1/2".. Sodium bicarbonate induced a significant but transient rise in pulsed Doppler cardiac output (CO) (+27.7%), aortic blood flow velocity (+15.3%), systolic blood pressure (BP) (+9.3%), (+14.6%), transcutaneous carbon dioxide pressure (PtcCO2) (+11.8%), and transcutaneous oxygen pressure (PtcO2) (+8%). In spite of the PaCO2 elevation, pH significantly improved (from a mean of 7.24 to 7.30), and the base deficit decreased (-39.3%). Calculated systemic vascular resistance (SVR) (-10.7%) and diastolic BP (-11.7%) decreased significantly, while PaO2 and heart rate (HR) did not change. Central venous pressure (CVP) (+6.5%) increased only slightly. By 30 min after bicarbonate administration all hemodynamic parameters, with the exception of the diastolic BP, had returned to baseline.. Sodium bicarbonate in neonates with metabolic acidosis induces an increase in contractility and a reduction in afterload.

Topics: Acidosis, Lactic; Bicarbonates; Birth Weight; Blood Gas Analysis; Blood Gas Monitoring, Transcutaneous; Critical Illness; Echocardiography, Doppler; Gestational Age; Hemodynamics; Humans; Infant, Newborn; Infant, Premature; Infusions, Intravenous; Intensive Care Units, Neonatal; Myocardial Contraction; Prospective Studies; Respiration, Artificial; Sodium; Sodium Bicarbonate

Carbicarb, sodium bicarbonate, and 5% dextrose were compared for effects on resuscitability in a canine model of electromechanical dissociation after ventricular fibrillation.. 21 healthy mongrel dogs were anesthetized with pentobarbital, intubated, and mechanically supported. They were instrumented to measure heart rate, arterial pressure, pulmonary artery pressure, right atrial pressure, cardiac output, and arterial and mixed venous blood gases. The dogs were then subjected to a protocol that consisted of three successive CPR episodes. During each episode they were treated with repeated injections of one of the three substances, randomly chosen. After two minutes of ventricular fibrillation and four minutes of electromechanical dissociation, CPR was started with a thumper (rate, 60; duty cycle, 50%). If recovery was not obtained after five minutes of CPR, 1 mEq/kg carbicarb or sodium bicarbonate or 5 mL D5W was injected in the right atrium. Half the dose of the same substance was injected every five minutes thereafter; 1 mg epinephrine was also injected every five minutes until recovery. Hemodynamic and gasometric evaluations were performed five and 20 minutes after recovery. This later evaluation served as baseline for the next CPR episode.. The duration and success rates of CPR are similar in the three CPR groups. Hemodynamic parameters were also similar during recovery. Bicarbicarb and sodium bicarbonate increased bicarbonate levels and corrected pH in the arterial and mixed venous blood. There was no difference in the blood gas values after carbicarb and sodium bicarbonate.. In this model of cardiac arrest, carbicarb was not superior to sodium bicarbonate in the correction of metabolic acidosis during CPR.

Topics: Acidosis, Lactic; Animals; Bicarbonates; Blood Gas Analysis; Carbonates; Clinical Protocols; Disease Models, Animal; Dogs; Drug Combinations; Glucose; Heart Arrest; Hemodynamics; Resuscitation; Sodium; Sodium Bicarbonate

To determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis.. Prospective, randomized, blinded, crossover study. Each patient sequentially received sodium bicarbonate and equimolar sodium chloride. The order of the infusions was randomized.. Intensive care unit of a tertiary care hospital.. Fourteen patients who had metabolic acidosis (bicarbonate less than 17 mmol/L and base excess less than -10) and increased arterial lactate (mean, 7.8 mmol/L). All had pulmonary artery catheters and 13 were receiving catecholamines.. Sodium bicarbonate (2 mmol/kg body weight over 15 minutes) increased arterial pH (7.22 to 7.36, P less than 0.001), serum bicarbonate (12 to 18 mmol/L, P less than 0.001), and partial pressure of CO2 in arterial blood (PaCO2) (35 to 40 mm Hg, P less than 0.001) and decreased plasma ionized calcium (0.95 to 0.87 mmol/L, P less than 0.001). Sodium bicarbonate and sodium chloride both transiently increased pulmonary capillary wedge pressure (15 to 17 mm Hg, and 14 to 17 mm Hg, P less than 0.001) and cardiac output (18% and 16%, P less than 0.01). The mean arterial pressure was unchanged. Hemodynamic responses to sodium bicarbonate and sodium chloride were the same. These data have more than 90% power of detecting a 0.5 L/min (7%) change in mean cardiac output after administration of sodium bicarbonate compared with that after sodium chloride. Even the 7 most acidemic patients (mean pH, 7.13; range, 6.90 to 7.20) had no significant hemodynamic changes after either infusion.. Correction of acidemia using sodium bicarbonate does not improve hemodynamics in critically ill patients who have metabolic acidosis and increased blood lactate or the cardiovascular response to infused catecholamines in these patients. Sodium bicarbonate decreases plasma ionized calcium and increases PaCO2.

Topics: Acidosis, Lactic; Adult; Aged; Aged, 80 and over; Bicarbonates; Calcium; Carbon Dioxide; Data Interpretation, Statistical; Double-Blind Method; Female; Hemodynamics; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Prospective Studies; Randomized Controlled Trials as Topic; Sodium; Sodium Bicarbonate

A 47-year-old female patient presented nausea and vomiting for half a year and elevated serum creatinine for 3 days. Proximal renal tubular acidosis (RTA) complicated with anemiawas confirmed after admission. Secondary factors, such as autoimmune disease, drugs, poison, monoclonal gammopathy, were excluded. Renal biopsy revealed acute interstitial nephritis. The patient was administrated with daily prednisone 50 mg, sodium bicarbonate 4 g, 3 times per day, erythropoietin 3 000 U, 2 times per week, combined with potassium, calcium, and calcitriol tablets. Serum creatinine reduced to 90 μmol/L. However nausea and vomiting deteriorated with lactic acidosis. Bone marrow biopsy indicated the diagnosis of non-Hodgkin lymphoma, therefore the patient was treated with chemotherapy. Although metabolic acidosis improved gradually after chemotherapy, severe pneumocystis carinii pneumonia developed two weeks later. The patient refused further treatment and was discharged.. 患者女性，47岁。因恶心、呕吐半年，发现肾功能异常（血肌酐255 μmol/L）3 d就诊，入院检查发现近端肾小管酸中毒合并贫血，排除自身免疫病、药物、毒物、单克隆免疫球蛋白病等继发因素，肾脏穿刺活检组织病理提示急性间质性肾炎，予泼尼松50 mg/d；碳酸氢钠4 g，3次/d；促红细胞生成素3 000 U，2次/周；氯化钾缓释片500 mg，3次/d；碳酸钙500 mg，3次/d；骨化三醇0.5 μg，1次/d。患者血肌酐恢复至90 μmol/L，但随诊期间患者恶心呕吐加重，再次检查发现合并乳酸酸中毒（乳酸14.1 mmol/L）。骨髓穿刺提示非霍奇金淋巴瘤，予CHOP方案化疗，期间乳酸酸中毒逐步好转（乳酸由14.5 mmol/L降至3.1 mmol/L），半个月后发生重症耶氏肺孢子菌肺炎，最终放弃治疗出院。.

Topics: Acidosis, Lactic; Acidosis, Renal Tubular; Anemia; Antineoplastic Agents; Biopsy; Creatinine; Erythropoietin; Female; Humans; Lymphoma, Non-Hodgkin; Middle Aged; Nausea; Pneumonia, Pneumocystis; Prednisone; Renal Insufficiency; Sodium Bicarbonate; Treatment Refusal; Vomiting

Topics: Acidosis, Lactic; Acute Kidney Injury; Aged; Alanine; Continuous Renal Replacement Therapy; Diabetes Mellitus, Type 2; Female; Heart Failure; HIV Infections; Humans; Oliguria; Reverse Transcriptase Inhibitors; Sodium Bicarbonate; Tenofovir

Lactic acidosis occurs commonly and can be a marker of significant physiologic derangements. However what an elevated lactate level and acidemia connotes and what should be done about it is subject to inconsistent interpretations. This review examines the varied etiologies of lactic acidosis, the physiologic consequences, and the known effects of its treatment with sodium bicarbonate. Lactic acidosis is often assumed to be a marker of hypoperfusion, but it can also result from medications, organ dysfunction, and sepsis even in the absence of malperfusion. Acidemia causes deleterious effects in almost every organ system, but it can also have positive effects, increasing localized blood flow and oxygen delivery, as well as providing protection against hypoxic cellular injury. The use of sodium bicarbonate to correct severe acidemia may be tempting to clinicians, but previous studies have failed to show improved patient outcomes following bicarbonate administration. Bicarbonate use is known to decrease vasomotor tone, decrease myocardial contractility, and induce intracellular acidosis. This suggests that mild to moderate acidemia does not require correction. Most recently, a randomized control trial found a survival benefit in a subgroup of critically ill patients with serum pH levels <7.2 with concomitant acute kidney injury. There is no known benefit of correcting serum pH levels ≥ 7.2, and sparse evidence supports bicarbonate use <7.2. If administered, bicarbonate is best given as a slow IV infusion in the setting of adequate ventilation and calcium replacement to mitigate its untoward effects.

Topics: Acidosis, Lactic; Humans; Sodium Bicarbonate

Short bowel syndrome (SBS) is a condition when a person's gastrointestinal function is insufficient to supply the body with essential nutrients and hydration. Patients with SBS suffer from diarrhoea and symptoms of malabsorption such as weight loss, electrolyte disturbances and vitamin deficiencies. Long-term management of this condition can be complicated by the underlying disease, the abnormal bowel function and issues related to treatment like administration of parenteral nutrition and the use of a central venous catheter. Here, we describe a case of D-lactic acid acidosis, a rarer complication of SBS, presenting with generalised weakness and severe metabolic acidosis.

Topics: Acidosis, Lactic; Aged; Anti-Infective Agents; C-Reactive Protein; Humans; Lactic Acid; Male; Parenteral Nutrition, Home; Rifamycins; Rifaximin; Short Bowel Syndrome; Sodium Bicarbonate

Metformin is an antidiabetic drug; used to treat type II diabetes mellitus, metformin associated lactic acidosis has an incidence of 2-9 cases / 100,000 patients / year with high mortality (30%). We have had the case of a 75-year-old woman with metabolic acidosis as a result of metformin assumption, treated by renal replacement therapy (CRRT) with continuous veno-venous hemodiafiltration (CVVHDF).. after a short treatment period there was a reduction in Lactates (from 16.8 mmol/L to 12.6 mmol/L) and a progressive improvement of acidosis. In 72 hours the recovery of diuresis and subsequent suspension of CRRT was achieved.. CRRT, in addition to ensuring support for renal failure and volume correction, allowed a rapid recovery from metformin-associated lactic acidosis.

