sodium-bicarbonate and Hypoglycemia

Hyperkalemia is a common problem in both inpatients and outpatients. Many disease states (eg, chronic kidney disease) and medications may precipitate hyperkalemia. There are several drugs now available to treat hyperkalemia. Many of these drugs are relatively new. This review provides information regarding drug-induced causes of hyperkalemia and provides detailed information on the medications used to treat this problem.

Topics: Acute Disease; Administration, Intravenous; Adrenergic beta-Agonists; Arrhythmias, Cardiac; Calcium; Cation Exchange Resins; Chronic Disease; Electrocardiography; Glucose; Humans; Hyperkalemia; Hypoglycemia; Hypoglycemic Agents; Insulin; Polymers; Polystyrenes; Potassium; Silicates; Sodium Bicarbonate; Sodium Potassium Chloride Symporter Inhibitors

Hyperkalemia is a common electrolyte disorder that can result in morbidity and mortality if not managed appropriately.. This review evaluates the classic treatments of hyperkalemia and discusses controversies and new medications for management.. Potassium (K+) plays a key role in determining the transmembrane potentials of "excitable membranes" present in nerve and muscle cells. K+ is the predominant intracellular cation, and clinical deterioration typically ensues when patients develop sufficiently marked elevation in extracellular fluid concentrations of K+ (hyperkalemia). Hyperkalemia is usually detected via serum clinical laboratory measurement. The most severe effect of hyperkalemia includes various cardiac dysrhythmias, which may result in cardiac arrest and death. Treatment includes measures to "stabilize" cardiac membranes, to shift K+ from extracellular to intracellular stores, and to promote K+ excretion. Calcium gluconate 10% dosed 10 mL intravenously should be provided for membrane stabilization, unless the patient is in cardiac arrest, in which case 10 mL calcium chloride is warranted. Beta-agonists and intravenous insulin should be given, and some experts recommend the use of synthetic short-acting insulins rather than regular insulin. Dextrose should also be administered, as indicated by initial and serial serum glucose measurements. Dialysis is the most efficient means to enable removal of excess K+. Loop and thiazide diuretics can also be useful. Sodium polystyrene sulfonate is not efficacious. New medications to promote gastrointestinal K+ excretion, which include patiromer and sodium zirconium cyclosilicate, hold promise.. Hyperkalemia can be deadly, and treatment requires specific measures including membrane stabilization, cellular shift, and excretion.

Topics: Acidosis; Buffers; Cation Exchange Resins; Dialysis; Drug Combinations; Electrocardiography; Glucose; Humans; Hyperkalemia; Hypoglycemia; Insulin; Polystyrenes; Potassium; Receptor, Insulin; Sodium Bicarbonate; Transcytosis; Treatment Outcome

Insulin autoimmune syndrome is a rare cause of hyperinsulinemic hypoglycemia characterized by autoantibodies to human insulin without previous insulin use. We report a case of a patient with hyperinsulinemic hypoglycemia possibly caused by insulin antibodies induced by insulin analogs and a novel therapeutic measure for this condition.. An 84-year-old Japanese man with a 28-year history of type 2 diabetes and chronic kidney disease, treated with biphasic insulin aspart 30, experienced persistent early morning hypoglycemia with daytime hyperglycemia. Despite discontinuation of biphasic insulin aspart 30, the condition persisted even after the patient ate small, frequent meals. Sodium bicarbonate was administered to correct the chronic metabolic acidosis, which then rectified the early morning glucose level.. We believe this to be the first published case of a therapeutic approach to the treatment of hyperinsulinemic hypoglycemia associated with insulin antibodies that factors in blood pH and the correction of acidosis using sodium bicarbonate, which physicians could consider.

Topics: Acidosis; Aged, 80 and over; Alkalies; Autoimmune Diseases; Humans; Hyperinsulinism; Hypoglycemia; Insulin Antibodies; Male; Sodium Bicarbonate; Syndrome

We report a rare fatal case of acute metformin overdose in a 19-year-old woman.

