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Background/Objectives: Hyperglycemic emergencies cause significant losses of body water, sodium, and potassium. This report presents a method for computing the actual losses of water and monovalent cations in these emergencies. Methods: We developed formulas for computing the losses of water and monovalent cations as a function of the presenting serum sodium and glucose levels, the sum of the concentrations of sodium plus potassium in the lost fluids, and body water at the time of hyperglycemia presentation as measured by bioimpedance or in the initial euglycemic state as estimated by anthropometric formulas. The formulas for computing the losses from hyperglycemia were tested in examples of hyperglycemic episodes. Results: The formulas were tested in two patient groups, those with or without known weight loss during the development of hyperglycemia. In the first group, these formulas were applied to estimate the losses of body water and monovalent cations in (a) a previously published case of a boy with diabetic ketoacidosis and known weight loss who, during treatment not addressing his water deficit, developed severe hypernatremia and (b) a comparison of water loss computed by this new method with the reported average fluid gained during treatment of the hyperglycemic hyperosmolar state in a published study. In the second group, the formulas were applied in hypothetical subjects with varying levels of initial body water, serum sodium, and glucose at the time of hyperglycemia and sums of sodium and potassium concentrations in the lost fluids. Conclusions: Losses of body water and monovalent cations, which determine the severity of dehydration and hypovolemia, vary significantly between patients with hyperglycemic emergencies presenting with the same serum glucose and sodium concentrations. These losses can be calculated using estimated or measured body water values. Prospective studies are needed to test this proof-of-concept report.

The key message from the 1958 Edelman study states that combinations of external gains or losses of sodium, potassium and water leading to an increase of the fraction (total body sodium plus total body potassium) over total body water will raise the serum sodium concentration ([Na]S), while external gains or losses leading to a decrease in this fraction will lower [Na]S. A variety of studies have supported this concept and current quantitative methods for correcting dysnatremias, including formulas calculating the volume of saline needed for a change in [Na]S are based on it. Not accounting for external losses of sodium, potassium and water during treatment and faulty values for body water inserted in the formulas predicting the change in [Na]S affect the accuracy of these formulas. Newly described factors potentially affecting the change in [Na]S during treatment of dysnatremias include the following: (a) exchanges during development or correction of dysnatremias between osmotically inactive sodium stored in tissues and osmotically active sodium in solution in body fluids; (b) chemical binding of part of body water to macromolecules which would decrease the amount of body water available for osmotic exchanges; and (c) genetic influences on the determination of sodium concentration in body fluids. The effects of these newer developments on the methods of treatment of dysnatremias are not well-established and will need extensive studying. Currently, monitoring of serum sodium concentration remains a critical step during treatment of dysnatremias.

PRESENTATION Three patients developed acute respiratory failure during treatment of diabetic ketoacidosis (DKA) diagnosed by the combination of hyperglycemia, anion gap metabolic acidosis, and presence of ketone bodies in serum. [...]

Respiratory failure complicating the course of diabetic ketoacidosis (DKA) is a source of increased morbidity and mortality. Detection of respiratory failure in DKA requires focused clinical monitoring, careful interpretation of arterial blood gases, and investigation for conditions that can affect adversely the respiration. Conditions that compromise respiratory function caused by DKA can be detected at presentation but are usually more prevalent during treatment. These conditions include deficits of potassium, magnesium and phosphate and hydrostatic or non-hydrostatic pulmonary edema. Conditions not caused by DKA that can worsen respiratory function under the added stress of DKA include infections of the respiratory system, pre-existing respiratory or neuromuscular disease and miscellaneous other conditions. Prompt recognition and management of the conditions that can lead to respiratory failure in DKA may prevent respiratory failure and improve mortality from DKA.

We analyzed abnormalities in serum potassium ([K]) in 40 episodes of diabetic ketoacidosis (DKA)--6 episodes in peritoneal dialysis (PD) and 34 episodes in hemodialysis (HD)--and in 245 episodes of nonketotic hyperglycemia (NKH)--70 episodes in PD and 175 episodes in HD. Serum glucose ([Glu]) was 25 mmol/L or higher in all episodes. We compared the PD and HD hyperglycemic episodes separately for DKA and NKH. For DKA, [Glu] was 55.5 + 4.8 mmol/L in PD and 51.9 +/- 12.2 mmol/L in HD [p = nonsignificant (NS)], and [K] was 6.4 +/- 1.5 mmol/L in PD and 6.3 +/- 1.1 mmol/L in HD (p=NS). Also for DKA, [K] was 5.5 mmol/L or higher in 4 episodes (66.7%) in PD and in 26 episodes (76.5%) in HD (p=NS), and 6.0 mmol/L or higher in 3 episodes (50.0%) in PD and in 22 (episodes 64.7%) in HD (p=NS). For NKH, [Glu] was 39.4 +/- 14.7 mmol/L in PD and 37.8 +/- 12.4 mmol/L in HD (p=NS), and [K] was 4.3 +/- 0.9 mmol/L in PD and 5.1 +/- 0.8 mmol/L in HD (p < 0.001). Also for NKH, [K] was 5.5 mmol/L or higher in 7 episodes (10.0%) in PD and in 55 episodes (31.4%) in HD (p < 0.001), and 6.0 mmol/L or higher in 4 episodes (5.7%) in PD and in 31 episodes (17.7%) in HD (p = 0.023). Serum sodium, tonicity, urea, osmolality, creatinine, chloride and anion gap, and arterial blood pH and partial pressure of carbon dioxide did not differ between PD and HDfor either DKA or NKH episodes, but serum total carbon dioxide content was lower in PD than in HD DKA episodes (6.5 + 3.8 mmol/L vs. 9.5 + 2.8 mmol/L, p = 0.038), and higher in PD than in HD NKH episodes (22.5 + 6.0 mmol/L vs. 20.9 + 4.4 mmol/L, p = 0.004). Although PD and HD DKA episodes appear not to differ in [K], the mean [K] and the frequency of hyperkalemia are both lower in PD than in HD NKH episodes. Differences between PD and HD in acid-base balance and, probably, in other factors affecting [K] (such as mineralocorticoid metabolism and blood levels) may account for the differences in [K] between PD and HD NKH episodes.