Correspondence

Hypernatremia

N Engl J Med 2000; 343:817-818September 14, 2000

Article

To the Editor:

In the review article on hypernatremia by Adrogué and Madias (May 18 issue),1 we wonder whether the patient described as having a pure water loss does not in fact have a sodium gain as well. Our reasoning is that if a 20 percent increase in the plasma sodium concentration is due to a pure water deficit, then there should be a corresponding 20 percent reduction in the total body water distributed equally among the intracellular-fluid and the extracellular-fluid compartments. A decline in the extracellular fluid of this degree should have been clinically apparent, identifiable at least by the presence of postural hypotension. Moreover, patients with hypovolemia who consume sodium tend to retain it in response to their reduced extracellular-fluid volume. If the clinical observations are taken at face value, the increase in the plasma sodium concentration of 28 mmol per liter (168 mmol per liter – 140 mmol per liter) in the presence of an extracellular-fluid volume of 13.2 liters means that the sodium content has increased by 370 mmol. This 20 percent increase in the plasma sodium concentration will reduce the intracellular-fluid volume by 4.2 liters (20 percent of 21 liters). If we are correct, the goals of therapy should be to cause a loss of 370 mmol of sodium from the extracellular-fluid compartment and an increase of 4.2 liters of electrolyte-free water in the intracellular-fluid compartment. The recognition of the events that occur in the intracellular-fluid and the extracellular-fluid compartments helps in the design of therapy.2

Mitchell L. Halperin, M.D.
David Z.I. Cherney, M.D.
University of Toronto, Toronto, ON M5B 1A6, Canada

2 References

1
Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med 2000;342:1493-1499
Full Text | Web of Science | Medline

2
Halperin ML, Goldstein MB. Fluid, electrolyte, and acid-base physiology: a problem-based approach. 3rd ed. Philadelphia: W.B. Saunders, 1999:346.

To the Editor:

My chief concern is the method of choosing a solution and its rate of administration suggested by Adrogué and Madias. The authors recommend formulas for use in estimating the effect of 1 liter of any solution on the serum sodium concentration. The derivation of these formulas is far from obvious. Most clinicians would use them in a “cookbook” approach. When the physiologic basis for formulas is not understood, they are often forgotten or used incorrectly. The method suggested by Feig and McCurdy in their now classic review1 is easily understood and therefore preferable. Although it is true that this conventional formula is only useful for calculating the water deficit, the approach of Adrogué and Madias really does no more; neither helps clinicians choose the best hypotonic solution to administer. What is needed is a method for estimating the cation deficits that are a critical factor in the choice of solutions. In the authors' example of the treatment of a patient with hypotonic sodium and potassium loss, they chose to administer 0.2 percent sodium chloride containing 20 mmol of potassium chloride per liter. But they could just as well have chosen another hypotonic solution (e.g., 0.45 percent sodium chloride containing 20 mmol of potassium chloride per liter or 0.2 percent sodium chloride containing 40 mmol of potassium chloride per liter); by varying the rates of infusion of these solutions, they would induce similar rates of decline in the serum sodium concentration but different rates of increase in cations.

Choosing the most appropriate solution for the correction of hypernatremia caused by hypotonic losses requires an estimate not only of the water deficit, but also of the cation deficit. Unfortunately, there is at present no reliable way to assess the latter. Until there is, choosing a solution will require educated guesses of the degree of cation deficit based on the patient's appearance, the clinician's experience, and careful observation of the response to initial therapy.

Aaron Spital, M.D.
Genesee Hospital, Rochester, NY 14607

1 References

1
Feig PU, McCurdy DK. The hypertonic state. N Engl J Med 1977;297:1444-1454
Full Text | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: Pure water loss reduces the size of the extracellular-fluid and intracellular-fluid compartments proportionately. But clinical experience indicates that even severe water deficits are generally not associated with physical findings of intravascular-volume depletion. The absence of hemodynamic compromise in the first patient described in our review, coupled with the remaining clinical information, led us to attribute the patient's hypernatremia to pure water loss. Indeed, water repletion alone returned the patient to his clinical base line. We see no reason to postulate that a sizable increase in hypertonic sodium contributed to the patient's hypernatremia, as suggested by Halperin and Cherney.

Our review cited the original work on our formula,1 so Dr. Spital and interested readers can examine its derivation. As is true of conventional formulas, our formula should not be used to devise therapy. Rather, it provides, simply and expeditiously, quantitative projections that can assist physicians in implementing the selected treatment plan for patients with dysnatremias. The advantages of our formula over those of conventional formulas have been reviewed.1 Chief among them are that our formula projects the effect of solutions of variable sodium (and potassium) concentrations (rather than only of electrolyte-free water) on the patient's serum sodium concentration and that it is applicable to both hypernatremia and hyponatremia. But no formula can substitute for rigorous pathophysiologic reasoning, sound clinical judgment, and frequent monitoring of the patient's condition and laboratory data. All these are essential for the effective management of the dysnatremias.

Horacio J. Adrogué, M.D.
Veterans Affairs Medical Center, Houston, TX 77030

Nicolaos E. Madias, M.D.
New England Medical Center, Boston, MA 02111

1 References