Prediction of the change in extracellular sodium concentration in hyperglycemia complicated by severe losses of water and solute (original) (raw)
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AND TYPE 2 DIAbetes now accounts for 20 to 50% of cases of new-onset diabetes in young people. 1 Electrolyte disturbances are common in patients with diabetes and may be the result of an altered distribution of electrolytes related to hyperglycemia-induced osmotic fluid shifts or of total-body deficits brought about by osmotic diuresis. Complications from end-organ injury and the therapies used in the management of diabetes may also contribute to electrolyte disturbances. In this review, we highlight the ways in which specific electrolytes may be influenced by dys-regulation in glucose homeostasis. S ODI UM Increases in plasma glucose concentration can lead to changes in plasma sodium concentration through several mechanisms. Elevations in glucose concentration increase plasma tonicity, creating an osmotic driving force that favors the movement of water from the intracellular space to the extracellular space, thereby diluting the extracellular concentration of sodium. The plasma sodium concentration is usually low as a result of this osmotic flux of water. Increased or normal plasma sodium concentrations in the presence of hyperglycemia indicate a clinically significant deficit in total body water. A consensus statement and clinical practice guidelines on the management of hyperglycemic crises in adults recommend the addition of a correction factor of 1.6 mg per deciliter to the measured plasma sodium concentration for each 100 mg per deciliter (5.6 mmol per liter) of glucose above 100 mg per deciliter to account for the dilutional effect of glucose. 2,3 Correcting the plasma sodium concentration in patients with glycemia helps to assess the magnitude of the deficit of sodium and water and provides a reasonable initial estimate of the required tonicity of replacement fluids during the course of therapy. Correction factors predicting plasma sodium concentration after the normalization of hyperglycemia vary from a low of 1.35 mmol per liter to as high as 4.0 mmol per liter 4,5 (for additional discussion, see the Supplementary Appendix, available with the full text of this article at NEJM.org). Such variability in the range of correction factors appears to be due to the fact that patients with preserved renal function represent an open hyperglycemic system that introduces a number of variables, all difficult to quantify, and renders the use of a standardized correction factor imprecise. It should be emphasized that the corrected sodium concentration at the time of sampling does not account for the effects of osmotic diuresis and fluid intake during treatment, both of which are highly variable and unpredictable. Frequent calculations of the corrected sodium concentration, along with
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.
Estimating excess glucose, sodium and water deficits in non-ketotic hyperglycaemia
Nephrology Dialysis Transplantation, 2007
Background. The treatment of solute addition, Na and water losses in hyperglycaemic hyponatraemia is guided by clinical judgement rather than by a quantitative assessment. Methods. We devised an iteration method to compute glucose appearance (G A ) within the extracellular space, to obtain the PNa (plasma sodium concentration) expected by glucose addition only (PNa G ). The difference between this and the actual measurement (PNa 1 ) was used to compute the attending Na and/or volume depletion, and the PNa expected during correction. The equations were validated on computer-built models, where the electrolyte derangements were simulated, generating true values of plasma glucose (P G ) and Na concentrations, from which surfeit and deficits were back-calculated with our formulas. We also computed G A and PNa G on 43 patients who were stratified into a group with normal hydration (PNa 1 ¼ PNa G ), one with prevalent Na depletion (PNa 1 < PNa G ), and one with prevalent volume depletion (PNa 1 > PNa G ). The volume conditions established by our computations were compared by logistic regression analysis with those assessed from clinical laboratory data.
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.
Role of hyperglycemia in the pathogenesis of Na+/K+ disturbance
International Journal of Research in Medical Sciences, 2016
Diabetes mellitus (DM) is a chronic disease characterized by disorders in carbohydrate, fat and protein metabolism, a consequence of insulin resistance or impaired -cell function, resulting in insulin deficiency or absence. Failure of some tissues, especially muscle and adipose tissue, to take up glucose due to insulin resistance (Type 2 diabetes mellitus) or absence of insulin (Type 1 diabetes mellitus) because GLUT-4 remains sequestered within cells , contributes greatly to hyperglycemia. 1 High glucose levels may cause retinopathy, nephropathy, neuropathy and also an increased risk for cardiovascular disease. The complications of diabetes are metabolic imbalance, blood vessel degeneration, electrolyte imbalance have become a leading cause of impairment of human health. 2,3 Electrolytes play an important role in maintaining acidbase balance, membrane potential, blood clotting, muscle contraction, nerve conduction and control body fluid. 2 ABSTRACT Background: Electrolytes play an important role in maintaining acid-base balance, blood-clotting, control body fluid, muscle contraction, nerve conduction. The diabetic patients develop frequently a constellation of electrolyte imbalance. Imbalance in electrolyte concentration may affect the course of diabetes and its management. It has been reported that there is an inverse relationship between serum sodium (Na+) and potassium (K+) levels in diabetic patients. The aim of present study was to determine whether such relation is seen in context of Nepal and whether this inverse relation depends upon serum glucose levels in diabetic patients for their glycemic control. Methods: This is a retrospective study performed on records of 135 diabetic patients who were treated at outpatient clinic of Kist Medical College and Teaching Hospital from 15 June 2015-15 July 2015. Fasting blood glucose (FPG) level was analyzed with semiautomatic analyzer-humalyzer 3000 by GOD-POD method and Na+ and K+ levels were analyzed with ion selective electrode-nova electrolyte. The relationship among serum Na+ level, serum K+ levels and Fasting plasma glucose levels were determined by SPSS version 20. Results: Serum Na+ level was insignificantly negatively correlated (r=-0.091, p=0.296) with FPG level while a positive correlation of serum K+ level (r=0.235, p=0.006) was seen with FPG level and an inverse relation between serum Na+ and K+ was found. Age showed insignificant negative correlation with serum Na+ (r=-0.203, p=0.018), insignificant positive correlation with K+ (r=0.067, p=0.443) and insignificant negative correlation with FPG (r=-0.045, p=0.608). Conclusions: Hyperglycemia disrupts the balance of serum Na+ and K+ in uncontrolled diabetes mellitus.
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.