The Safety and Efficacy of Desmopressin in Patients With Intracranial Hemorrhage and a History of Alcohol Use

Abstract

Background: Patients with a history of alcohol use disorder are at an increased risk of hematoma expansion following intracranial hemorrhage (ICH) due to the effects of alcohol on platelet aggregation. Desmopressin (DDAVP) improves platelet aggregation and may decrease hematoma expansion in patients with ICH. However, DDAVP may also increase the risk of hyponatremia and thrombotic events. Evidence is limited regarding the safety and efficacy of DDAVP in alcohol use (AU)-associated ICH. Methods: This was a retrospective chart review of adult patients with radiographic evidence of ICH and a confirmed or suspected history of alcohol use upon admission. Patients were categorized into groups based on DDAVP administration. Safety outcomes included hyponatremia (serum sodium <135 mEq/L or decrease in serum sodium of ≥ 5 mEq/L for patients with baseline sodium <135 mEq/L) within 24 hours of ICH and thrombotic events within 7 days of ICH. The primary efficacy outcome was the incidence of hematoma expansion, defined as any expansion of the hemorrhage noted on repeat imaging within 32 hours. Results: In total, 52 patients were included in the safety analysis (27 DDAVP and 25 non-DDAVP). Although hyponatremia was numerically higher in the DDAVP group, there was no significant difference between groups (19.2% vs 4.2%, P = 0.192). Thrombotic complications were similar between the DDAVP and non-DDAVP groups (11.1% vs. 8%, P = 1.0). Thirty-nine patients met criteria for hemostatic efficacy analysis. There was no difference in hematoma expansion between the DDAVP and non-DDAVP groups (23.1% vs 34.6%, P = 0.71) and these findings were consistent after adjusting for differences in baseline characteristics (OR 0.63, 95% CI 0.1-3.3). Conclusion: The administration of DDAVP was not associated with adverse safety events, but did not significantly reduce the incidence of hematoma expansion in patients with AU-associated ICH.

Ultra-Early Hemostatic Therapy for Acute Intracerebral Hemorrhage: An Updated Review

“…10–12 One retrospective study reported a decrease in hematoma expansion, but this was limited to the first 24 hours of treatment as the researchers only looked at the first 24 hours as their primary endpoint. 13 A single-center, nonrandomized study of patients with spontaneous ICH on antiplatelet therapy who received combined desmopressin and platelet transfusion had results in line with the PATCH 9 trial: there was no benefit found with early platelet transfusion, and desmopressin failed to decrease hematoma expansion or improve functional outcome. 14 Finally, a meta-analysis of the use of desmopressin to reduce hematoma expansion in antiplatelet-associated ICH found that the literature did not support the routine use of desmopressin for this purpose.…”

“…They found that the incidence of hyponatremia in the DDAVP-treated group was higher, but this number was not statistically significant, and thrombotic complications were likewise similar. 9 The authors concluded that while the use of DDAVP in this population was safe, it did not significantly reduce hematoma expansion.…”

“…8 Patients receiving desmopressin after symptom onset also experienced minor adverse effects and small changes in hematoma volume. Gunther et al 9 recently performed a retrospective cohort study of 52 patients who presented with alcohol use-associated intracranial bleeding and were treated with either DDAVP (n = 27) or not (n = 25). They found that the incidence of hyponatremia in the DDAVP-treated group was higher, but this number was not statistically significant, and thrombotic complications were likewise similar.…”

Effect of Desmopressin on Bleeding After Heart Surgeries: A Narrative Review

“…Desmopressin is an analog of the antidiuretic hormone (vasopressin), which is particularly interesting due to its antidiuretic and anticoagulant role. This hormone exerts its anticoagulant activity by increasing the adhesion of platelets to vascular endothelium and vWF multimers, thereby causing the formation of platelet plaques ( 1 , 2 ). The role of desmopressin is well revealed in patients with VWD type 1 who have defects in platelet aggregation due to birth defects or drug side effects ( 3 ).…”