Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA 02114, USA.
Anesth Analg. 2010 Mar 1;110(3):895-902. doi: 10.1213/ANE.0b013e3181cc9ed8.
Vasospasm is a potentially devastating complication after aneurysmal subarachnoid hemorrhage. Although endovascular treatment with intraarterial nicardipine and milrinone is an accepted clinical treatment strategy, there is little information either on hemodynamic management during treatment or on outcome and consequences of the hemodynamic management. We tested 2 hypotheses: (1) intraarterial administration of nicardipine and milrinone to treat cerebral vasospasm would require increased administration of vasoconstrictor to support arterial blood pressure at target levels; and (2) high-dose vasopressors administered to increase blood pressure in these patients would lead to systemic acidosis and end-organ ischemic damage.
We conducted a single-center, retrospective review of consecutive patients with clinically symptomatic vasospasm after aneurysmal subarachnoid hemorrhage that failed medical management with "triple H therapy" and subsequently received intraarterial nicardipine and/or milrinone between March 2005 and July 2007.
Of 160 endovascular interventions in 73 patients (aged 52 +/- 10 years; 50 women), 96 received only nicardipine, 5 only milrinone, and 59 both drugs. General anesthesia with muscle relaxation was performed for 93% of procedures. During treatment, both the number and dose of vasopressors required to maintain arterial blood pressure at target levels increased; the median dose of phenylephrine increased from 200 (n = 121) to 325 microg/min (n = 122), norepinephrine increased from 12 (n = 60) to 24.5 microg/min (n = 87), and vasopressin infusions increased from 7 to 24. Nonetheless, arterial blood pressure decreased 13% during treatment. In >90% of procedures, the postprocedure angiogram showed improved vessel caliber. A single patient demonstrated troponin T increase; no patients had a decrease in renal function, bowel or peripheral ischemia, systemic acidosis, or acute stroke. Overall mortality was 11%.
Intraarterial administration of nicardipine and/or milrinone requires use of vasopressors to maintain arterial blood pressure. Despite high doses of vasoconstrictors, treatment has low mortality, minimal end-organ ischemic damage or systemic acidosis, and results in improved caliber of cerebral vessels affected by vasospasm.
血管痉挛是蛛网膜下腔出血后一种潜在的破坏性并发症。虽然血管内应用尼卡地平联合米力农是一种公认的临床治疗策略，但关于治疗期间的血液动力学管理或血液动力学管理的结果和后果的信息却很少。我们检验了 2 个假设：（1） 用尼卡地平联合米力农治疗脑动脉痉挛会需要增加血管收缩剂的使用来维持目标水平的动脉血压；（2） 为了升高血压而在这些患者中使用大剂量的升压药会导致全身酸中毒和终末器官缺血性损伤。
我们进行了一项单中心、回顾性研究，纳入了 2005 年 3 月至 2007 年 7 月期间因接受“三重 H 治疗”后仍出现临床症状性血管痉挛而接受血管内尼卡地平联合/或米力农治疗的连续患者。
73 例患者（年龄 52 ± 10 岁；50 例女性）共进行了 160 次血管内介入治疗，其中 96 例仅接受尼卡地平，5 例仅接受米力农，59 例同时接受两种药物。93%的操作均使用全身麻醉伴肌松。治疗期间，维持目标水平的动脉血压所需的血管加压剂的种类和剂量均增加；去氧肾上腺素的中位数剂量从 200μg/min（n=121）增加到 325μg/min（n=122），去甲肾上腺素从 12μg/min（n=60）增加到 24.5μg/min（n=87），加压素输注从 7 单位增加到 24 单位。尽管如此，治疗期间动脉血压仍下降了 13%。>90%的操作后血管造影显示血管口径改善。仅有 1 例患者出现肌钙蛋白 T 升高；无患者出现肾功能下降、肠或外周缺血、酸中毒或急性卒中。总的死亡率为 11%。
血管内给予尼卡地平联合/或米力农治疗需要使用升压药来维持动脉血压。尽管使用了大剂量的血管收缩剂，该治疗方法的死亡率低，终末器官缺血性损伤或全身酸中毒发生率低，且能改善血管痉挛导致的血管口径。
