DISORDERS OF FLUIDS AND ELECTROLYTES Electrolyte and Acid–Base Disturbances in Patients with Diabetes Mellitus THE PREVALENCE OF DIABETES IS INCREASING RAPIDLY (original) (raw)
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Principles of Quantitative Fluid and Cation Replacement in Extreme Hyperglycemia
Cureus, 2013
Hyperglycemia may cause profound deficits of water, sodium and potassium through osmotic diuresis, which continues during treatment as long as there is glucosuria. Replacement fluids should cover both the deficits at presentation and the ongoing losses during treatment. At presentation with hyperglycemia, quantitative estimates of the deficits in water, sodium and potassium are based on rapid body weight changes, which indicate changes in body water, and on the serum sodium concentration corrected to a normal serum glucose level. The corrected serum sodium concentration provides a measure of the water deficit relative to the cation deficit (sodium, plus potassium) that is useful in guiding the choice of monovalent cation concentration in the initial replacement fluids. Monitoring clinical status, serum chemistries (glucose, sodium, potassium, total carbon dioxide), urine flow rate, and urine chemistries (sodium and potassium) during the course of fluid and cation replacement therapy is critical. This monitoring guides the volume and composition of replacement solutions for deficits developing during treatment and the management of potassium balance and acid-base abnormalities, including metabolic acidosis, respiratory acidosis, rarely, and others.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 1986
When serum glucose concentration is nearly normal, serum sodium concentration and tonicity are usually normal in ambulatory outpatient diabetics on chronic hemodialysis or peritoneal dialysis. In hyperglycemia, patients on hemodialysis do not undergo osmotic diuresis and are able to nearly normalize their serum tonicity by increasing the intake of water. Patients on peritoneal dialysis differ from hemodialysis patients because of continued loss of water in the peritoneal dialysate and achieve only partial correction of tonicity by water consumption. The model currently used to predict changes in serum sodium concentration and in tonicity from hyperglycemia assumes no changes in external balance of body water or solute during development of hyperglycemia and, therefore, is not applicable in ambulatory dialysis patients with intact thirst mechanism, because of water retention. In ambulatory patients on chronic dialysis, clinical manifestations of hyperglycemia include thirst, water in...
EVALUATION OF HYDRATION STATUS OF PATIENTS WITH HYPERGLYCEMIA
Background: Acute hyperglycemia increases serum osmolality which leads to a rapid decline in serum sodium levels. Consequently, assessment of hydration status in individuals with hyperglycemia remains difficult. The goal of this study was to compare common equations that estimate osmolality to measured serum osmolality in patients hospitalized with hyperglycemia. Methods: In this cross-sectional study, data was collected from adult patients with serum glucose levels greater than 200 mg/dL. Serum osmolality was measured directly and compared to osmolality estimates using the Dorwart equation and the Rasouli equation. Sodium correction factors for hyperglycemia of 1.6 and 2.4 were also utilized for each equation, yielding six total equations. Patients greater than 18 years of age with measured serum osmolality ≥ 295 mOsm/L were included in the analysis. Regression analysis was performed in order to determine the best equation to predict hydration status of patients with hyperglycemia. Results: A total of 195 hospitalized adults with hyperglycemia were evaluated for inclusion in the study. Twelve of 195 hyperglycemic patients had normal hydration (serum osmolality 280-294 mOsm/L), and thus were excluded from the analysis. Among the equations utilized, the Rasouli equation utilizing a sodium correction factor of 2.4 was the most accurate predictor of dehydration, correctly identifying 94% of those patients. Conclusions: The two commonly used equations to estimate osmolality consistently underestimated the actual measured osmolality level of patients with hyperglycemia. The Rasouli equation utilizing a sodium correction factor of 2.4 was the most accurate equation for predicting measured osmolality; however, it still tended to underestimate osmolality. In order to determine the hydration status of patients with hyperglycemia rapidly, we recommend direct measurement of serum osmolality.
Kidney International, 1993
Role of hyperglycemia and insulin resistance in determining sodium retention in non-insulin-dependent diabetes. Sodium retention has been advocated to give rise to hypertension in humans. Increases in blood glucose and insulin concentrations ensue in the stimulation of sodium reabsorption by the kidney. Although the combined occurrence of hyperglycemia and hyperinsulinemia, frequently secondary to insulin resistance with regard to carbohydrate metabolism, is a hallmark of non-insulin dependent diabetes (NIDDM), the role of these abnormalities in determining an impaired natriuresis in NLDDM is not yet fully understood. We studied sodium homeostasis in 14 control subjects and 59 NIDDM normotensive, normoalbuminuric patients who were divided into two groups with markedly impaired (Group 2 NIDDM: 30) and less severely impaired (Group 1 NIDDM: 29) insulin sensitivity during euglycemic-hyperinsulinemic (80 to 90 U/ml plasma insulin) clamp. A hyperglycemic (9 mmol/liter plasma glucose)-nearly euinsulinemic (20 to 40 U/ml plasma insulin) clamp was also performed in the same 14 controls and in two cohorts of 22 Group 2 and 17 Group 1 NIDDM patients. The two groups of patients had similar overnight fasting glucose levels (Group 1 NIDDM vs. Group 2 NIDDM: 176 13 vs. 185 15 mg/dl, mean SE). Conversely, overnight fasting plasma insulin was significantly higher in Group 2 NIDDM than in Group I NIDDM patients (Group 1 NIDDM vs. Group 2 NIDDM: 12 3 vs. 18 3 U/ml, P < 0.05). Both NIDDM Groups had higher plasma glucose and insulin than controls (75 4 mg/dl and 6 3 U/ml). Blood pressure levels and albumin excretion rates were slightly but significantly higher in Group 2 NIDDM, but not in Group I NIDDM patients, than in controls. Insulin administration during the euglycemic-hyperinsulinemic clamp decreased in a similar manner the sodium excretion rate in controls and in both NIDDM groups. Conversely, the sodium excretion rate was always significantly lower in Group 2 than in Group I NIDDM patients and in controls during the hyperglycemic, near euinsulinemic clamp (euglycemia and hyperglycemia; Controls vs.
Diabetes mellitus and electrolyte disorders
World journal of clinical cases, 2014
Diabetic patients frequently develop a constellation of electrolyte disorders. These disturbances are particularly common in decompensated diabetics, especially in the context of diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. These patients are markedly potassium-, magnesium- and phosphate-depleted. Diabetes mellitus (DM) is linked to both hypo- and hyper-natremia reflecting the coexistence of hyperglycemia-related mechanisms, which tend to change serum sodium to opposite directions. The most important causal factor of chronic hyperkalemia in diabetic individuals is the syndrome of hyporeninemic hypoaldosteronism. Impaired renal function, potassium-sparing drugs, hypertonicity and insulin deficiency are also involved in the development of hyperkalemia. This article provides an overview of the electrolyte disturbances occurring in DM and describes the underlying mechanisms. This insight should pave the way for pathophysiology-directed therapy, thus contribut...