Topics: Acidosis, Lactic; Aged; Anticoagulants; Bronchial Spasm; Combined Modality Therapy; Female; Furosemide; Hemodiafiltration; Humans; Hypoglycemic Agents; Hypotension; Metformin; Piperacillin, Tazobactam Drug Combination; Sodium Bicarbonate; Sodium Citrate

The purpose was to determine prognosis of patients presenting extreme acidosis (pH <7) on admission to the intensive care unit (ICU) and to identify mortality risk factors.. We retrospectively analyzed all patients who presented with extreme acidosis within 24 hours of admission to a polyvalent ICU in a university hospital between January 2011 and July 2013. Multivariate analysis and survival analysis were used.. Among the 2156 patients admitted, 77 patients (3.6%) presented extreme acidosis. Thirty (39%) patients suffered cardiac arrest before admission. Although the mortality rate predicted by severity score was 93.6%, death occurred in 52 cases (67.5%) in a median delay of 13 (5-27) hours. Mortality rate depended on reason for admission, varying between 22% for cases linked to diabetes mellitus and 100% for cases of mesenteric infarction (P = .002), cardiac arrest before admission (P < .001), type of lactic acidosis (P = .007), high Simplified Acute Physiology Score II (P = .008), and low serum creatinine (P = .012).. Patients with extreme acidosis on admission to ICU have a less severe than expected prognosis. Whereas mortality is almost 100% in cases of cardiac arrest before admission, mortality is much lower in the absence of cardiac arrest before admission, which justifies aggressive ICU therapies.

Topics: Acidosis; Acidosis, Lactic; Acidosis, Respiratory; Adult; Aged; Diabetes Mellitus; Extracorporeal Membrane Oxygenation; Female; Heart Arrest; Hemorrhage; Hospital Mortality; Hospitalization; Hospitals, University; Humans; Hypoglycemic Agents; Infarction; Intensive Care Units; Male; Mesenteric Ischemia; Metformin; Middle Aged; Multivariate Analysis; Prognosis; Renal Dialysis; Respiration, Artificial; Retrospective Studies; Risk Factors; Severity of Illness Index; Sodium Bicarbonate; Survival Analysis; Vasoconstrictor Agents

Metformin-associated lactic acidosis (MALA) is one of the most important drug toxicities with a high morbidity and mortality rate. We report herein a case of suicide attempt with metformin presenting as MALA and acute renal failure on admission to emergency department and acute myocardial injury later on hospitalisation. An obvious improvement of metabolic parameters was seen in our patient provided by anti-ischaemic treatment together with bicarbonate infusion and haemodialysis. Although myocardial injury due to MALA is not a common disorder, we must be aware that metformin overdose with lack of tissue oxygenation, hypoperfusion, and arrhythmias may cause myocardial ischaemia.

Topics: Acidosis, Lactic; Acute Kidney Injury; Emergency Medical Services; Humans; Hypoglycemic Agents; Male; Metformin; Middle Aged; Myocardial Ischemia; Renal Dialysis; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome

Mortality rates associated with severe lactic acidosis (blood pH<7.2) due to sepsis or low-flow states are high. Eliminating the triggering conditions remains the most effective therapy. Although recommended by some, administration of sodium bicarbonate does not improve cardiovascular function or reduce mortality. This failure has been attributed to both reduction in serum calcium concentration and generation of excess carbon dioxide with intracellular acidification. In animal studies, hyperventilation and infusion of calcium during sodium bicarbonate administration improves cardiovascular function, suggesting that this approach could allow expression of the positive aspects of sodium bicarbonate. Other buffers, such as THAM or Carbicarb, or dialysis might also provide base with fewer untoward effects. Examination of these therapies in humans is warranted. The cellular injury associated with lactic acidosis is partly due to activation of NHE1, a cell-membrane Na(+)/H(+) exchanger. In animal studies, selective NHE1 inhibitors improve cardiovascular function, ameliorate lactic acidosis, and reduce mortality, supporting future research into their possible use in humans. Two main mechanisms contribute to lactic acid accumulation in sepsis and low-flow states: tissue hypoxia and epinephrine-induced stimulation of aerobic glycolysis. Targeting these mechanisms could allow for more specific therapy. This Acid-Base and Electrolyte Teaching Case presents a patient with acute lactic acidosis and describes current and future approaches to treatment.

Topics: Acidosis, Lactic; Drug Combinations; Forecasting; Humans; Male; Middle Aged; Sodium Bicarbonate

Lactic acidosis occurs when lactate production exceeds its metabolism. There are many possible causes of lactic acidosis, and in any given patient, several causes may coexist. This Attending Rounds presents a case in point. Metformin's role in the pathogenesis of lactic acidosis in patients with diabetes mellitus is complex, as the present case illustrates. The treatment of lactic acidosis is controversial, except for the imperative to remedy its underlying cause. The use of sodium bicarbonate to treat the often alarming metabolic derangements may be quite efficacious in that regard but is of questionable benefit to patients. Renal replacement therapies (RRTs) have particular appeal in this setting for a variety of reasons, but their effect on clinical outcomes is untested.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Biomarkers; Diabetes Mellitus, Type 2; Fatal Outcome; Humans; Hypoglycemic Agents; Male; Metformin; Middle Aged; Renal Dialysis; Sodium Bicarbonate; Treatment Outcome

Lactic acidosis is a very common biological issue for shock patients. Experimental data clearly demonstrate that metabolic acidosis, including lactic acidosis, participates in the reduction of cardiac contractility and in the vascular hyporesponsiveness to vasopressors through various mechanisms. However, the contributions of each mechanism responsible for these deleterious effects have not been fully determined and their respective consequences on organ failure are still poorly defined, particularly in humans. Despite some convincing experimental data, no clinical trial has established the level at which pH becomes deleterious for hemodynamics. Consequently, the essential treatment for lactic acidosis in shock patients is to correct the cause. It is unknown, however, whether symptomatic pH correction is beneficial in shock patients. The latest Surviving Sepsis Campaign guidelines recommend against the use of buffer therapy with pH ≥7.15 and issue no recommendation for pH levels <7.15. Furthermore, based on strong experimental and clinical evidence, sodium bicarbonate infusion alone is not recommended for restoring pH. Indeed, bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. This review addresses the principal hemodynamic consequences of shock-associated lactic acidosis. Despite the lack of formal evidence, this review also highlights the various adapted supportive therapy options that could be putatively added to causal treatment in attempting to reverse the hemodynamic consequences of shock-associated lactic acidosis.

Topics: Acidosis, Lactic; Carbon Dioxide; Hemodynamics; Hospital Mortality; Humans; Shock; Sodium Bicarbonate

Metformin-associated lactic acidosis or lacticemia has been widely reported as an adverse drug effect in diabetic patients with other significant comorbidities and in acute overdose in adults. Lacticemia has been reported twice in a previously healthy pediatric population, both of which were suicide attempts and required hemodialysis. We report a case of a 17-year-old, nondiabetic, healthy adolescent girl with metformin-associated lacticemia who intentionally overdosed on metformin, had no coingestants, and was treated only with crystalloids. Furthermore, she did not require intravenous bicarbonate administration or extracorporeal removal.

Topics: Acidosis, Lactic; Adolescent; Drug Overdose; Female; Humans; Hypoglycemic Agents; Metformin; Renal Dialysis; Sodium Bicarbonate; Suicide, Attempted

Lactic acidosis is associated with cardiovascular failure. Buffering with sodium bicarbonate is proposed in severe lactic acidosis. Bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. The authors thus investigated the cardiovascular and metabolic effects of an adapted sodium bicarbonate therapy, including prevention of carbon dioxide increase with hyperventilation and ionized calcium decrease with calcium administration.. Lactic acidosis was induced by hemorrhagic shock. Twenty animals were randomized into five groups: (1) standard resuscitation with blood retransfusion and norepinephrine (2) adapted sodium bicarbonate therapy (3) nonadapted sodium bicarbonate therapy (4) standard resuscitation plus calcium administration (5) hyperventilation. Evaluation was focused in vivo on extracellular pH, on intracellular pH estimated by P nuclear magnetic resonance and on myocardial contractility by conductance catheter. Aortic rings and mesenteric arteries were isolated and mounted in a myograph, after which arterial contractility was measured.. All animals in the hyperventilation group died prematurely and were not included in the statistical analysis. When compared with sham rats, shock induced extracellular (median, 7.13; interquartile range, [0.10] vs. 7.30 [0.01]; P = 0.0007) and intracellular acidosis (7.26 [0.18] vs. 7.05 [0.13]; P = 0.0001), hyperlactatemia (7.30 [0.01] vs. 7.13 [0.10]; P = 0.0008), depressed myocardial elastance (2.87 [1.31] vs. 0.5 [0.53] mmHg/μl; P = 0.0001), and vascular hyporesponsiveness to vasoconstrictors. Compared with nonadapted therapy, adapted bicarbonate therapy normalized extracellular pH (7.03 [0.12] vs. 7.36 [0.04]; P < 0.05), increased intracellular pH to supraphysiological values, improved myocardial elastance (1.68 [0.41] vs. 0.72 [0.44] mmHg/μl; P < 0.05), and improved aortic and mesenteric vasoreactivity.. A therapeutic strategy based on alkalinization with sodium bicarbonate along with hyperventilation and calcium administration increases pH and improves cardiovascular function.

Topics: Acidosis, Lactic; Adrenergic alpha-Agonists; Animals; Blood Transfusion; Calcium; Disease Models, Animal; Heart; Hydrogen-Ion Concentration; Hyperventilation; Magnetic Resonance Spectroscopy; Male; Norepinephrine; Random Allocation; Rats; Rats, Wistar; Severity of Illness Index; Shock, Hemorrhagic; Sodium Bicarbonate

An intoxication with drugs, ethanol or cleaning solvents may cause a complex clinical scenario if multiple agents have been ingested simultaneously. The situation can become even more complex in patients with (multiple) co-morbidities. A 59-year-old man with type 2 diabetes mellitus (without treatment two weeks before the intoxication) intentionally ingested a substantial amount of ethanol along with ~750 mL of laminate floor cleaner containing citric acid. The patient was admitted with severe metabolic acidosis (both ketoacidosis and lactic acidosis, with serum lactate levels of 22 mM). He was treated with sodium bicarbonate, insulin and thiamine after which he recovered within two days. Diabetic ketoacidosis and lactic acidosis aggravated due to ethanol intoxication, thiamine deficiency and citrate. The high lactate levels were explained by excessive lactate formation caused by the combination of untreated diabetes mellitus, thiamine deficiency and ethanol abuse. Metabolic acidosis in diabetes is multi-factorial, and the clinical situation may be further complicated, when ingestion of ethanol and toxic agents are involved. Here, we reported a patient in whom diabetic ketoacidosis was accompanied by severe lactic acidosis as a result of citric acid and mainly ethanol ingestion and a possible thiamine deficiency. In the presence of lactic acidosis in diabetic ketoacidosis, physicians need to consider thiamine deficiency and ingestion of ethanol or other toxins.

