sodium-bicarbonate and Diabetes-Mellitus--Type-1

Diabetic ketoacidosis is a common, serious acute complication in children with diabetes mellitus. Diabetic ketoacidosis can accompany new-onset type 1 diabetes mellitus or it can occur with established type 1 diabetes mellitus during the increased demands of an acute illness or with decreased insulin delivery due to omitted doses or insulin pump failure. Additionally, diabetic ketoacidosis episodes in children with type 2 diabetes mellitus are being reported with greater frequency. Although the diagnosis is usually straightforward in a known diabetes patient with expected findings, a fair proportion of patients with new-onset diabetes present in diabetic ketoacidosis. The initial management of children with diabetic ketoacidosis frequently occurs in an emergency department. Physicians must be aware that diabetic ketoacidosis is an important consideration in the differential diagnosis of pediatric metabolic acidosis. This review will acquaint emergency medicine clinicians with the pathophysiology, treatment, and potential complications of this disorder.

Topics: Ambulatory Care; Blood Urea Nitrogen; Brain Edema; Child; Contraindications; Creatinine; Critical Pathways; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Ketoacidosis; Diagnosis, Differential; Dose-Response Relationship, Drug; Electrolytes; Emergency Medicine; Emergency Service, Hospital; Fluid Therapy; Humans; Hypoglycemic Agents; Insulin; Phosphates; Potassium; Risk Management; Sodium Bicarbonate

Topics: Blood Glucose; Combined Modality Therapy; Continuous Renal Replacement Therapy; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Emergencies; Fluid Therapy; Humans; Insulin; Male; Middle Aged; Respiration, Artificial; Sodium Bicarbonate; Sodium-Glucose Transporter 2 Inhibitors

Hyperkalemia generally is attributable to cell shifts or abnormal renal potassium excretion. Cell shifts account for transient increases in serum potassium levels, whereas sustained hyperkalemia generally is caused by decreased renal potassium excretion. Impaired renal potassium excretion can be caused by a primary decrease in distal sodium delivery, a primary decrease in mineralocorticoid level or activity, or abnormal cortical collecting duct function. Excessive potassium intake is an infrequent cause of hyperkalemia by itself, but can worsen the severity of hyperkalemia when renal excretion is impaired. Before concluding that a cell shift or renal defect in potassium excretion is present, pseudohyperkalemia should be excluded.

Topics: Adult; Aldosterone; Chronic Disease; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Glomerular Filtration Rate; Humans; Hyperkalemia; Kidney; Kidney Tubules; Liddle Syndrome; Male; Potassium, Dietary; Renin-Angiotensin System; Sodium Bicarbonate

To ascertain whether initial depression of conscious level in children with diabetic ketoacidosis (DKA) is related to hyperosmolality, acidosis or other factors.. In 225 episodes of DKA without evidence of cerebral edema, we examined the relationship between conscious level and initial biochemical variables. We contrasted these findings with those in 42 children who later developed cerebral oedema.. On admission, 42/225 (19%) had mild (pH 7.26-7.35); 96 (44%) moderate (pH 7.11-7.25); and 80 (37%) severe DKA (pH

Topics: Adolescent; Age Factors; Blood Glucose; Brain Edema; Child; Child, Preschool; Consciousness; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Female; Humans; Hydrogen-Ion Concentration; Infant; Male; Multivariate Analysis; Osmolar Concentration; Sodium Bicarbonate; Unconsciousness

Insulin deficiency was recently shown to stimulate splanchnic protein synthesis in vivo, whereas insulin enhances small intestinal mucosal cell proliferation in vitro. Because insulin is a postprandial hormone, it was hypothesized that it has an important role in regulating small intestinal protein synthesis in humans.. Small intestinal mucosal protein synthesis was measured in C-peptide-negative patients with type 1 diabetes mellitus during insulin deprivation (n = 6) and during insulin treatment (n = 6) and in nondiabetic control subjects (n = 6). Mucosal protein synthesis was measured from the increment of [(13)C]leucine enrichment in endoscopically obtained duodenal mucosa samples during a primed continuous infusion of L-[1-(13)C]leucine.. During insulin treatment, the rate of mucosal protein synthesis in patients with type 1 diabetes was similar (1.32% +/- 0.05%/h) to that of nondiabetic controls (1.33% +/- 0.06%/h). However, during insulin deprivation, the mucosal protein synthesis rate in patients with type 1 diabetes was significantly lower (1.15% +/- 0.33%/h) than during either insulin treatment (P = 0.01) or in nondiabetic controls (P = 0.04).. These studies show that insulin is required for the maintenance of normal rates of protein synthesis in small intestinal mucosa. Because protein synthesis is an essential component of the remodeling process of this fast turning over tissue, the decline in the synthesis rate of small intestinal mucosa during insulin deprivation may be a contributing factor in the development of gastrointestinal complications that occur in poorly controlled type 1 diabetic patients.