Topics: Acidosis; Blood Gas Analysis; Cardiotonic Agents; Drug Overdose; Fatal Outcome; Female; Heart Arrest; Humans; Hypoglycemia; Hypoglycemic Agents; Hypotension; Long QT Syndrome; Metformin; Sodium Bicarbonate; Young Adult

Current recommendations for nutritional interventions in basketball are largely extrapolated from laboratory-based studies that are not sport-specific. We therefore adapted and validated a basketball simulation test relative to competitive basketball games using well-trained basketball players (n = 10), then employed this test to evaluate the effects of two common preexercise nutritional interventions on basketball-specific physical and skilled performance. Specifically, in a randomized and counterbalanced order, participants ingested solutions providing either 75 g carbohydrate (sucrose) 45 min before exercise (Study A; n = 10) or 2 × 0.2 g · kg(-1) sodium bicarbonate (NaHCO3) 90 and 20 min before exercise (Study B; n = 7), each relative to appropriate placebos (H2O and 2 × 0.14 g · kg(-1) NaCl, respectively). Heart rate, sweat rate, pedometer count, and perceived exertion did not systematically differ between the 60-min basketball simulation test and competitive basketball, with a strong positive correlation in heart rate response (r = .9, p < .001). Preexercise carbohydrate ingestion resulted in marked hypoglycemia (< 3.5 mmol · l(-1)) throughout the first quarter, coincident with impaired sprinting (+0.08 ± 0.05 second; p = .01) and layup shooting performance (8.5/11 versus 10.3/11 baskets; p < .01). However, ingestion of either carbohydrate or sodium bicarbonate before exercise offset fatigue such that sprinting performance was maintained into the final quarter relative to placebo (Study A: -0.07 ± 0.04 second; p < .01 and Study B: -0.08 ± 0.05 second; p = .02), although neither translated into improved skilled (layup shooting) performance. This basketball simulation test provides a valid reflection of physiological demands in competitive basketball and is sufficiently sensitive to detect meaningful changes in physical and skilled performance. While there are benefits of preexercise carbohydrate or sodium bicarbonate ingestion, these should be balanced against potential negative side effects.

Topics: Athletic Performance; Basketball; Blood Glucose; Dietary Carbohydrates; Eating; Fatigue; Heart Rate; Humans; Hypoglycemia; Male; Physical Endurance; Physical Exertion; Sodium Bicarbonate; Sports Nutritional Physiological Phenomena; Sweat; Task Performance and Analysis; Time Factors; Young Adult

We report on a child with moyamoya disease combined with von Gierke's disease. A 7-year-old girl with von Gierke's disease had a stroke associated with moyamoya disease. She had had many episodes of hypoglycemia and severe metabolic acidosis before surgery. General anesthesia was induced with midazolam 3 mg and fentanyl 100 microg followed by rocuronium 12 mg. After tracheal intubation, anesthesia was maintained with sevoflurane 2.5% in 33% oxygen and 66% nitrous oxide. We used mainly mixture of saline and glucose as intraoperative fluid instead of acetated Ringer solution, and controlled administration of glucose according to blood glucose levels. The patient's plasma lactate levels and base excess during operation showed changes compared with those before operation, because sodium bicarbonate was used during the surgery. The duration of anesthesia was 374 minutes. The patient woke up and spontaneous respiration returned, and the trachea was extubated in the operating room. We were able to manage this case safely without any complications.

Topics: Acidosis; Anesthesia, General; Child; Female; Glucose; Glycogen Storage Disease Type I; Humans; Hypoglycemia; Infusions, Intravenous; Intraoperative Care; Intraoperative Complications; Moyamoya Disease; Sodium Bicarbonate; Vascular Surgical Procedures

Topics: Evidence-Based Medicine; Glucose; Humans; Hyperkalemia; Hypoglycemia; Insulin; Intensive Care Units; Sodium Bicarbonate

Topics: Acidosis; Ampicillin; Animals; Anti-Bacterial Agents; Atropine; Blood Cell Count; Blood Chemical Analysis; Cephalosporins; Electrolytes; Female; Fluid Therapy; Gentamicins; Glucose; Horse Diseases; Horses; Hydrogen-Ion Concentration; Hypoglycemia; Infusions, Intravenous; Sepsis; Shock; Sodium Bicarbonate; Uveitis

