Friday, November 13, 2009

DDAVP for prevention and treatment of overcorrection of hyponatremia

Osmotic demyelination is a much feared complication of treatment of hyponatremia. Slow and limited correction minimizes the risk and recommended rates of correction have been widely published. In spite of this, overcorrection is common. This occurs inadvertently because renal diluting capacity is often restored during treatment. A frequent example is treatment of hypovolemic hyponatremia with isotonic saline in which case volume expansion eliminates the signal for vasopressin secretion, resulting in a water diuresis. These changes are unpredictable, calculations of sodium deficits are unreliable, and the rise in serum sodium is often more rapid than anticipated or desired.

These issues were discussed, with a focus on the use of DDAVP, in a paper from last year in the Clinical Journal of the American Society of Nephrology.

I first read about this use of DDAVP several years ago in UptoDate but could find little to support it in the primary literature. The paper referenced here is the largest published experience that I'm aware of. It is based on a retrospective chart review and its findings and conclusions are as follows:

Results: Six patients (group 1) were given desmopressin acetate after the 24-h limit of 12 mmol/L had already been reached or exceeded; correction was prevented from exceeding the 48-h limit of 18 mmol/L in five of the six. Fourteen patients (group 2) were given desmopressin acetate in anticipation of overcorrection after the plasma sodium concentration had increased by 1 to 12 mmol/L. In all 14 patients who were treated with desmopressin acetate as a preventive measure, correction was prevented from exceeding either the 24- or 48-h limits. After desmopressin acetate was administered, the plasma sodium concentration of 14 of the 20 patients fell by 2 to 9 mmol/L. In all six group 1 patients and in five of the group 2 patients, the plasma sodium concentration was actively lowered again by the concurrent administration of desmopressin acetate and 5% dextrose in water; no serious adverse consequences from this maneuver were observed.

Conclusion: Desmopressin acetate is effective in preventing and reversing inadvertent overcorrection of hyponatremia.

The link above is to the entire paper free of access controls, which is worth reading in its entirety. I was struck be several points:

The authors are experienced clinicians who are thoroughly familiar with the pathophysiologic rationale for the use of DDAVP. When used by such clinicians DDAVP is safe and effective in preventing and mitigating overcorrection of hyponatremia. The authors present several pearls governing effective use.

Impending overcorrection is often signaled early by a return of renal diluting capacity evidenced by urine volume, urine osmolality, or the initial rate of rise in sodium concentration.

Hyponatremia in this series was often multifactorial but the frequency with which thiazides and SSRIs were involved was impressive.

Clinical scenarios of inadvertent overcorrection include volume expansion, discontinuation of thiazides and SSRIs, and treatment of adrenal crisis with glucocorticoids.

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