Topics: Acidosis; Acidosis, Lactic; Alcoholic Intoxication; Citric Acid; Diabetes Mellitus, Type 2; Humans; Insulin; Male; Middle Aged; Severity of Illness Index; Sodium Bicarbonate; Thiamine; Thiamine Deficiency

Lactic acidosis is a common cause of high anion gap metabolic acidosis. Sodium bicarbonate may be considered for an arterial pH <7.15 but paradoxically depresses cardiac performance and exacerbates acidosis by enhancing lactate production. This study aimed to evaluate the cause and mortality rate of lactic acidosis and to investigate the effect of factors, including sodium bicarbonate use, on death.. We conducted a single center analysis from May 2011 through April 2012. We retrospectively analyzed 103 patients with lactic acidosis among 207 patients with metabolic acidosis. We used SOFA and APACHE II as severity scores to estimate illness severity. Multivariate logistic regression analysis and Cox regression analysis models were used to identify factors that affect mortality.. Of the 103 patients with a mean age of 66.1±11.4 years, eighty-three patients (80.6%) died from sepsis (61.4%), hepatic failure, cardiogenic shock and other causes. The percentage of sodium bicarbonate administration (p = 0.006), catecholamine use, ventilator care and male gender were higher in the non-survival group than the survival group. The non-survival group had significantly higher initial and follow-up lactic acid levels, lower initial albumin, higher SOFA scores and APACHE II scores than the survival group. The mortality rate was significantly higher in patients who received sodium bicarbonate. Sodium bicarbonate administration (p = 0.016) was associated with higher mortality. Independent factors that affected mortality were SOFA score (Exp (B) = 1.72, 95% CI = 1.12-2.63, p = 0.013) and sodium bicarbonate administration (Exp (B) = 6.27, 95% CI = 1.10-35.78, p = 0.039).. Lactic acidosis, which has a high mortality rate, should be evaluated in patients with metabolic acidosis. In addition, sodium bicarbonate should be prescribed with caution in the case of lactic acidosis because sodium bicarbonate administration may affect mortality.

Topics: Acidosis, Lactic; Aged; Female; Hospital Mortality; Humans; Logistic Models; Male; Middle Aged; Multivariate Analysis; Proportional Hazards Models; Retrospective Studies; Sepsis; Sodium Bicarbonate; Treatment Outcome

To evaluate the preferences and self-reported practices of pediatric acute care physicians with respect to sodium bicarbonate administration to infants and children in shock or cardiac arrest.. National survey study utilizing a self-administered questionnaire.. Thirteen Canadian pediatric tertiary care centers.. Canadian pediatric critical care physicians, pediatric emergency physicians, and trainees in these subspecialties.. None.. Survey items were evaluated based on Yes/No responses, frequency responses, and Likert scales. Overall response rate was 53% (151/284) with 49.0% (74/151) citing pediatric critical care as their primary practice. 82.0% of respondents (123/150) indicated they would administer sodium bicarbonate as part of ongoing resuscitation for septic shock, whereas 58.3% (88/151) would administer sodium bicarbonate in a cardiac arrest scenario (p=0.004). 47.3% (71/150) selected a pH threshold at or below which they would administer sodium bicarbonate (mean, 6.94±0.013; median, 7.00; range, 6.50-7.20; interquartile range, 6.90-7.00), whereas 20.5% (31/151) selected a base excess threshold (mean, -15.62±0.78; median, -16; range, -20 to -4; interquartile range, -20 to -14). Both pH and duration of resuscitation were strongly associated with the decision to administer sodium bicarbonate (p<0.0001). Respondents' perceptions regarding a colleague's likelihood of administering sodium bicarbonate to the same patient under the same circumstances reflect an acknowledgment of disparate practices with respect to sodium bicarbonate use. 53.0% (79/149) felt current American Heart Association guidelines help them in deciding whether to administer sodium bicarbonate to critically ill patients, and 84% would support a randomized trial.. Differences of opinion exist among pediatric acute care physicians with respect to the timing and appropriateness of sodium bicarbonate administration during resuscitation. Most indicated they would support moving forward with a clinical trial.

Topics: Acidosis, Lactic; Attitude of Health Personnel; Canada; Child; Child, Preschool; Emergency Service, Hospital; Health Care Surveys; Health Knowledge, Attitudes, Practice; Heart Arrest; Hospitals, Pediatric; Humans; Infant; Practice Patterns, Physicians'; Resuscitation; Shock; Sodium Bicarbonate

Drunken lamb syndrome (DLS) has recently been described as lamb D-lactic acidosis syndrome (LDLAS). In 2012, 18 lambs aged between 7 days and 28 days with LDLAS were identified. Biochemically, each lamb had a metabolic acidosis characterised by D-lactic acidosis and exhibited clinical signs including: not hyperthermic, no evidence of dehydration, demonstrating an ataxic gait tending to recumbency (DLS) and possibly somnolence. These lambs received 50 mmol of sodium bicarbonate as an 8.4 per cent solution given orally, together with parenteral long-acting amoxicillin. All 18 cases made a full clinical recovery. This study demonstrates a novel effective treatment for a disease that is usually fatal, and also demonstrates a strong correlation between venous plasma bicarbonate concentrations and venous plasma D-lactate concentrations (R(2)=0.49).

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Amoxicillin; Animals; Animals, Newborn; Anti-Bacterial Agents; Female; Lactates; Male; Sheep; Sheep Diseases; Sodium Bicarbonate; Treatment Outcome

Topics: Acidosis, Lactic; Heart Arrest; Humans; Practice Patterns, Physicians'; Shock; Sodium Bicarbonate

Topics: Acidosis, Lactic; Animals; Female; Lactates; Male; Sheep Diseases; Sodium Bicarbonate

Topics: Acidosis, Lactic; Acute Kidney Injury; Anti-Bacterial Agents; Comorbidity; Female; Humans; Hypothermia; Infusions, Intravenous; Metformin; Middle Aged; Multiple Organ Failure; Penicillanic Acid; Piperacillin; Piperacillin, Tazobactam Drug Combination; Renal Replacement Therapy; Sodium Bicarbonate; Urinary Tract Infections; Vasoconstrictor Agents

Lactic acidosis is a frequent cause of poor outcome in the intensive care settings. We set up an experimental model of lactic acid infusion in normoxic and normotensive rats to investigate the systemic effects of lactic acidemia per se without the confounding factor of an underlying organic cause of acidosis.. Sprague Dawley rats underwent a primed endovenous infusion of L(+) lactic acid during general anesthesia. Normoxic and normotensive animals were then randomized to the following study groups (n = 8 per group): S) sustained infusion of lactic acid, S+B) sustained infusion+sodium bicarbonate, T) transient infusion, T+B transient infusion+sodium bicarbonate. Hemodynamic, respiratory and acid-base parameters were measured over time. Lactate pharmacokinetics and muscle phosphofructokinase enzyme's activity were also measured.. Following lactic acid infusion blood lactate rose (P<0.05), pH (P<0.05) and strong ion difference (P<0.05) drop. Some rats developed hemodynamic instability during the primed infusion of lactic acid. In the normoxic and normotensive animals bicarbonate treatment normalized pH during sustained infusion of lactic acid (from 7.22 ± 0.02 to 7.36 ± 0.04, P<0.05) while overshoot to alkalemic values when the infusion was transient (from 7.24 ± 0.01 to 7.53 ± 0.03, P<0.05). When acid load was interrupted bicarbonate infusion affected lactate wash-out kinetics (P<0.05) so that blood lactate was higher (2.9 ± 1 mmol/l vs. 1.0 ± 0.2, P<0.05, group T vs. T+B respectively). The activity of phosphofructokinase enzyme was correlated with blood pH (R2 = 0.475, P<0.05).. pH decreased with acid infusion and rose with bicarbonate administration but the effects of bicarbonate infusion on pH differed under a persistent or transient acid load. Alkalization affected the rate of lactate disposal during the transient acid load.

Topics: Acidosis, Lactic; Animals; Hemodynamics; Hydrogen-Ion Concentration; Lactic Acid; Phosphofructokinases; Rats; Rats, Sprague-Dawley; Respiratory Rate; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Aged, 80 and over; Comorbidity; Diabetes Mellitus, Type 2; Diuretics; Drug Monitoring; Female; Humans; Hypoglycemic Agents; Kidney Failure, Chronic; Lactates; Metformin; Polypharmacy; Renal Dialysis; Sodium Bicarbonate

Topics: Acidosis, Lactic; Adrenergic alpha-Agonists; Anti-Inflammatory Agents; Antidiuretic Agents; Drug Overdose; Epinephrine; Glucose; Humans; Hydrocortisone; Hypoglycemic Agents; Insulin; Male; Metformin; Middle Aged; Norepinephrine; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome; Vasopressins

Metformin, widely used in the treatment of diabetes mellitus, is known to cause lactic acidosis in both therapeutic use and after an overdose. We report the case of a 40-year-old woman who claimed to have ingested between 75 and 100 grams of metformin and subsequently developed severe lactic acidosis. She eventually developed a peak serum lactate level of 40.0 mmol/L and a serum pH nadir of 6.59 and became obtunded, hypotensive, and hypothermic. After aggressive supportive therapy with mechanical ventilation, vasopressor agents, sodium bicarbonate, and hemodialysis, her metabolic derangements steadily improved and she made a complete recovery without any residual sequelae. Her admission serum metformin concentration was later determined to be 160 microg/mL (therapeutic range is 1-2 microg/mL). There are several case reports and case series describing lactic acidosis secondary to metformin ingestion, although the exact mechanism remains unclear. The overall management of metformin overdose is reviewed. This case represents the largest reported amount of ingested metformin, the lowest serum pH, and the highest serum lactate concentration in any intentional metformin overdose survivor in the literature. Despite potentially lethal metabolic derangements, such patients can survive with aggressive supportive care.

