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Incidence of Diabetes Insipidus After Cessation of Vasopressin Infusion for Treatment of Shock
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A6008 - Incidence of Diabetes Insipidus After Cessation of Vasopressin Infusion for Treatment of Shock
Author Block: H. Ferenchick, N. Ferguson, P. Dicpinigaitis; Department of Medicine/ Critical Care Division, Montefiore Medical Center, Bronx, NY, United States.
Rationale: Vasopressin, a peptide hormone released from the posterior pituitary gland, has multiple physiologic effects, including vasoconstriction. Patients in septic shock may have a relative deficiency of vasopressin. Thus, vasopressin infusion has achieved common usage in catecholamine-requiring and catecholamine-resistant shock. Diabetes insipidus (DI) is a syndrome associated with excretion of large volumes of dilute urine and hypernatremia. Despite the common usage of vasopressin, only 12 cases of DI associated with cessation of vasopressin infusion have been reported to date (J Clin Pharm Ther, 2017). The actual incidence of this phenomenon is unknown; thus, investigation of this question formed the basis of this study.
Methods: Montefiore Medical Center electronic health records for the 5-year period from 1/1/2012 through 12/31/2016 were retrospectively analyzed incorporating Looking Glass™ Clinical Analytics (Streamline Health, Atlanta, GA) to identify a target population comprised of adult (age ≥ 18) patients treated for hypotension with intravenous vasopressin infusion, and who survived at least 24 hours after its discontinuation. Initial evaluation yielded 1896 patients who received the drug in intravenous (IV) form. When we introduced a screening tool to assist in capturing potential DI patients, i.e., requirement for a serum sodium level of 147 meq/dl or higher subsequent to vasopressin administration, 341 patients were identified. To date 260 of these 341 medical records have been manually reviewed to select only patients receiving vasopressin infusion (rather than single or multiple one-time IV doses without continuous infusion) and to evaluate changes in serum sodium pre- and post-vasopressin infusion.
Results: 37 of 260 subjects evaluated to date demonstrated the onset of hypernatremia (serum sodium ≥ 147 meq/dl) and a rise in serum sodium of 10 meq/dl or greater after cessation of vasopressin infusion compared with baseline levels. Extrapolation of these data to the entire group of 341 hypernatremic subjects yields an incidence of 2.6% among the 1896 identified patients who received vasopressin infusion.
Conclusions: Our results demonstrate a 2.6% incidence of hypernatremia, as defined by serum sodium ≥ 147 meq/dl, and an increase in serum sodium of ≥ 10 meq/dl after cessation of vasopressin infusion compared with pre-treatment levels. Given the common usage of vasopressin for the treatment of shock, clinicians should be aware of this effect, which may represent DI or a DI-type phenomenon, the mechanism of which remains to be elucidated.
Author Block: H. Ferenchick, N. Ferguson, P. Dicpinigaitis; Department of Medicine/ Critical Care Division, Montefiore Medical Center, Bronx, NY, United States.
Rationale: Vasopressin, a peptide hormone released from the posterior pituitary gland, has multiple physiologic effects, including vasoconstriction. Patients in septic shock may have a relative deficiency of vasopressin. Thus, vasopressin infusion has achieved common usage in catecholamine-requiring and catecholamine-resistant shock. Diabetes insipidus (DI) is a syndrome associated with excretion of large volumes of dilute urine and hypernatremia. Despite the common usage of vasopressin, only 12 cases of DI associated with cessation of vasopressin infusion have been reported to date (J Clin Pharm Ther, 2017). The actual incidence of this phenomenon is unknown; thus, investigation of this question formed the basis of this study.
Methods: Montefiore Medical Center electronic health records for the 5-year period from 1/1/2012 through 12/31/2016 were retrospectively analyzed incorporating Looking Glass™ Clinical Analytics (Streamline Health, Atlanta, GA) to identify a target population comprised of adult (age ≥ 18) patients treated for hypotension with intravenous vasopressin infusion, and who survived at least 24 hours after its discontinuation. Initial evaluation yielded 1896 patients who received the drug in intravenous (IV) form. When we introduced a screening tool to assist in capturing potential DI patients, i.e., requirement for a serum sodium level of 147 meq/dl or higher subsequent to vasopressin administration, 341 patients were identified. To date 260 of these 341 medical records have been manually reviewed to select only patients receiving vasopressin infusion (rather than single or multiple one-time IV doses without continuous infusion) and to evaluate changes in serum sodium pre- and post-vasopressin infusion.
Results: 37 of 260 subjects evaluated to date demonstrated the onset of hypernatremia (serum sodium ≥ 147 meq/dl) and a rise in serum sodium of 10 meq/dl or greater after cessation of vasopressin infusion compared with baseline levels. Extrapolation of these data to the entire group of 341 hypernatremic subjects yields an incidence of 2.6% among the 1896 identified patients who received vasopressin infusion.
Conclusions: Our results demonstrate a 2.6% incidence of hypernatremia, as defined by serum sodium ≥ 147 meq/dl, and an increase in serum sodium of ≥ 10 meq/dl after cessation of vasopressin infusion compared with pre-treatment levels. Given the common usage of vasopressin for the treatment of shock, clinicians should be aware of this effect, which may represent DI or a DI-type phenomenon, the mechanism of which remains to be elucidated.
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