Emily Bowers1, Eric Shaw2,3, William Bromberg4, Audrey Johnson5. 1. Department of Pharmacy, Memorial Health University Medical Center, 4700 Waters Avenue, Savannah, GA, 31404, USA. Emily.bowers@hcahealthcare.com. 2. Department of Clinical Trials, Memorial Health University Medical Center, 4700 Waters Avenue, Savannah, GA, 31404, USA. 3. Mercer University School of Medicine, Savannah, Savannah, GA, USA. 4. Department of Surgery, Memorial Health University Medical Center, 4700 Waters Avenue, Savannah, GA, 31404, USA. 5. Department of Pharmacy, Memorial Health University Medical Center, 4700 Waters Avenue, Savannah, GA, 31404, USA.
Abstract
INTRODUCTION: Desmopressin improves hemostasis through the release of factor VIII, von Willebrand factor, and tissue plasminogen activator, and increases platelet adhesion. Neurocritical Care guidelines recommend consideration of desmopressin in antiplatelet-associated intracranial hemorrhage. Studies supporting its use have not evaluated the potential impact of desmopressin on serum sodium levels in patients receiving hypertonic saline therapy. The purpose of this study was to assess the impact of desmopressin on sodium levels and hypertonic saline effectiveness in intracranial hemorrhage. METHODS: This was a single center retrospective observational chart review. Patients were included in the desmopressin group if they were diagnosed with intracranial hemorrhage, administered desmopressin, and received hypertonic saline infusion. Patients in the hypertonic saline alone group were then matched 1:1 to the patients in the desmopressin group. The primary end point was the effect of desmopressin on reaching a sodium goal of 145-155 mEq/L. The secondary end points included intensive care unit and hospital length of stay, change in sodium, time to reach sodium goal, thrombotic events, mortality, and a composite of increased cerebral edema, hematoma expansion, midline shift, herniation, need for neurosurgical intervention, and neurologic decompensation. RESULTS: Of 112 patients screened, 25 patients met inclusion criteria for the desmopressin group, and 25 patients were matched with patients in the hypertonic saline alone group. The percentage of patients who reached goal sodium in the desmopressin group compared with hypertonic saline alone was similar (80% vs. 88%, respectively). There were no differences in the secondary end points. In the subgroup analysis, patients in the hypertonic saline group met the predefined sodium goal of 150-155 mEq/L within 48 h more often than those in the desmopressin group (82% vs. 60%, respectively, p = 0.042). CONCLUSIONS: The use of desmopressin in intracranial hemorrhage does not appear to negatively impact the ability for patients to reach goal sodium of 145-155 mEq/L. However, in patients with higher sodium goals, desmopressin may decrease hypertonic saline effectiveness.
INTRODUCTION: Desmopressin improves hemostasis through the release of factor VIII, von Willebrand factor, and tissue plasminogen activator, and increases platelet adhesion. Neurocritical Care guidelines recommend consideration of desmopressin in antiplatelet-associated intracranial hemorrhage. Studies supporting its use have not evaluated the potential impact of desmopressin on serum sodium levels in patients receiving hypertonic saline therapy. The purpose of this study was to assess the impact of desmopressin on sodium levels and hypertonic saline effectiveness in intracranial hemorrhage. METHODS: This was a single center retrospective observational chart review. Patients were included in the desmopressin group if they were diagnosed with intracranial hemorrhage, administered desmopressin, and received hypertonic saline infusion. Patients in the hypertonic saline alone group were then matched 1:1 to the patients in the desmopressin group. The primary end point was the effect of desmopressin on reaching a sodium goal of 145-155 mEq/L. The secondary end points included intensive care unit and hospital length of stay, change in sodium, time to reach sodium goal, thrombotic events, mortality, and a composite of increased cerebral edema, hematoma expansion, midline shift, herniation, need for neurosurgical intervention, and neurologic decompensation. RESULTS: Of 112 patients screened, 25 patients met inclusion criteria for the desmopressin group, and 25 patients were matched with patients in the hypertonic saline alone group. The percentage of patients who reached goal sodium in the desmopressin group compared with hypertonic saline alone was similar (80% vs. 88%, respectively). There were no differences in the secondary end points. In the subgroup analysis, patients in the hypertonic saline group met the predefined sodium goal of 150-155 mEq/L within 48 h more often than those in the desmopressin group (82% vs. 60%, respectively, p = 0.042). CONCLUSIONS: The use of desmopressin in intracranial hemorrhage does not appear to negatively impact the ability for patients to reach goal sodium of 145-155 mEq/L. However, in patients with higher sodium goals, desmopressin may decrease hypertonic saline effectiveness.