Topics: Acidosis, Lactic; Adult; Drug Overdose; Female; Humans; Hypoglycemic Agents; Hypotension; Metformin; Poisoning; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Animals; Animals, Suckling; Autopsy; Fatal Outcome; Female; Male; Sheep; Sheep Diseases; Sodium Bicarbonate; Treatment Outcome

Topics: Acidosis, Lactic; Anti-Bacterial Agents; Drug Therapy, Combination; Ethanol; Humans; Length of Stay; Male; Middle Aged; Proton Pump Inhibitors; Sodium Bicarbonate; Treatment Outcome

d-lactic acidosis is a rare and severe complication of short bowel syndrome in children that may result from important ileal bacterial overgrowth by lactobacilli. Intestinal flora (Lactobacilli) is responsible for the production of d-lactic acid after fermentation of food carbohydrates.. We report on the case of a 6-year-old child with a short bowel syndrome treated with both home enteral and parenteral nutrition. The patient suddenly presented with acute neurological symptoms including dysarthria and disorientation. Biological analysis revealed metabolic acidosis, increased plasma d-lactic acid assessed by organic acid chromatography analysis and a very important increase in expired hydrogen during glucose breath test. Lactobacillus fermentum (known to produce d and L isomers of lactic acid) was isolated in the gastric liquid and rectal swabs. Clinical and biological evolution was rapidly favourable after treatment with intravenous sodium bicarbonate, antibiotic therapy and interruption of enteral nutrition.. d-lactic acidosis should be suspected when neurological symptoms occur in a child with short bowel syndrome. They can be prevented by treating intestinal bacterial overgrowth.

Topics: Acidosis, Lactic; Anti-Bacterial Agents; Child; Follow-Up Studies; Humans; Intestines; Lactic Acid; Lactobacillus; Male; Parenteral Nutrition; Short Bowel Syndrome; Sodium Bicarbonate; Time Factors; Treatment Outcome

Topics: Acidosis, Lactic; Angiography, Digital Subtraction; Blood Gas Analysis; Contrast Media; Diabetes Mellitus, Type 2; Fatal Outcome; Heart Arrest; Humans; Hypoglycemic Agents; Intubation, Intratracheal; Iohexol; Male; Metformin; Middle Aged; Postoperative Complications; Radiographic Image Enhancement; Renal Insufficiency; Respiration, Artificial; Respiratory Distress Syndrome; Sodium Bicarbonate; Subarachnoid Hemorrhage; Tomography, X-Ray Computed

Polypharmacy may lead to synergistic complications from the different medications. We report the case of a 50-year-old woman who was prescribed 11 drugs, including a diuretic, celecoxib, metformin, and candesartan, and who developed acute kidney dysfunction while on these drugs, manifesting as severe proteinuria, acute azotemia, hyperkalemia. The kidney injury caused the accumulation of metformin, leading to lactic acidosis and acute pancreatitis. Sodium bicarbonate hemodialysis not only improved the metabolic abnormalities but also hastened the removal of metformin.

Topics: Acidosis, Lactic; Acute Disease; Acute Kidney Injury; Angiotensin II Type 1 Receptor Blockers; Benzimidazoles; Biphenyl Compounds; Celecoxib; Cyclooxygenase Inhibitors; Diuretics; Drug Interactions; Drug Therapy, Combination; Drug-Related Side Effects and Adverse Reactions; Humans; Hydrochlorothiazide; Hypoglycemic Agents; Metformin; Middle Aged; Pancreatitis; Pharmaceutical Preparations; Polypharmacy; Pyrazoles; Renal Dialysis; Sodium Bicarbonate; Sulfonamides; Tetrazoles

Metformin-associated lactic acidosis is a rare but serious condition and potentially even more hazardous during pregnancy. We reported a case of lactic acidosis in a 28-year-old pregnant woman (gravida 3, para 0, abortion 2, ante-partum 22 weeks) after ingestion of 39.50 g (approximately 80 tablets) metformin in a suicide attempt. She had no pre-existing systemic illness. Analysis of arterial blood gases revealed a high anion gap (28.1 mEq/l) and a normal osmol gap (8 mEq/l) metabolic acidosis. Other etiologies of high anion gap and normal osmol gap metabolic acidosis were excluded by laboratory investigation. The patient was treated on an emergency basis and received aggressive fluid management, intravenous sodium bicarbonate (1 mEq/kg) and activated charcoal, orally. The fetal condition was monitored intensively. The fetus was delivered smoothly via vaginal delivery in a healthy state at the 38th gestational week. Clinical follow-up over the next 2 years confirmed no congenital abnormality. We present a case of successful management of metformin-associated lactic acidosis during pregnancy, treated simply, with intravenous sodium bicarbonate and intensive fetal monitoring. This relatively noninvasive method is an effective treatment option. However, hemodialysis still has a valuable role in the management of acidosis which proves refractory to conservative treatment, such as that described.

Topics: Acidosis, Lactic; Adult; Birth Weight; Charcoal; Female; Humans; Hypoglycemic Agents; Infant, Newborn; Metformin; Pregnancy; Pregnancy Complications; Sodium Bicarbonate; Suicide, Attempted

Acute severe metabolic acidosis associated with lactic acidosis or ketoacidosis can have severe detrimental effects on organ function, and might contribute to mortality. A general consensus exists that elimination of the cause of the acidosis is essential for treatment, but there is controversy concerning the use of base for the treatment of these disorders. Some physicians advocate administration of base when the acidosis is severe to prevent a decrease in cardiac output, whereas others oppose administration of base even when the acidosis is severe given the potential compromise of cardiac function. Nephrologists and critical care specialists are often the physicians developing recommendations for the treatment of severe acid-base disorders.. A short online survey of 20 questions was developed to assess the approach to the treatment of acute metabolic acidosis of program directors of fellowship programs and experts from the specialties of critical care and nephrology.. Although there was variability among individual physicians from both specialties, a larger percentage of nephrologists than critical care physicians queried recommended administration of base for the treatment of lactic acidosis (86% vs 67%) and ketoacidosis (60% vs 28%). Also, critical care physicians in general used a lower level of blood pH when deciding when to initiate treatment. Of the physicians who gave base, most utilized sodium bicarbonate as the form of base given.. The results of this survey indicate that the decisions whether to use base for the treatment of acute severe metabolic acidosis, and under which circumstances, vary among physicians, and indicate the need for further studies to develop evidence-based guidelines for therapy.

Topics: Acidosis; Acidosis, Lactic; Blood; Critical Care; Diabetic Ketoacidosis; Humans; Hydrogen-Ion Concentration; Nephrology; Online Systems; Sodium Bicarbonate; Surveys and Questionnaires

In this report of a near-fatal metformin ingestion successfully treated with alkalinization and high-volume hemofiltration, we discuss the management of severe lactic acidosis and demonstrate that early aggressive intervention resulted in a positive outcome.. Case report.. A tertiary pediatric intensive care unit.. The patient was a healthy 14-yr-old female found by a sibling following a seizure of unknown duration, thought to be secondary to hypoglycemia as a consequence of a self-ingestion of metformin, atenolol, and diclofenac. She responded well to advanced resuscitation but progressively developed severe lactic acidosis, bradycardia, and hypotension in addition to persistent hypoglycemia. The peak lactate level was 37.5 mmol/L with an albumin corrected anion gap of 65 mmol/L.. She was treated with high-volume venovenous hemofiltration and aggressive alkalinization therapy. The latter facilitated control of severe acidosis, whereas the hemofiltration removed the ingested drugs in addition to endogenously produced lactate precipitated by metformin.. In this case, early and aggressive treatment of the acidosis and cardiovascular compromise with inotropes, venovenous hemofiltration, and large doses of sodium bicarbonate in metformin overdose resulted in a successful outcome even in the presence of severe acidosis and very high lactate levels.

Topics: Acidosis, Lactic; Adolescent; Drug Overdose; Female; Fluid Therapy; Hemofiltration; Humans; Hypoglycemic Agents; Metformin; Sodium Bicarbonate

Mitochondrial cytopathy is a multisystemic disease that requires different pharmacological and specialist approaches; although most therapies are usually of scarce effectiveness. We describe a clinical management of a very young girl with Pearson's syndrome that developed the symptoms of Kearns-Sayre syndrome. Many of symptoms were temporarily improved by the replacement therapy with hydrocortisone introduced to treat the partial adrenal insufficiency. During her life, she showed an ample clinical spectrum of symptoms because of multiple organs involvements: firstly bone marrow and, thereafter, brain, retina, inner ear, and kidney. Partial adrenal insufficiency, rarely described in mitochondrial disorders, was a distinctive characteristic of this case. When our patient was treated with hydrocortisone, in addition to ubiquinone and carnitine, the episodes of decompensation regressed and an improvement of the adrenal insufficiency, but only temporary reversion of the weakness of muscle, ophthalmoplegia and of the fatigue, were testified. Nevertheless, after a brief period of recovery, she developed the de Toni-Debré-Fanconi syndrome and the reappearance of the neurological symptoms.

Topics: Acidosis, Lactic; Bone Marrow Diseases; Calcium; Child, Preschool; Disease Progression; DNA, Mitochondrial; Ergocalciferols; Fanconi Syndrome; Female; Humans; Kearns-Sayre Syndrome; Levetiracetam; Neutropenia; Nootropic Agents; Pancreas, Exocrine; Pancreatic Diseases; Piracetam; Sodium Bicarbonate; Thrombocytopenia

Metformin, an antihyperglycemic, is widely used in the treatment of type 2 diabetes mellitus (DM). A rare, but important complication associated with this drug is the development of lactic acidosis: Overall mortality of lactic acidosis is approximately 50%. Certain subsets of patients taking metformin are at greater risk of developing lactic acidosis. This report discusses the development of metformin-associated lactic acidosis in four older adults admitted to an institution during a 2-month period, treatments, and outcomes. We recommend an aggressive treatment strategy of hemodialysis followed by peritoneal dialysis, continuous bicarbonate infusion, and tight glucose control. We review the cautions and contraindications of metformin use for the treatment of type 2 DM and report an educational plan for residents and staff instituted to improve drug complication awareness and reduce mortality.

Topics: Acidosis, Lactic; Aged; Aged, 80 and over; Diabetes Mellitus, Type 2; Female; Follow-Up Studies; Humans; Hydrogen-Ion Concentration; Hypoglycemic Agents; Infusions, Intravenous; Male; Metformin; Risk Factors; Sodium Bicarbonate

Nucleoside reverse transcriptase inhibitors (NRTIs), which are used for the treatment of human immunodeficiency virus (HIV) infection have been associated with a wide spectrum of clinical manifestations, including hepatic steatosis, lipodystrophy, myopathy, and lactic acidosis. Such adverse effects are postulated to result from the inhibition of mitochondrial DNA gamma polymerase, which causes the depletion of mitochondrial DNA and eventual the disruption of oxidative phosphorylation. Although cases of severe decompensated lactic acidosis are rare, this syndrome is associated with a high mortality rate. We report upon the first Korean case, of severe lactic acidosis in an acquired immunodeficiency syndrome (AIDS) patient receiving stavudine, an anti-HIV drug.

Topics: Acidosis, Lactic; Acquired Immunodeficiency Syndrome; Adult; Anti-HIV Agents; Female; Humans; Sodium Bicarbonate; Stavudine

The respiratory compensation point (RCP) marks the onset of hyperventilation ("respiratory compensation") during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body's buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally.. During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51-3.73 l x min(-1) oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26-42; body mass index (BMI) 20.7-23.9 kg x m(-2); Vo(2peak) 51.3-62.1 ml x min(-1) x kg(-1)). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test.. In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l x min(-1)) compared with the first test.. For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms.