Topics: Adult; Amino Acids; Blood Glucose; Carbon Isotopes; Diabetes Mellitus, Type 1; Female; Hormones; Humans; Insulin; Intestinal Mucosa; Intestine, Small; Kinetics; Leucine; Male; Middle Aged; Protein Biosynthesis; Reference Values; Sodium Bicarbonate

The reliability of urine glucose testing to monitor diabetic control was investigated in patients attending the Diabetic Clinic of the Tikur Anbassa Hospital in Addis Ababa between October 1994 and January 1995 with the aim of utilising it for those with a normal renal threshold who cannot afford the cost of home blood glucose monitoring. Clinically important fasting blood glucose values were taken as those > 180 mg/dl and important urine glucose values as those > or = 0.25% by Clinitest. Capillary blood glucose was determined by visual and metre readings. Urine was tested for glucose by the standard Clinitest method. There were 265 patients, 126 IDDM and 139 NIDDM. Urine glucose corresponded satisfactorily with FBG in 80% of the patients. The sensitivity, specificity, positive and negative predictive values of urine glucose results by Clinitest in comparison with FBG by metre determination were 71%, 90%, 90% and 70% and by visual determination 71%, 86%, 80%, 79% respectively. On the basis of these results we conclude that urine glucose testing by Clinitest provides reliable information in more than 70% of our diabetic patients the majority of whom cannot afford the cost of home blood glucose monitoring.

Topics: Adult; Blood Glucose; Blood Glucose Self-Monitoring; Citric Acid; Copper Sulfate; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Drug Combinations; Female; Glycosuria; Humans; Indicators and Reagents; Male; Reproducibility of Results; Sensitivity and Specificity; Sodium Bicarbonate

We have attempted to identify any characteristics which could be used to predict the development of cerebral edema in four children under 5 years of age with new onset insulin-dependent diabetes mellitus and diabetic ketoacidosis. We retrospectively analysed and compared the concentration of serum sodium (corrected for serum glucose value) and effective serum osmolality of these 4 children with values of 10 age-matched controls with new onset insulin-dependent diabetes mellitus who did not develop cerebral edema during treatment of diabetic ketoacidosis. The initial serum sodium values of the two groups were not statistically different. Patients who developed cerebral edema had lower initial serum glucose values and effective serum osmolality. During treatment, patients who developed cerebral edema had consistently lower mean serum sodium and osmolality than controls at each 4-h interval after the first 4 h of therapy. Serum sodium and osmolality declined progressively after the initiation of therapy in cerebral edema patients, while remaining stable in controls. These data suggest that children who develop cerebral edema during treatment for diabetic ketoacidosis initially may have a relatively normal serum osmolality and subsequently develop progressive hyponatremia and/or a trend of declining serum sodium before developing cerebral edema.

Topics: Brain Edema; Child, Preschool; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Hyponatremia; Infant; Insulin; Prognosis; Retrospective Studies; Sodium; Sodium Bicarbonate

Topics: Bicarbonates; Brain Edema; Child, Preschool; Dexamethasone; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Infusions, Intravenous; Insulin; Intubation, Intratracheal; Male; Mannitol; Oxygen Inhalation Therapy; 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

We have investigated whole body protein turnover in the fasted state in five normal men, five male Type 1 diabetic patients off insulin therapy, and five obese women, using IV 13C-leucine as a tracer. In diabetic patients, there was, as expected, a greater net loss of protein in the fasted state than in normal subjects. However, contrary to animal and studies in vitro, our diabetic patients in the fasted state showed a greater rate of protein synthesis than normal subjects (p less than 0.01). The increased net loss of protein in diabetic patients compared with normal subjects arose because, in the diabetic patients, protein breakdown was increased even more than protein synthesis under the conditions of this study. Plasma leucine concentration was higher in diabetic and in insulin-insensitive obese patients than in normal subjects (p less than 0.01), and higher in diabetic than in obese patients (p less than 0.05). The rate of protein synthesis per kg lean body mass was also higher in diabetic patients than in obese or normal subjects (p less than 0.01), and higher in obese than normal subjects (p less than 0.05). We conclude that, in human subjects, whole body leucine and protein metabolism are very sensitive to the action of insulin.

Topics: Adult; Bicarbonates; Blood Glucose; C-Peptide; Carbon Isotopes; Diabetes Mellitus, Type 1; Female; Humans; Insulin; Leucine; Male; Obesity; Proteins; Reference Values; Sodium Bicarbonate