sodium-lactate and Hyperglycemia

A consensus has not been established for the standard treatment of hyperkalemia in the neonatal population. Most treatment regimens include a dextrose/insulin infusion. Additional agents used include calcium, sodium bicarbonate, polystyrene sulfonate, and albuterol. This study assessed the safety and efficacy of a potassium cocktail (k-cocktail) containing dextrose, insulin, calcium gluconate, and sodium lactate for treatment of neonatal hyperkalemia.. To determine whether modifications to a potassium cocktail formulation, based on a prior quality improvement project, resulted in a decrease in the incidence of hyperglycemia and acidosis associated with its use, and to evaluate the effectiveness of the k-cocktail in lowering serum potassium levels and the incidence of adverse effects.. We conducted a retrospective cohort study of neonates with hyper-kalemia who received 2 k-cocktail formulations (group 1 [n = 13], original formulation, dextrose:insulin 5:1; group 2 [n = 26], modified formulation, dextrose: insulin 3.3:1). Group 2 subjects were matched 2:1 by gestational age and birth weight with those in group 1. Variables related to safety and effectiveness of therapy were assessed by medical record review. The following tests were used to assess group differences: χ(2), Fisher exact, 2-tailed t-tests, and mixed linear models.. The incidence of hyperglycemia during the modified k-cocktail infusion in group 2 decreased from 76.9% to 21.7% (p = 0.001). Serum blood glucose concentrations increased during the infusion, on average, for group 1 infants and were unchanged during the infusion for those in group 2. The incidence of acidosis during the infusion was similar between groups (group 1 [76.9%] vs group 2 [68.2%]; p = 0.58). No significant adverse events were observed. Serum potassium concentrations decreased similarly in both groups.. An intravenous infusion including a dextrose:insulin ratio of 3.3:1, compared with a higher ratio, results in less hyperglycemia and appears to be as effective in decreasing potassium concentrations in newborns.

Topics: Acidosis; Blood Glucose; Calcium Gluconate; Cohort Studies; Drug Therapy, Combination; Glucose; Humans; Hyperglycemia; Hyperkalemia; Infant; Infusions, Intravenous; Insulin; Medical Records; Potassium Compounds; Retrospective Studies; Sodium Lactate; Treatment Outcome

Hyperlactatemia is a prominent feature of cardiogenic shock. It can be attributed to increased tissue production of lactate related to dysoxia and to impaired utilization of lactate caused by liver and tissue underperfusion. The aim of this prospective observational study was to determine the relative importance of these mechanisms during cardiogenic shock.. Two groups of subjects were compared: seven cardiac surgery patients with postoperative cardiogenic shock and seven healthy volunteers.. Lactate metabolism was assessed by using two independent methods: a) a pharmacokinetic approach based on lactate plasma level decay after the infusion of 2.5 mmol x kg(-1) of sodium lactate; and b) an isotope dilution technique for which the transformation of [13C]lactate into [13C]glucose and 13CO2 was measured. Glucose turnover was determined using 6,62H2-glucose.. All patients suffered from profound shock requiring high doses of inotropes and vasopressors. Mean arterial lactate amounted to 7.8 +/- 3.4 mmol x L(-1) and mean pH to 7.25 +/- 0.07. Lactate clearance was not different in the patients and controls (7.8 +/- 3.4 vs. 10.3 +/- 2.1 mL x kg(-1) x min(-1)). By contrast, lactate production was markedly enhanced in the patients (33.6 +/- 16.4 vs. 9.6 +/- 2.2 micromol x kg(-1) x min(-1); p < .01). Exogenous [13C]lactate oxidation was not different (107 +/- 37 vs. 103 +/- 4 mmol), and transformation of [13C]lactate into [13C]glucose was not different (20.0 +/- 13.7 vs. 15.2% +/- 6.0% of exogenous lactate). Endogenous glucose production was markedly increased in the patients (1.95 +/- 0.26 vs. 5.3 +/- 3.0 mg x kg(-1) x min(-1); p < .05 [10.8 +/- 1.4 vs. 29.4 +/- 16.7 micromol x kg(-1) x min(-1)]), whereas net carbohydrate oxidation was not different (1.7 +/- 0.5 vs. 1.3 +/- 0.3 mg x kg(-1) x min(-1) [9.4 +/- 2.8 vs. 7.2 +/- 1.7 micromol x kg(-1) x min(-1)]).. Hyperlactatemia in early postoperative cardiogenic shock was mainly related to increased tissue lactate production, whereas alterations of lactate utilization played only a minor role. Patients had hyperglycemia and increased nonoxidative glucose disposal, suggesting that glucose-induced stimulation of tissue glucose uptake and glycolysis may contribute significantly to hyperlactatemia.

Topics: Acidosis, Lactic; Adult; Aged; Bilirubin; Cardiac Surgical Procedures; Case-Control Studies; Female; Glucose; Glycolysis; Hemodynamics; Humans; Hydrocortisone; Hyperglycemia; Lactic Acid; Liver; Male; Middle Aged; Oxidation-Reduction; Prospective Studies; Shock, Cardiogenic; Sodium Lactate; Survival Analysis; Tissue Distribution

Both hyperglycemia and hyperinsulinemia stimulate whole body and muscle glucose disposal. To define the impact of increased lactate concentration (4-5 mM) on muscle glucose disposal during hyperglycemia, we studied anesthetized normal rats infused with either sodium lactate or sodium bicarbonate as control. Animals were studied under hyperglycemic clamp (13 mM) using [3-3H]glucose (study 1) and 2-deoxy-[1-3H]glucose (study 2) to assess glucose rate of disappearance (Rd), glycolytic flux (GF), glycogen synthesis, and glucose utilization index by different tissues. Moreover, in study 3, the effect of lactate on the pattern of plasma insulin response to hyperglycemia was evaluated. In study 1, lactate infusion resulted in an increased Rd (38.7 +/- 1.7 vs. 32.3 +/- 1.3 mg.min-1.kg-1; P < 0.01), which was explained by an enhanced rate of glycogen synthesis (23.0 +/- 1.7 vs. 14.7 +/- 1.2 mg.min-1.kg-1; P < 0.001), whereas GF was unchanged. In study 2, lactate-infused animals showed an increased 2-deoxy-glucose disposal and a stimulated glycogen synthase activity as well as an increased glycogen accumulation at the end of the study in several skeletal muscles. In study 3, lactate did not induce any change in either early or late insulin response to hyperglycemia. In conclusion, our results show that muscle glycogen deposition may be enhanced by elevated lactate levels under hyperglycemic conditions and support a role for lactate in the regulation of glucose homeostasis.

Topics: Animals; Deoxyglucose; Glucose; Glucose Clamp Technique; Glycogen; Glycogen Synthase; Glycolysis; Hyperglycemia; Infusions, Intravenous; Kinetics; Male; Muscle, Skeletal; Rats; Rats, Sprague-Dawley; Sodium Bicarbonate; Sodium Lactate; Tritium