Topics: Acidosis, Lactic; Adult; Body Mass Index; Exercise; Exercise Test; Humans; Hydrogen-Ion Concentration; Hyperventilation; Oxygen Consumption; Sodium Bicarbonate

Topics: Acidosis, Lactic; Blood Chemical Analysis; Critical Care; Humans; Hydrogen-Ion Concentration; Infusions, Intravenous; Intensive Care Units; Prognosis; Risk Assessment; Sensitivity and Specificity; Severity of Illness Index; Sodium Bicarbonate; Survival Rate; Treatment Outcome

Topics: Acidosis, Lactic; Aged; Aged, 80 and over; Diabetes Mellitus, Type 2; Humans; Hypoglycemic Agents; Male; Metformin; Sodium Bicarbonate

Topics: Acidosis, Lactic; Adenocarcinoma; Aged; Antineoplastic Combined Chemotherapy Protocols; Bleomycin; Colonic Neoplasms; Cyclophosphamide; Doxorubicin; Etoposide; Fatal Outcome; Humans; Lactates; Liver; Lymphoma, Large B-Cell, Diffuse; Male; Neoplasms, Second Primary; Prednisone; Sodium Bicarbonate; Vincristine

We report the survival of a multiply injured patient with exanguinating haemorrhage and an arterial pH of 6.5, following a road vehicle crash. The previously healthy 38 years old male driver veered off the motorway and collided with a tree. The ambulance arrived at the scene 9 min after being called by an eyewitness and, following rapid extrication from the wreckage; the patient arrived in hospital 27 min later (with a GCS of 6), and was immediately intubated. The patient had suffered near-complete amputation of the left leg at upper femoral shaft level, along with multiple distal fractures and open wounds. He also sustained a head injury and closed displaced fractures of left radius and ulna. The patient received 2 l of crystalloids in the pre-hospital phase. Once in hospital the haemorrhage was controlled with a pressure dressing and intra-venous fluids were kept to a minimum until he was taken promptly to theatre. His initial arterial blood sample revealed a pH of 6.57, pCo(2) of 9.18 kPa, a pO(2) of 70.11 kPa and a base excess of -27.5 mmol l(-1). The co-oximeter Hb was 5.8 g dl(-1). Haemorrhage was controlled in theatre where he was transfused a total of 30 U of blood, 1 pack of platelets, 12 U of fresh frozen plasma, 3.5 l of crystalloids and 1.5 l of colloid. Sodium bicarbonate was administered three times. He subsequently remained ventilated in intensive care unit (ICU). Over the following week he survived sepsis, disseminated intravascular coagulation and myoglobinuria (with transient renal failure) attributable to rhabdomyolysis secondary to muscle necrosis. He later underwent diversion colostomy and disarticulating amputation of the left femur after several debridements. After 6 weeks on ICU he made an excellent recovery will full return of his mental abilities. In this case, the serial arterial blood samples obtained were reliable. The lactic acidosis observed was the result of profound tissue hypo-perfusion and its rate of clearance seems to have greater prognostic value than its peak or initial value. Several factors may have contributed to the patient's survival: rapid retrieval from the scene; early intubation with excellent subsequent oxygenation (thus avoiding the dangerous combination of hypoxia and acidosis with synergistic influence on cardiac depression) and limited initial fluid resuscitation in the emergency department with prompt surgical intervention and vigorous restoration of organ perfusion after surgical haemostasis. Immediat

Topics: Accidents, Traffic; Acidosis, Lactic; Adult; Amputation, Traumatic; Blood Gas Analysis; Hemorrhage; Humans; Hydrogen-Ion Concentration; Intensive Care Units; Male; Multiple Trauma; Shock, Hemorrhagic; Sodium Bicarbonate

We describe a preterm neonate with documented group B Streptococcus sepsis and associated metabolic acidosis whose lactic acidemia was refractory to conventional sodium bicarbonate therapy but responded well to dichloroacetate treatment.

Topics: Acidosis, Lactic; Dichloroacetic Acid; Humans; Infant, Newborn; Sepsis; Sodium Bicarbonate; Streptococcal Infections

To examine the impact of administration of NaHCO3 on contractility and energy metabolism of the myocardium during hypoxemia.. Regional myocardial hypoxia was induced in the left anterior descending (LAD) artery myocardium in anesthetized, open-chest dogs, using a perfusion circuit between the right atrium and the LAD artery, and a membrane oxygenator. The rate of flow in LAD artery was maintained constant with the use of a roller pump. During hypoxia, eight dogs were administered isotonic NaHCO3 in the circuit and six other dogs received equimolar NaCl. Myocardial contractile function was assessed using sonomicrometry for measurement of percentage of systolic shortening and preload recruitable stroke work. Oxygen consumption and the rate of appearance of lactate were measured. Clamp-frozen tissue samples were obtained at the end of the experiment from the hypoxic LAD myocardium and the nonhypoxic circumflex myocardium for measurement of tissue lactate level.. During hypoxia, there was a significant decrease in oxygen consumption by the LAD myocardium (35 +/- 7 micromol/min in the NaCl group and 40 +/- 7 micromol/min in the NaHCO3 group during hypoxia vs. 131 +/- 11 micromol/min during aerobic perfusion). There was also a significant decrease in myocardial contractility as measured by percentage of systolic shortening (14 +/- 3% to -8 +/- 3%); NaHCO3 infusion during hypoxia did not improve myocardial contractility (-7 +/- 2%). Similar results were obtained with measurements of preload recruitable stroke work. The rate of production of lactate during hypoxia was substantially lower than expected, based on the calculated oxygen deficit, and was not significantly increased by the administration of NaHCO3 (33 +/- 9 micromol/min in the NaCl group and 51 +/- 5 micromol/min in the NaHCO3 group). Tissue lactate was not statistically different in the hypoxic myocardium supplied by the LAD artery and the nonhypoxic myocardium supplied by the circumflex artery in either group.. The response of the myocardium to hypoxia is to decrease its mechanical work and metabolic demand. The infusion of NaHCO3 did not enhance myocardial contractile function or flux in glycolysis during hypoxia. We speculate that this diminished mechanical work and metabolic demand may represent an adaptive response to preserve cellular integrity until oxygen delivery is restored.

Topics: Acidosis, Lactic; Analysis of Variance; Animals; Blood Gas Analysis; Disease Models, Animal; Dogs; Drug Evaluation, Preclinical; Energy Metabolism; Female; Hemodynamics; Hydrogen-Ion Concentration; Hypoxia; Lactic Acid; Male; Myocardial Contraction; Myocardial Ischemia; Myocardial Stunning; Oxygen Consumption; Sodium Bicarbonate; Stroke Volume

A 16-year-old man with mitochondrial encephalomyopathy underwent biopsy and nephrectomy under general anesthesia. Mitochondrial encephalomyopathy is caused by mitochondrial dysfunction, and frequently accompanies elevation of lactic and pyruvic acid levels in the blood. It has been considered that problems of anesthesia for the patient with mitochondrial encephalomyopathy are the probability of hyperlactacidemia, the relevance to malignant hyperthermia, the possibility of myocardial disease and dysfunction of heart conduction system, respiratory depression due to muscle weakness, and so on. Therefore, to prevent hyperlactacidemia, we prepared the extracellular fluid solution including bicarbonic acid but no lactic and acetic acid, and infused the solution to the patient during anesthesia. By use of this solution, his lactic acid level was kept within the normal range during anesthesia and no metabolic acidosis occurred. His hemodynamics was stable and he showed normal response to vecuronium, recovering from anesthesia smoothly and postoperative course was uneventful.

Topics: Acidosis, Lactic; Adolescent; Anesthesia, General; Humans; Intraoperative Complications; Isotonic Solutions; Male; Mitochondrial Encephalomyopathies; Nephrectomy; Perioperative Care; Ringer's Solution; Sodium Bicarbonate

Topics: Acidosis, Lactic; Humans; Sodium Bicarbonate

Topics: Acidosis, Lactic; Animals; Buffers; HEPES; Humans; Sodium Bicarbonate

Severe acidemia (blood pH < 7.1 to 7.2) suppresses myocardial contractility, predisposes to cardiac arrhythmias, causes venoconstriction, and can decrease total peripheral vascular resistance and blood pressure, reduce hepatic blood flow, and impair oxygen delivery. These alterations in organ function can contribute to increased morbidity and mortality. Although it seemed logical to administer sodium bicarbonate to attenuate acidemia and therefore lessen the impact on cardiac function, the routine use of bicarbonate in the treatment of the most common causes of severe acidemia, diabetic ketoacidosis, lactic acidosis, and cardiac arrest, has been an issue of great controversy. Studies of animals and patients with these disorders have reported conflicting data on the benefits of bicarbonate, showing both beneficial and detrimental effects. Alternative alkalinizing agents, tris-hydroxymethyl aminomethane and Carbicarb, have shown some promise in studies of animals and humans, and reevaluation of these buffers in the treatment of severe acidemic states seems warranted. The potential value of base therapy in the treatment of severe acidemia remains an important issue, and further studies are required to determine which patients should be administered base therapy and what base should be used.

Topics: Acidosis; Acidosis, Lactic; Animals; Arrhythmias, Cardiac; Bicarbonates; Buffers; Calcium; Carbonates; Cardiac Output; Diabetic Ketoacidosis; Drug Combinations; Heart Arrest; Humans; Myocardial Contraction; Oxygen; Potassium; Sodium Bicarbonate; Tromethamine; Vascular Resistance; Water-Electrolyte Balance

Topics: Acidosis, Lactic; Adult; Fatal Outcome; Female; Humans; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma; Sodium Bicarbonate; Tumor Lysis Syndrome

Topics: Acidosis, Lactic; Cell Hypoxia; Humans; Lactic Acid; Severity of Illness Index; Shock; Sodium Bicarbonate

Topics: Acidosis, Lactic; Humans; Infusions, Intravenous; Lactic Acid; Sodium Bicarbonate; Treatment Outcome

We report the case of a child in whom severe lactic acidosis (LA) and hyperammonemia developed after twenty days of total parenteral nutrition (TPN) for diffuse esophageal damage due to caustic ingestion. The revision of TPN preparation revealed that thiamine was never included and the hypothesis of thiamine deficiency was later confirmed measuring the serum thiamine level. Because severe metabolic acidosis the dialytic treatment with hemodiafiltration (HDF) and bicarbonate infusion were performed: the patient very quickly recovered with dramatic reestablishment of the acid-basic balance. Thiamine administration restored lactate metabolism. We emphasize that HDF is a useful and prompt treatment for LA to get over the critical phase of neurological and cardiological damage.

