Estimation of the sodium deficit in patients with hyponatremia
- Richard H Sterns, MD
Richard H Sterns, MD
- Editor-in-Chief — Nephrology
- Section Editor — Fluid and Electrolytes
- Professor of Medicine
- University of Rochester School of Medicine and Dentistry
Hyponatremia represents a relative excess of water in relation to sodium. It can be induced by a marked increase in water intake (primary polydipsia) or, in the great majority of cases, by impaired water excretion resulting from advanced renal failure or from persistent release of antidiuretic hormone (ADH) induced by effective volume depletion, the syndrome of inappropriate ADH secretion (SIADH), thiazide diuretics, adrenal insufficiency, or hypothyroidism. (See "Causes of hyponatremia in adults".)
Patients with true volume depletion and some with SIADH require saline administration to raise the serum sodium. Isotonic saline is typically sufficient in true volume depletion but is ineffective in SIADH where, if saline is given, a hypertonic solution is typically required. The mechanisms responsible for these conclusions are described elsewhere. (See "Overview of the treatment of hyponatremia in adults".)
When treating patients with moderate to severe hyponatremia with saline, formulas have been used to estimate the sodium deficit as a guide to initial therapy and to estimate the effect of a given volume of saline. The utility and limitations of these formulas will be reviewed here. An overview of the treatment of hyponatremia is presented separately. (See "Overview of the treatment of hyponatremia in adults".)
SODIUM DEFICIT FORMULA
When saline is given to treat hyponatremia, the quantity of sodium required to achieve the desired elevation in the serum sodium concentration can be estimated from the product of the serum sodium deficit per liter and the total body water (TBW):
Sodium deficit = TBW x (desired serum Na - actual serum Na)
- Oh MS, Uribarri J, Barrido D, et al. Danger of central pontine myelinolysis in hypotonic dehydration and recommendation for treatment. Am J Med Sci 1989; 298:41.
- Mohmand HK, Issa D, Ahmad Z, et al. Hypertonic saline for hyponatremia: risk of inadvertent overcorrection. Clin J Am Soc Nephrol 2007; 2:1110.
- Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med 2000; 342:1581.
- Wendland EM, Kaplan AA. A proposed approach to the dialysis prescription in severely hyponatremic patients with end-stage renal disease. Semin Dial 2012; 25:82.
- Kamel KS, Bear RA. Treatment of hyponatremia: a quantitative analysis. Am J Kidney Dis 1993; 21:439.
- Rose BD. New approach to disturbances in the plasma sodium concentration. Am J Med 1986; 81:1033.
- Fichman MP, Vorherr H, Kleeman CR, Telfer N. Diuretic-induced hyponatremia. Ann Intern Med 1971; 75:853.
- Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol 2009; 29:282.
- Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001. p.716.
- Verbalis JG, Goldsmith SR, Greenberg A, et al. Hyponatremia treatment guidelines 2007: expert panel recommendations. Am J Med 2007; 120:S1.
- Greenberg A, Verbalis JG. Vasopressin receptor antagonists. Kidney Int 2006; 69:2124.
- EDELMAN IS, LEIBMAN J. Anatomy of body water and electrolytes. Am J Med 1959; 27:256.
- Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med 2006; 355:2099.
- Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 8: advanced challenges in resuscitation: section 1: life-threatening electrolyte abnormalities. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000; 102:I217.