In response to hypoglycemia, healthy individuals rapidly antagonize insulin action on glucose and lipid metabolism, but the effects on protein metabolism are unclear. Because amino acids are an important substrate for gluconeogenesis and a fuel alternative to glucose for oxidation, we evaluated whether hypoglycemia antagonizes the hypoaminoacidemic and the antiproteolytic effects of insulin and changes the de novo synthesis of glutamine, a gluconeogenic amino acid. To this purpose, in 7 healthy subjects, we performed 2 studies, 3.5 h each, at similar insulin but different glucose concentrations (i.e., 4.9 +/- 0.1 mmol/l [euglycemic clamp] or 2.9 +/- 0.2 mmol/l [hypoglycemic clamp]). As expected, hypoglycemia antagonized the insulin suppression of glucose production achieved in euglycemia (from 21 +/- 15 to 116 +/- 12% of basal, P < 0.001), the stimulation of glucose uptake (from 207 +/- 28 to 103 +/- 7% of basal, P < 0.01) and the suppression of circulating free fatty acids (from 30 +/- 5 to 80 +/- 17% of basal, P < 0.001). In contrast, hypoglycemia increased the insulin suppression of circulating leucine (from 63 +/- 1 to 46 +/- 2% of basal, P < 0.001) and phenylalanine (from 79 +/- 3 to 64 +/- 3% of basal, P < 0.001) concentrations. Hypoglycemia did not change the insulin suppression of proteolysis (from 79 +/- 2 to 82 +/- 4% of basal, P < 0.001). However, hypoglycemia doubled the insulin suppression of the glutamine concentrations (from 84 +/- 3 to 63 +/- 3% of basal, P < 0.01) in the absence of significant changes in the glutamine rate of appearance, but it also caused an imbalance between glutamine uptake and release. This study demonstrates that successful counterregulation does not affect proteolysis. Moreover, it does not increase the availability of circulating amino acids by de novo synthesis. In contrast, despite the lower concentration of circulating amino acids, hypoglycemia increases the uptake of glutamine that can be used for gluconeogenesis and as a fuel alternative to glucose.

Topics: Adult; Blood Glucose; C-Peptide; Carbon Isotopes; Fatty Acids, Nonesterified; Female; Glucose Clamp Technique; Glutamine; Humans; Hypoglycemia; Insulin; Insulin Secretion; Kinetics; Leucine; Male; Nitrogen Isotopes; Proteins; Reference Values; Sodium Bicarbonate

To investigate the effect of low-dose versus high-dose insulin treatment of Kussmaul's coma, the authors treated 2 groups of relevant patients. Group I treated with low-dose insulin in combination with other therapeutic measures achieved a progressive decrease of glycemia within 8 hours. Complications were not registered. Group II on high-dose insulin scheme exhibited a drop in blood sugar resultant in hypoglycemia in 4, hypotonia in 2, brain edema in 1 patient. The absence of complications, availability and simplicity support the advantages of the low-dose regime which is now widely introduced into clinical practice.

Topics: Adolescent; Adult; Aged; Bicarbonates; Diabetic Coma; Diabetic Ketoacidosis; Drug Therapy, Combination; Female; Humans; Hyperglycemia; Hypoglycemia; Infusions, Intravenous; Injections, Intramuscular; Insulin; Male; Middle Aged; Sodium; Sodium Bicarbonate

The recovery of weanling mice from insulin-induced hypoglycemic stupor-coma after injection of sodium -L(+)-lactate (18 mmol/kg) was as rapid (10 min) as in litter-mates treated with glucose (9 mmol/kg). Stimulated by this dramatic action, we studied the effects of lactate injection on brain carbohydrate and energy metabolism in normal and hypoglycemic mice; blood and liver tissue were also studied. Ten minutes after lactate injection in normal mice, plasma lactate levels increased by 15 mmol/L; plasma glucose levels were unchanged, but the beta-hydroxybutyrate concentration fell 59%. In the brains of these animals, glucose levels increased 2.3-fold, and there were significant increases in brain glycogen (10%), glucose-6-phosphate (27%), lactate (68%), pyruvate (37%), citrate (12%), and malate (19%); the increase in alpha-ketoglutarate (32%) was not significant. Lactate injection reduced the cerebral glucose-use rate 40%. These changes were not due to lactate-induced increases in blood [HCO-3] and pH (examined by injection of 15 mmol/kg sodium bicarbonate). Although lactate injection of hypoglycemic mice doubled levels of glucose in plasma and brain (not significant) and most of the cerebral glycolytic intermediates, values were far below normal (still in the range seen in hypoglycemic animals). By contrast, citrate and alpha-ketoglutarate levels returned to normal; the large increase in malate was not significant. Reduced glutamate levels increased to normal, and elevated aspartate levels fell below normal. Thus, recovery from hypoglycemic stupor does not necessarily depend on normal levels of plasma and/or brain glucose (or glycolytic intermediates).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Animals, Suckling; Bicarbonates; Brain; Energy Metabolism; Hydrogen-Ion Concentration; Hypoglycemia; Insulin Coma; Lactates; Lactic Acid; Liver; Mice; Oxidation-Reduction; Sodium Bicarbonate