Topics: Acidosis, Lactic; Burns, Chemical; Child, Preschool; Esophageal Stenosis; Hemodiafiltration; Humans; Male; Parenteral Nutrition, Total; Sodium Bicarbonate; Thiamine Deficiency

We conducted experiments to determine whether preference for barley was affected when lambs ate various amounts of barley and whether lambs ate more barley when it contained lasalocid and sodium bicarbonate (NaHCO3), both of which attenuate acidosis. In Exp. 1, lambs were assigned to two treatments (six lambs/treatment). For 2 d, lambs in two treatments were offered either 400 or 1,200 g of rolled barley from 0600 to 0700 as a preload meal. A preference ratio [PR = barley ingested/(total amount of alfalfa + barley ingested)] was calculated based on lambs' intake when offered a choice of 200 g each of rolled barley and alfalfa pellets hourly from 0700 to 1100. After the preload meal, lambs in Treatment 1 (400 g preload) showed equal preference for barley (.52) and alfalfa (.48) for 4 h on d 1 (P > .05); their preference for barley was less after the meal of barley on d 1 (.52) than on d 2 (.72), but their preference for barley declined between h 3 (.81) and 4 (.55) of d 2 (P = .11). Lambs in Treatment 2 (1,200 g preload) showed a low preference for barley on d 1 (.29) and 2 (.19) (P < .001). In Exp. 2, lambs were assigned to four treatments (six lambs/treatment): 1) rolled barley + NaHCO3 (2%) + lasalocid (33 ppm); 2) rolled barley + NaHCO3 (2%); 3) rolled barley + lasalocid (33 ppm); or 4) rolled barley. Intake of barley by lambs offered NaHCO3 + lasalocid (Treatment 1) was greater (P = .07) than that by lambs offered NaHCO3 (Treatment 2), whereas intake by lambs offered lasalocid (Treatment 3) was similar (P > .05) to that by controls. We conclude that eating barley too frequently or in excess caused a decrease in lambs' preference for barley and that NaHCO3 and lasalocid attenuated the aversion.

Topics: Acidosis, Lactic; Animal Feed; Animals; Buffers; Eating; Food Preferences; Hordeum; Ionophores; Lasalocid; Medicago sativa; Sheep; Sheep Diseases; Sodium Bicarbonate

Reports of acute toxicity following sulfasalazine ingestion are rare. A case of an acute ingestion of sulfasalazine 50 g and paracetamol 50 g resulting in severe lactic acidosis, seizures, coagulopathy, hyperglycemia, ketosis, and methemoglobinemia is reported. Despite the ingestion of a large amount of paracetamol with serum paracetamol 5486 nmol/L (844 mg/L), significant hepatotoxicity did not occur. The patient recovered fully following administration of intravenous N-acetylcysteine, methylene blue, sodium bicarbonate, and supportive therapy.

Topics: Acetaminophen; Acetylcysteine; Acidosis, Lactic; Acute Disease; Adult; Anti-Inflammatory Agents; Blood Coagulation Disorders; Blood Platelets; Drug Combinations; Drug Overdose; Humans; Hyperglycemia; Infusions, Intravenous; Male; Methemoglobinemia; Methylene Blue; Partial Thromboplastin Time; Sodium Bicarbonate; Suicide, Attempted; Sulfasalazine

Topics: Acidosis, Lactic; Adult; Bicarbonates; Buffers; Drug Overdose; Humans; Hypoglycemic Agents; Lactic Acid; Male; Metformin; Renal Dialysis; Sodium Bicarbonate

Although peritoneal equilibration testing (PET) is increasingly used in chronic peritoneal dialysis, there is little knowledge about the clinical impact of PET in the acute setting. We report about more than threefold increases in lactate removal by adjusting the dialysis prescription according to the results of PET in an infant with severe congenital lactic acidosis.

Topics: Acidosis, Lactic; Bicarbonates; Body Weight; Dialysis Solutions; Fatal Outcome; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Lactates; Peritoneal Cavity; Peritoneal Dialysis; Sodium Bicarbonate; Time Factors

1. The correction of metabolic acidosis with sodium bicarbonate remains controversial. Experiments in vitro have suggested possible deleterious effects after alkalinization of the extracellular fluid. Disequilibrium of carbon dioxide and bicarbonate across cell membranes after alkali administration, leading to the phenomenon of 'paradoxical' intracellular acidosis, has been held responsible for some of these adverse effects. 2. Changes in intracellular pH in suspensions of leucocytes from healthy volunteers were monitored using a fluorescent intracellular dye. The effect in vitro of increasing extracellular pH with sodium bicarbonate was studied at different sodium bicarbonate concentrations. Lactic acid and propionic acid were added to the extracellular buffer to mimic conditions of metabolic acidosis. 3. The addition of a large bolus of sodium bicarbonate caused intracellular acidification as has been observed previously. The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate was added as a series of small boluses the reduction in intracellular pH was small. Under conditions of initial acidosis this was rapidly followed by intracellular alkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect is minimal when the conditions approximate those seen in clinical practice. We suggest that the observed small and transient lowering of intracellular pH is insufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis.

Topics: Acidosis, Lactic; Adult; Buffers; Cell Membrane; Cells, Cultured; Extracellular Space; Female; Humans; Hydrogen-Ion Concentration; Intracellular Fluid; Leukocytes; Male; Middle Aged; Sodium Bicarbonate

Use of sodium bicarbonate (NaHCO3) may result in intracellular acidosis due to the generation of CO2. Carbicarb, has been reported to be superior to sodium bicarbonate (NaHCO3) because of lesser generation of CO2. The present study was designed to investigate whether Carbicarb or NaHCO3 is superior to normal saline in the treatment of hypoxic lactic acidosis.. Hypoxia was induced by ventilation with 8% O(2) in 30 piglets with fixed ventilation. When the pH fell to < 7.2, hypoxia was reversed by placing the animals in 21% O2 (experiment 1) or 100% O(2) (experiment 2) and either saline, Carbicarb or NaHCO3 were given. Data were collected for 120 minutes after therapy.. In both experiment 1 (severe acidosis, pH < or = 7.1) and 2 (moderate acidosis, pH < or = 7.2) use of Carbicarb and NaHCO3 increased the arterial carbon dioxide tension (pCO2) significantly (p < 0.05). With moderate acidosis: 1) use of alkalinizing agents compared to saline resulted in an initial improvement in arterial pH at 1 minute, but thereafter, the differences were not statistically significant; and 2) there were no differences in hemodynamic variables and plasma lactic acid concentration between the three groups.. The data demonstrate that 1) both Carbicarb and NaHCO3 significantly increase arterial pCO2; and 2) use of either alkalinizing agent in moderate acidosis does not alter the course of acidosis.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Animals; Animals, Newborn; Carbonates; Drug Combinations; Female; Fetal Hypoxia; Male; Sodium Bicarbonate; Swine

The goal of this study was to evaluate whether sodium bicarbonate might be a useful form of therapy for hypoxic L-lactic acidosis; our aim was to determine if alkali could extend the time of survival in this setting. Hypoxia was induced in anesthetized, paralyzed, artificially ventilated rats by lowering inspired O2 to 5.5%, an amount sufficient to develop a severe degree of L-lactic acidosis. Measuring arterial blood gases frequently permitted maintenance of a near-constant arterial O2 content. Three groups of hypoxic rats were studied: first, no infusions (n = 10); second, sodium bicarbonate at a rate equal to H+ production in the no-infusion group (n = 12); and third, a control for the Na load in the second group as NaCl (n = 17). Survival was close to twofold longer in the sodium bicarbonate group. Part of this beneficial effect seemed to be increased anaerobic glycolysis, producing ATP along with L-lactic acid. In addition, there was a large decrease in the metabolic demand (consumption of O2) in the 7- to 15-min period in the sodium bicarbonate group. Rats exposed to hypoxia and infused with NaCl for 15 min or alkali for 15, 27, or 40 min were then returned to room air; all survived for the subsequent experimental period of 150 min. We found that there is both a rationale and experimental evidence for giving sodium bicarbonate to prolong survival during hypoxia.

Topics: Acidosis, Lactic; Adenosine Triphosphate; Alkalies; Anaerobiosis; Animals; Glycolysis; Hypoxia; Lactic Acid; Male; Oxygen Consumption; Rats; Rats, Wistar; Sodium Bicarbonate; Survival Analysis

Topics: Acidosis, Lactic; Humans; Liver Transplantation; Sodium Bicarbonate

The effects of HCO3Na load on acid-base balance and muscle intracellular bioenergetics have been investigated using 31P-magnetic resonance spectroscopy in an experimental model of endotoxinic shock. Anesthetized, mechanically ventilated, and paralyzed rats (n = 16) were given an intravenous bolus of Escherichia coli lipopolysaccharide (15 mg/kg). When shock was established they were randomly assigned to receive either HCO3Na intravenously (2 mmol/kg in 2 min) or an equimolar saline injection. Lipopolysaccharide induced a significant decrease in the levels of mean arterial pressure (58 +/- 6 vs. 120 +/- 8 mmHg), arterial pH (7.20 +/- .03 vs. 7.35 +/- .01), intracellular pH (6.86 +/- .04 vs. 7.08 +/- .01), a marked hyperlactatemia (7 +/- 3 vs. 1.2 +/- .2 mmol/L) and a drop in the phosphocreatine-inorganic phosphate ratio. In the bicarbonate-loaded rats, mean arterial pressure further decreased whereas it remained unchanged in the saline group. Bicarbonate increased arterial pH and PaCO2 transiently. In the saline group, arterial pH decreased and PaCO2 remained stable. In both groups, intracellular pH and high energy phosphates had a similar evolution. In this model of septic shock, partial correction of arterial pH using HCO3Na did not reduce the metabolic cellular injury in skeletal muscle. Based on these results, HCO3Na may be of limited therapeutic value in severe septic metabolic acidosis.

Topics: Acidosis, Lactic; Animals; Blood Pressure; Disease Models, Animal; Hindlimb; Hydrogen-Ion Concentration; Lipopolysaccharides; Magnetic Resonance Spectroscopy; Muscle, Skeletal; Physical Phenomena; Physics; Rats; Rats, Sprague-Dawley; Shock, Septic; Sodium Bicarbonate; Sodium Chloride

Topics: Acidosis, Lactic; Animals; Carbonates; Dogs; Drug Combinations; Hydrogen-Ion Concentration; Saline Solution, Hypertonic; Sodium Bicarbonate

Several recent studies evaluated alkali therapy for lactic acidosis (LA). We studied the effects of sodium bicarbonate (NaHCO3) on LA due to hemorrhagic shock in dogs. After inducing hemorrhagic shock in twelve mongrel dogs, we divided them into two groups: the first group was treated with 7% NaHCO3 and the second with 4.9% sodium chloride (NaCl). We measured pyruvate, lactate, acetoacetate (AcAc) and 3-hydroxybutyrate (3OHBA) while monitoring hemodynamics and blood gases, and calculated pyruvate/lactate and AcAc/3OHBA ratios. There was no statistically significant difference between the two groups in hemodynamic parameters, except for stroke volume index, and oxygen consumption throughout this experiment. Arterial pH and base excess increased significantly in the NaHCO3 group. The increases of pyruvate and lactate were significantly greater in the NaHCO3 group than in the NaCl group, but the other metabolic data were not significantly different. We did not find that NaHCO3 had greater beneficial effect than NaCl in hemorrhagic shock model, and the use of NaHCO3 for LA due to hemorrhagic shock may not be recommended.

