Hypernatremia in Hyperglycemia: Clinical Features and Relationship to Fractional Changes in Body Water and Monovalent Cations during Its Development

Author:

Wagner Brent123ORCID,Ing Todd S.4,Roumelioti Maria-Eleni1,Sam Ramin5,Argyropoulos Christos P.1ORCID,Lew Susie Q.6,Unruh Mark L.7,Dorin Richard I.8ORCID,Degnan James H.9,Tzamaloukas Antonios H.10

Affiliation:

1. Division of Nephrology, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87122, USA

2. Kidney Institute of New Mexico, University of New Mexico Health Sciences Center, Albuquerque, NM 87122, USA

3. Raymond G. Murphy Veterans Affairs Medical Center, Albuquerque, NM 87108, USA

4. Department of Medicine, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA

5. Department of Medicine, Zuckerberg San Francisco General Hospital, University of California in San Francisco School of Medicine, San Francisco, CA 94110, USA

6. Department of Medicine, School of Medicine and Health Sciences, George Washington University, Washington, DC 20037, USA

7. Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87122, USA

8. Department of Medicine, Division of Endocrinology, Raymond G. Murphy Veterans Affairs Medical Center, University of New Mexico, Albuquerque, NM 87108, USA

9. Department of Mathematics and Statistics, University of New Mexico, Albuquerque, NM 87131, USA

10. Research Service, Department of Medicine, Raymond G. Murphy Veterans Affairs Medical Center, University of New Mexico School of Medicine, Albuquerque, NM 87108, USA

Abstract

In hyperglycemia, the serum sodium concentration ([Na]S) receives influences from (a) the fluid exit from the intracellular compartment and thirst, which cause [Na]S decreases; (b) osmotic diuresis with sums of the urinary sodium plus potassium concentration lower than the baseline euglycemic [Na]S, which results in a [Na]S increase; and (c), in some cases, gains or losses of fluid, sodium, and potassium through the gastrointestinal tract, the respiratory tract, and the skin. Hyperglycemic patients with hypernatremia have large deficits of body water and usually hypovolemia and develop severe clinical manifestations and significant mortality. To assist with the correction of both the severe dehydration and the hypovolemia, we developed formulas computing the fractional losses of the body water and monovalent cations in hyperglycemia. The formulas estimate varying losses between patients with the same serum glucose concentration ([Glu]S) and [Na]S but with different sums of monovalent cation concentrations in the lost fluids. Among subjects with the same [Glu]S and [Na]S, those with higher monovalent cation concentrations in the fluids lost have higher fractional losses of body water. The sum of the monovalent cation concentrations in the lost fluids should be considered when computing the volume and composition of the fluid replacement for hyperglycemic syndromes.

Publisher

MDPI AG

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