![]() Hypertonicity is seen routinely in severe hyperglycemia ( 1– 5), causes potentially life-threatening neurological manifestations ( 6, 7), and represents an important component of the treatment ( 1, 2). This report addresses the management of hyperglycemic hypertonicity. These imbalances, which cause extracellular and intracellular volume deficits, changes in the concentrations of key serum ions, and hypertonicity, constitute major treatment targets ( 1). Imbalances that develop in patients with severe hyperglycemia and preserved renal function include extracellular gain of solute (glucose) and deficits of water, sodium, potassium, and other ions resulting from glycosuria. However, the corrected may change during treatment because of ongoing fluid losses and should be monitored during treatment. The corrected, computed as increase by 1.6 mmol/L per 5.6 mmol/L decrease in, provides a reasonable estimate of the degree of hypertonicity due to losses of hypotonic fluids through osmotic diuresis at presentation of DKH or HHS and should guide the tonicity of replacement solutions. However, in DKA corrected was in the hypernatremic range in several reports and rose during treatment with adverse neurological consequences in other reports. In patients with preserved renal function, mean corrected was within the eunatremic range (141.1 mmol/L) in 7,812 DKA cases, and in the range of severe hypernatremia (160.8 mmol/L) in 755 cases of HHS. Mean corrected was 139.0 mmol/L in 772 hyperglycemic episodes in CKD stage 5 patients. The theoretical prediction of increase by 1.6 mmol/L per 5.6 mmol/L decrease in in most clinical settings, except in extreme hyperglycemia or profound hypervolemia, was supported by studies of hyperglycemia in CKD stage 5 treated only with insulin. Corrected was computed separately in reports of DKA, HHS and hyperglycemia in CKD stage 5. Theoretical methods calculating the corrected and clinical reports allowing its calculation were reviewed. Prediction of the serum sodium after normalization (the corrected ) estimates the part of hypertonicity caused by osmotic diuresis. Hypertonicity from glucose gain is reversed with normalization of serum glucose () hypertonicity due to osmotic diuresis requires infusion of hypotonic solutions. Patients with stage 5 chronic kidney disease (CKD) and hyperglycemia have minimal or no osmotic diuresis patients with preserved renal function and diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS) have often large osmotic diuresis. In hyperglycemia, hypertonicity results from solute (glucose) gain and loss of water in excess of sodium plus potassium through osmotic diuresis. Murphy Veterans Affairs Medical Center, University of New Mexico School of Medicine, Albuquerque, NM, United States
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