Topics: Acidosis, Lactic; Animals; Dogs; Hemodynamics; Lactates; Shock, Hemorrhagic; Sodium Bicarbonate

Topics: Acidosis, Lactic; Animals; Bicarbonates; Cattle; Cattle Diseases; Infusions, Intravenous; Male; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Bicarbonates; Hemodynamics; Humans; Infant, Newborn; Research Design; Sodium; Sodium Bicarbonate

The effects of Carbicarb, sodium bicarbonate, and sodium chloride on arterial blood gases, lactate concentrations, hemodynamics, and myocardial intracellular pH were compared in hypoxic lactic acidosis with controlled carbon dioxide elimination. Twenty-one young mongrel dogs were anesthetized, mechanically ventilated, and randomly allocated into one of three treatment groups. After hypoxic lactic acidosis was induced and maintained, 2.5 mEq/kg of one of the agents was infused over 30 min. Arterial blood gases, pH, lactate concentrations, and hemodynamic variables were measured immediately prior to the infusion of the agent and 30 min after the infusion was completed. With sodium bicarbonate administration, there was a significant increase in arterial PCO2 as compared to both Carbicarb or sodium chloride administration. With Carbicarb administration, there was a significant increase in arterial pH, base excess, and cardiac index, without a significant increase in arterial lactate concentration as compared to sodium bicarbonate or sodium chloride administration. Stroke volume index was also increased significantly with decreased heart rate. The data suggest that Carbicarb administration in hypoxic lactic acidosis improved hemodynamics compared with sodium bicarbonate or sodium chloride administration. The increased stroke volume and cardiac contractility appear to be due to improved myocardial intracellular pH.

Topics: Acidosis, Lactic; Animals; Bicarbonates; Carbon Dioxide; Carbonates; Dogs; Drug Combinations; Hemodynamics; Hydrogen-Ion Concentration; Lactates; Magnetic Resonance Spectroscopy; Myocardium; Sodium; Sodium Bicarbonate; Sodium Chloride

To evaluate the effectiveness of continuous arteriovenous hemodiafiltration (CAVHD) using citrate as the anticoagulant for the treatment of lactic acidosis in patients with renal failure.. Case series with careful monitoring of the clinical course of patients being treated in a medical or surgical ICU.. University hospital ICU.. Two patients with lactic acidosis are described, along with our experience using CAVHD and citrate in other clinical settings.. CAVHD was used to manage renal failure, while a continuous infusion of citrate was administered to maintain patency of the extracorporeal circuit.. Total and ionized serum calcium concentrations and citrate concentrations were monitored.. CAVHD with citrate as the anticoagulant proved to be a convenient means of managing vascular volume, serum electrolyte concentrations, acid-base balance, and replacement renal function requirements in the setting of severe lactic acidosis, oliguric renal failure, and hemorrhagic diathesis.. CAVHD with citrate as the anticoagulant can be recommended as effective therapy for selected patients, but careful monitoring is needed to avoid serious complications.

Topics: Acidosis, Lactic; Adult; Aged; Bicarbonates; Chlorides; Citrates; Citric Acid; Female; Hemofiltration; Humans; Hypernatremia; Kidney Failure, Chronic; Male; Middle Aged; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Bicarbonates; Humans; Liver Diseases; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Adult; Aged; Bicarbonates; Female; Humans; Hydrogen-Ion Concentration; Lymphoma, T-Cell; Lymphoma, T-Cell, Peripheral; Prognosis; Remission Induction; Sodium; Sodium Bicarbonate

The patient with theophylline overdose commonly presents with gastrointestinal, cardiovascular, neurologic, and electrolyte abnormalities. Respiratory alkalosis is the most common acid-base alteration, but mild metabolic acidosis has been reported. Two cases of severe lactic acidosis (pH 6.67 and 6.63) in patients without hypoxemia, shock, or prolonged seizure activity are reported. Possible causative mechanisms and aspects of therapy are discussed. Theophylline toxicity should be considered when an unconscious patient with concurrent severe metabolic acidosis presents to the emergency department.

Topics: Acidosis, Lactic; Adult; Bicarbonates; Charcoal; Coma; Drug Overdose; Emergencies; Female; Glasgow Coma Scale; Humans; Sodium; Sodium Bicarbonate; Theophylline

Topics: Acidosis, Lactic; Adolescent; Adult; Aged; Bicarbonates; Blood Glucose; Diabetic Ketoacidosis; Dichloroacetic Acid; Female; Humans; Insulin; Lactates; Lactic Acid; Male; Middle Aged; Sodium; Sodium Bicarbonate; Tromethamine

Sodium bicarbonate (BC) and dichloroacetate (DCA) were studied in 7- to 14-day-old (n = 25) anesthetized swine with hypoxic acidosis. BC (base deficit X kg X 0.3, n = 10), DCA (300 mg/kg, n = 7) or saline (n = 8) was infused for 1 h. Blood lactic acid, dP/dtmax, heart rate and cardiac output increased and base excess and total arterial and carotid resistances (R) decreased with acidosis; aortic pressure, renal and mesenteric R did not change. BC induced higher pH, base excess and lactic acid. Heart rate in all and dP/dtmax with BC and DCA were restored; renal and mesenteric R and aortic pressure decreased in all. Cardiovascular responses to DCA and BC did not differ except for renal R.. BC is a more effective alkalizer than DCA, which induced a greater renal vasodilation; both restored contractility.

Topics: Acidosis, Lactic; Animals; Animals, Newborn; Bicarbonates; Blood Pressure; Cardiac Output; Dichloroacetic Acid; Heart Rate; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Pulmonary Gas Exchange; Sodium; Sodium Bicarbonate; Swine

We report an 8-year-old patient with clinical features suggesting Leigh's syndrome and with a decreased activity of the E1 component of the pyruvate dehydrogenase complex in cultured skin fibroblasts. A nerve biopsy showed the presence of severe peripheral neuropathy, rarely described in the literature. The partial correction of lactic acidosis with oral sodium bicarbonate chronic therapy may result in a slow evolution of the clinical symptoms.

Topics: Acidosis, Lactic; Bicarbonates; Biopsy; Brain Diseases, Metabolic; Child; Fibroblasts; Humans; Leigh Disease; Male; Peripheral Nervous System Diseases; Pyruvate Dehydrogenase Complex Deficiency Disease; Skin; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Bicarbonates; Critical Care; Humans; Sodium; Sodium Bicarbonate

A patient with a history of previous mechanical ventilation for asthma was hospitalized with acute, severe asthma; metabolic acidosis; and hyperlactatemia. In addition to standard therapy, she was successfully treated with face-mask CPAP and IV sodium bicarbonate infusion. This therapy may help prevent mechanical ventilation in some patients with acute, severe asthma and lactic acidosis.

Topics: Acidosis, Lactic; Adult; Asthma; Bicarbonates; Female; Humans; Infusions, Intravenous; Positive-Pressure Respiration; Sodium; Sodium Bicarbonate

The effects of iv sodium bicarbonate (NaHCO3) and Carbicarb, an experimental buffer, were compared in a rat model of lactic acidosis induced by controlled hemorrhage and asphyxia. Although both NaHCO3 and Carbicarb were effective at alkalinizing the arterial blood in this model, NaHCO3 administration resulted in a rise in PaCO2 where Carbicarb did not (+9 +/- 2 vs. +2 +/- 2 torr at 2 min after infusion, p less than .01). Moreover, NaHCO3 resulted in a small decrease in intracellular brain pH as measured with P-31 nuclear magnetic resonance where Carbicarb afforded intracellular brain alkalinization (-0.03 +/- 0.01 vs. +0.08 +/- 0.02 pH units at 2 min, p less than .01). If these data are confirmed clinically, Carbicarb may offer advantages over NaHCO3 under conditions of fixed or limited ventilation.

Topics: Acidosis, Lactic; Animals; Bicarbonates; Brain; Carbon Dioxide; Carbonates; Drug Combinations; Hydrogen-Ion Concentration; Magnetic Resonance Spectroscopy; Partial Pressure; Rats; Sodium; Sodium Bicarbonate

We report two diabetic patients who developed lactic acidosis following the use of Buformin. Treatment consisted of mechanical ventilation, massive bicarbonate administration, circulatory support with dopamine and peritoneal dialysis. Despite this, both patients died.

Topics: Acidosis, Lactic; Aged; Bicarbonates; Biguanides; Buformin; Diabetes Mellitus; Diabetic Angiopathies; Dopamine; Humans; Hypertension; Male; Peritoneal Dialysis; Respiration, Artificial; Sodium; Sodium Bicarbonate

Carbicarb is a mixture of Na2CO3/NaHCO3 that buffers similarly to NaHCO3, but without net generation of CO2. We studied the effects of carbicarb in an animal preparation of hypoxic lactic acidosis (HLA). HLA was induced by ventilating dogs with an hypoxic gas mixture (8% O2/92% N2). Dogs with HLA (n = 28) were then treated with 2.5 meq/kg of either NaHCO3 or carbicarb over 1 hr. Measurements were made, after 1 hr of hypoxia and 1 hr of therapy, of: cardiac hemodynamics, blood gases, liver intracellular pH (pHi), oxygen consumption, and regional lactate production. After therapy, the arterial pH rose with carbicarb (7.22 to 7.27, p less than .01), and fell with NaHCO3 (7.18 to 7.13, p less than .01). Mixed venous PCO2 did not change with carbicarb but increased with NaHCO3 (p less than .05). Arterial lactates stabilized with carbicarb but rose with NaHCO3 (by 3.1 mmol/liter, p less than .005). Lactate use by muscle, gut, and liver all improved with carbicarb and decreased with NaHCO3. The liver pHi (normal = 6.99, hypoxia = 6.80) improved with carbicarb (to 6.92), but decreased further with NaHCO3 (to 6.40). Muscle O2 consumption rose with carbicarb, whereas it decreased with NaHCO3. Arterial pressure fell less with carbicarb (-12 vs -46 mm Hg, p less than .006) and the cardiac output was stable with carbicarb but decreased with NaHCO3 (from 143 to 98 ml/kg/min, p less than .004). Stroke volume also improved with carbicarb but there was no change in pulmonary capillary wedge pressure, suggesting that carbicarb had a beneficial effect on myocardial contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acidosis, Lactic; Animals; Bicarbonates; Blood Gas Analysis; Carbonates; Cardiac Output; Dogs; Drug Combinations; Hemodynamics; Hypoxia; Lactates; Lactic Acid; Oxygen Consumption; Sodium; Sodium Bicarbonate

