DDAVP is effective in preventing and reversing inadvertent overcorrection of hyponatremia

Abstract

Background and objectives: Adherence to therapeutic guidelines for the treatment of hyponatremia becomes difficult when water diuresis emerges during therapy. The objective of this study was to assess the effectiveness and safety of desmopressin acetate as a therapeutic agent to avoid overcorrection of hyponatremia and to lower the plasma sodium concentration again after inadvertent overcorrection.

Design, setting, participants, & measurements: Retrospective chart review was conducted of all patients who were given desmopressin acetate during the treatment of hyponatremia during 6 yr in a 528-bed community teaching hospital.

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.

Figure 1.

Patient 2, who presented with delirium as a result of a plasma sodium concentration (PNa) of 115 mmol/L and alcohol withdrawal, was given multiple doses of desmopressin acetate (DDAVP; filled arrows) in the intensive care unit after a spontaneous water diuresis had increased her PNa by 20 mmol/L over 21 h despite infusion of 0.45% saline (1/2 NS) at 150 ml/h. The final dose of DDAVP was given just before transfer from the intensive care unit, and it was followed by excessive re-lowering of the PNa because of the unintentional continuation of 5% dextrose in water (D5W). After the PNa had fallen from 133 to 122 mmol/L over 24 h (with no worsening of the patient's neurologic condition), a final water diuresis emerged, increasing the PNa to 138 over 17 h despite continued infusion of D5W at 150 ml/h without DDAVP.