From the Department of Neurology (A.M.N., M.B.M., E.M.L., J.C.G., M.B., S.P., R.A.B.), Department of Neurosurgery (J.M.R., B.R.B.), Department of Pathology (P.F.L.), and Department of Hematology (H.C.K.), Northwestern University, Chicago, IL; and Department of Pharmacy, Northwestern Memorial Hospital, Chicago, IL (K.E.L.-F.).
Stroke. 2014 Aug;45(8):2451-3. doi: 10.1161/STROKEAHA.114.006061. Epub 2014 Jul 8.
Minimizing hematoma growth in high-risk patients is an attractive strategy to improve outcomes after intracerebral hemorrhage. We tested the hypothesis that desmopressin (DDAVP), which improves hemostasis through the release of von Willebrand factor, improves platelet activity after intracerebral hemorrhage.
Patients with reduced platelet activity on point-of-care testing alone (5), known aspirin use alone (1), or both (8) received desmopressin 0.4 μg/kg IV. We measured Platelet Function Analyzer-epinephrine (Siemens AG, Germany) and von Willebrand factor antigen from baseline to 1 hour after infusion start and hematoma volume from the diagnostic to a follow-up computed tomographic scan.
We enrolled 14 patients with of mean age 66.8±14.6 years, 11 (85%) of whom were white and 8 (57%) were men. Mean Platelet Function Analyzer-epinephrine results shortened from 192±18 seconds pretreatment to 124±15 seconds (P=0.01) 1 hour later, indicating improved plate activity. von Willebrand factor antigen increased from 242±96% to 289±103% activity (P=0.004), indicating the expected increase in von Willebrand factor. Of 7 (50%) patients who received desmopressin within 12 hours of intracerebral hemorrhage symptom onset, changes in hematoma volume were modest, -0.5 (-1.4 to 8.4) mL and only 2 had hematoma growth. One patient had low blood pressure and another had a new fever within 6 hours of desmopressin administration.
Intravenous desmopressin was well tolerated and improved platelet activity after acute intracerebral hemorrhage. Larger studies are needed to determine its potential effects on reducing hematoma growth versus platelet transfusion or placebo.
http://www.clinicaltrials.gov. Unique identifier: NCT00961532.
降低高危患者的血肿增长是改善脑出血后预后的一种有吸引力的策略。我们检验了这样一个假设,即通过释放血管性血友病因子来改善止血的去氨加压素(DDAVP)可以改善脑出血后的血小板活性。
仅通过即时检测发现血小板活性降低的患者(5 例)、已知单独使用阿司匹林的患者(1 例)或两者均有的患者(8 例)接受去氨加压素 0.4 μg/kg IV 治疗。我们测量了血小板功能分析仪-肾上腺素(德国西门子公司)和输注开始后 1 小时的血管性血友病因子抗原以及从诊断到随访 CT 扫描的血肿体积。
我们共纳入了 14 名平均年龄为 66.8±14.6 岁的患者,其中 11 名(85%)为白人,8 名(57%)为男性。血小板功能分析仪-肾上腺素的平均结果从预处理时的 192±18 秒缩短至 1 小时后的 124±15 秒(P=0.01),表明血小板活性得到改善。血管性血友病因子抗原从 242±96%增加到 289±103%(P=0.004),表明血管性血友病因子预期增加。在脑出血症状发作后 12 小时内接受去氨加压素治疗的 7 名(50%)患者中,血肿体积的变化较小,为-0.5(-1.4 至 8.4)mL,只有 2 名患者出现血肿增大。一名患者在去氨加压素给药后 6 小时内出现低血压,另一名患者出现新发热。
静脉内给予去氨加压素耐受性良好,并改善了急性脑出血后的血小板活性。需要更大规模的研究来确定其在减少血肿增长方面与血小板输注或安慰剂相比的潜在效果。