Serum lactic acidosis is characterized by a pH less than 7.25 and lactate greater than 5 mEq. Although sodium bicarbonate (NaHCO3) is standard treatment for this condition, clinical and experimental studies suggest that high doses of NaHCO3 may be ineffectual or even detrimental to brain, cardiovascular, and respiratory function, as well as survival. For this reason, low dose therapy with NaHCO3 has been recommended. Sodium dichloroacetate (NaDCA) has been used successfully to treat clinical and experimentally-induced lactic acidosis. The present study was designed to compare the effects of low dose NaHCO3 with NaDCA on blood pressure, blood chemistries and brain metabolites in rats with a low flow-induced (Type A, the most common type) lactic acidosis. Fasted male Wistar rats were subjected to cerebral ischemia and systemic hypotension for 30 min at which time, if the pH or HCO-3 fell to 7.2 or 10, respectively, the rat was treated with NaHCO3, NaDCA, or an equal volume of sterile water. Over the 30 min of recirculation that followed ischemia, treatment had no effect on blood pressure or glucose or on brain glucose or glycogen. NaHCO3 had no effect on lactate but appeared to stabilize pH and increase HCO3- more than in sham- or NaDCA-treated rats. Although NaDCA caused a greater increase in HCO3- than sham treatment, pH continued to decline. However, lactate decreased more in NaDCA- than in sham- or NaHCO3- treated rats. These results suggest that low dose NaHCO3 is not detrimental in this model; however, although NaHCO3 stabilized pH, it did not rapidly correct the acidosis. NaDCA at this dose had no effect on the acidosis but was effective in decreasing lactate. Since serum lactate has previously correlated with survival and since higher doses of NaDCA have corrected lactic acidosis in other studies, future evaluation of postischemic treatment with higher doses of NaDCA is warranted.

Topics: Acetates; Acidosis, Lactic; Animals; Bicarbonates; Blood Glucose; Brain Chemistry; Brain Ischemia; Dichloroacetic Acid; Glycogen; Lactates; Male; Rats; Rats, Inbred Strains; Resuscitation; Sodium; Sodium Bicarbonate

A case is presented of severe metabolic acidosis in a previously healthy man. The cause was attributed to lactic acidosis secondary to exertion. Although lactic acid is commonly produced with increased physical activity, it is usually cleared and buffered rapidly. The pathophysiology of lactic acidosis is discussed.

Topics: Acidosis, Lactic; Adult; Bicarbonates; Fluid Therapy; Humans; Infusions, Intravenous; Male; Physical Exertion; Sodium; Sodium Bicarbonate

We studied the use of sodium bicarbonate administration in a canine model of hemorrhagic shock to determine its effect on hemodynamics, arterial and venous blood gases, respiratory gases, and blood lactate levels. Thirteen dogs were anesthetized, paralyzed, mechanically ventilated, and hemodynamically monitored. Hypotension was induced and maintained at a mean arterial pressure of 40 to 45 mm Hg using controlled hemorrhage and reinfusion. After 2.5 h of shock, the dogs were randomized into two groups: one group (n = 6) received NaCl infusion; the other (n = 7) received sodium bicarbonate (1 mEq/kg followed by a continuous infusion of 2.5 mEq/kg.h for 2.5 h). CO2 production was increased in the alkali group, but there was no statistically significant difference between groups in any measured hemodynamic, blood gas, or respiratory gas variable. These included heart rate, BP, cardiac output, arterial and venous pH, CO2 production, and bicarbonate levels. Blood lactate levels, however, in the bicarbonate treated animals were significantly (p less than .01) higher than in the group treated with NaCl alone (10.1 +/- 3.2 vs. 5.1 +/- 1.2 mEq/L). These results are similar to the effects of bicarbonate found in other models of lactic acidosis, and suggest that bicarbonate therapy may have limited usefulness in the treatment of lactic acidosis.

Topics: Acidosis, Lactic; Animals; Bicarbonates; Dogs; Hemodynamics; Lactates; Shock, Hemorrhagic; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Bicarbonates; Humans; Lactates; Lactic Acid; Male; Middle Aged; Sodium; Sodium Bicarbonate

Lactic acidosis in diabetics on metformin therapy is rare but still associated with poor prognosis. The authors report here five cases. Three patients were initially with a cardiovascular collapse and all had an acute renal failure. Sodium bicarbonate haemodialysis therapy led to a dramatic improvement. Consciousness and hemodynamic status recovered rapidly. Severe metabolic and blood gases derangements were also rapidly corrected. Plasma metformin removal, appreciated by repeated blood samplings in 3 cases, was satisfactory. All patients survived. However, blood metformin levels remained abnormally high at the end of the dialytic therapy. In conclusion, (1) bicarbonate dialysis is an adequate treatment of lactic acidosis observed in diabetic patients treated with metformin since it rapidly corrects the acid-base disorders and partially removes metformin; (2) the sole accumulation of metformin is not sufficient to explain lactic acidosis since this latter might be corrected in spite of persisting high levels of blood metformin.

Topics: Acidosis, Lactic; Aged; Aged, 80 and over; Bicarbonates; Diabetes Mellitus; Female; Humans; Male; Metformin; Middle Aged; Renal Dialysis; Sodium; Sodium Bicarbonate

Carbicarb (Na2CO3 0.33 molar NaHCO3 0.33 molar), a mixture formulated to avoid the objections to sodium bicarbonate therapy, has been compared with 1 mol/L NaHCO3 and 1 mol/L NaCl in the treatment of mixed respiratory and metabolic acidosis (pH 7.17) produced by asphyxia in rats. In clinically appropriate doses, intravenous NaHCO3 raised arterial pH only 0.03 unit, elevated arterial carbon dioxide pressure, and doubled lactate concentration. With Carbicarb, the pH rise was three times as great and the blood lactate level was unchanged. The new drug should be effective in treating the acidosis of cardiopulmonary failure without raising blood carbon dioxide pressure or lactate levels and at lower sodium doses than required for NaHCO3.

Topics: Acidosis, Lactic; Acidosis, Respiratory; Animals; Bicarbonates; Blood Gas Analysis; Blood Pressure; Carbonates; Drug Combinations; Hydrogen-Ion Concentration; Lactates; Rats; Respiration; Sodium; Sodium Bicarbonate

We used 31P spectroscopy to determine whether administration of a neutralizing dose of bicarbonate in rabbits with lactic acidosis caused a paradoxical brain intracellular acidosis. Ten 10- to 16-day-old rabbits were anesthetized with 0.75% halothane/oxygen and their lungs mechanically ventilated. Metabolic acidosis was induced by decreasing PaO2 to 25 to 35 mm Hg for 1 to 2 hours until the base deficit was 10 to 15 mEq/L. Cerebral ischemia was prevented by maintaining arterial blood pressure at +/- 20% of control value with a venous infusion of epinephrine. Hypoxia was then terminated by administration of 100% oxygen, which was continued for the remainder of the study. After 15 minutes 100% oxygen, 5 mEq/kg 4.2% bicarbonate was administered to five animals; 5 minutes later the same dose was repeated. Control rabbits were given equal volumes of saline solution. In all animals, arterial pH decreased from 7.43 +/- 0.06 to 7.25 +/- 0.08 (SE) during hypoxia, and brain intracellular pH from 7.22 +/- 0.06 to 7.09 +/- 0.09 (SE). Both pH values remained low during reoxygenation. Bicarbonate administration normalized arterial pH (7.41 +/- 0.03), whereas treatment with saline solution did not (7.23 +/- 0.01, P less than 0.05). PaCO2 rapidly increased by 10 mm Hg in the bicarbonate group, and remained elevated; it was unaffected by saline solution administration. Brain intracellular pH in the bicarbonate group increased by 0.12 U over 40 minutes, but intracellular pH in the saline solution group decreased 0.05 pH U (P less than 0.05) over the same period. We conclude that administering a total dose of 10 mEq/kg sodium bicarbonate to neonatal rabbits recovering from hypoxic lactic acidosis increases arterial pH, brain intracellular pH, and PaCO2; it does not produce paradoxical intracellular acidosis in the brain.

Topics: Acidosis, Lactic; Animals; Bicarbonates; Brain; Carbon Dioxide; Hydrogen-Ion Concentration; Hypoxia; Magnetic Resonance Spectroscopy; Partial Pressure; Rabbits; Sodium; Sodium Bicarbonate

Topics: Acetates; Acidosis, Lactic; Animals; Bicarbonates; Dichloroacetic Acid; Dogs; Hemodynamics; Hypoxia; Lactates; Lactic Acid; Sodium; Sodium Bicarbonate

Topics: Acidosis; Acidosis, Lactic; Animals; Bicarbonates; Calcium; Dogs; Heart Arrest; Humans; Hydrogen-Ion Concentration; Sodium; Sodium Bicarbonate

Lactic acidosis is seen frequently after severe anoxia and circulatory failure. Because dichloroacetate (DCA) has been shown to be effective in the treatment of lactic acidosis, we studied its effect on lactate levels and pH in arterial and sagittal sinus blood specimens in a pediatric canine model of anoxic cardiac arrest followed by CPR. Lactate levels rose steadily in all puppies receiving DCA alone (group 1), DCA plus bicarbonate (group 2), bicarbonate alone (group 3), or neither drug (group 4). Arterial and sagittal-sinus lactate levels were in the range of 2 mmol/L during the baseline period, 6 mmol/L after anoxic arrest, and 10 mmol/L after 20 min of CPR. Bicarbonate, but not DCA, significantly raised arterial pH. Neither drug reversed the progression of acidosis in the sagittal sinus; mean pH ranged from 6.85 to 6.92 among the four groups after 20 min of CPR. We speculate that DCA did not decrease lactate levels or raise the pH in either the peripheral circulation or the CNS (sagittal sinus) because of poor perfusion achieved during closed-chest cardiac compression.

Topics: Acetates; Acidosis, Lactic; Animals; Bicarbonates; Carbon Dioxide; Dichloroacetic Acid; Dogs; Heart Arrest; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Models, Biological; Oxygen; Resuscitation; Sodium; Sodium Bicarbonate

A case report of extreme acidosis associated with diabetic metabolic decompensation is described. Treatment with conventional therapy and sodium bicarbonate resulted in complete recovery.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Adult; Bicarbonates; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Infusions, Intravenous; Lactates; Male; Sodium; Sodium Bicarbonate