Abstract
In hyperglycemia, hypertonicity results from solute (glucose) gain and loss of water in excess of sodium plus potassium through osmotic diuresis. 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. Hypertonicity from glucose gain is reversed with normalization of serum glucose ([Glu]); hypertonicity due to osmotic diuresis requires infusion of hypotonic solutions. Prediction of the serum sodium after [Glu] normalization (the corrected [Na]) estimates the part of hypertonicity caused by osmotic diuresis. Theoretical methods calculating the corrected [Na] and clinical reports allowing its calculation were reviewed. Corrected [Na] was computed separately in reports of DKA, HHS and hyperglycemia in CKD stage 5. The theoretical prediction of [Na] increase by 1.6 mmol/L per 5.6 mmol/L decrease in [Glu] 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. Mean corrected [Na] was 139.0 mmol/L in 772 hyperglycemic episodes in CKD stage 5 patients. In patients with preserved renal function, mean corrected [Na] 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. However, in DKA corrected [Na] was in the hypernatremic range in several reports and rose during treatment with adverse neurological consequences in other reports. The corrected [Na], computed as [Na] increase by 1.6 mmol/L per 5.6 mmol/L decrease in [Glu], 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, the corrected [Na] may change during treatment because of ongoing fluid losses and should be monitored during treatment.
Highlights
Imbalances that develop in patients with severe hyperglycemia and preserved renal function include extracellular gain of solute and deficits of water, sodium, potassium, and other ions resulting from glycosuria
Glucose accumulation in the extracellular compartment contributes to tonicity (Ton), which is expressed by the formula [9]: Ton = 2 × [Na] + Glu mOsm/L
In hyperglycemic crises occurring in patients with preserved renal function, who represent an open system, [Na] receives influences from three pathophysiologic processes: rise in [Glu] and water gain cause [Na] decreases, while osmotic diuresis causes [Na] increase. In these patients, quantitating the isolated effect of glucose gain is imperative because this effect is predictable with a reasonable degree of certainty, as shown in the previous section, and more importantly, it will disappear with correction of hyperglycemia without requiring additional measures
Summary
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. In hyperglycemic crises occurring in patients with preserved renal function, who represent an open system, [Na] receives influences from three pathophysiologic processes: rise in [Glu] and water gain cause [Na] decreases, while osmotic diuresis causes [Na] increase In these patients, quantitating the isolated effect of glucose gain is imperative because this effect is predictable with a reasonable degree of certainty, as shown, and more importantly, it will disappear with correction of hyperglycemia without requiring additional measures. Mean corrected [Na] was in the eunatremic range in hyperglycemia of patients with CKD stage 5
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