Using propranolol in traumatic brain injury to reduce sympathetic storm phenomenon: A prospective randomized clinical trial.
Using propranolol in traumatic brain injury to reduce sympathetic storm phenomenon: A prospective randomized clinical trial.
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DOI：
10.4103/sja.sja_33_18
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发表时间：
2018-10
影响因子：
1.2
通讯作者：
Hussein NS
中科院分区：
文献类型：
--
作者：
Ammar MA;Hussein NS
创伤性脑损伤（Traumatic brain injury，TBI）与脑损伤后皮质控制丧失导致交感神经活动增加，副交感神经系统受损有关。交感神经风暴的表现包括心动过速、高血压、呼吸急促和体温过高。创伤后早期通过降低脑代谢、降低O2和葡萄糖消耗而发挥神经保护作用。β受体阻滞剂减少交感神经活动。我们认为，使用普萘洛尔钝化交感神经风暴现象，因为它是一种非选择性β抑制剂，具有亲脂性，可以稳定地穿透血脑屏障。60例患者随机分为两组，每组30例。A组开始普萘洛尔，B组在前24 h内接受安慰剂。主要结果是第7天的儿茶酚胺水平，次要结果是生理指标（心率[HR]、呼吸频率[RR]、平均动脉血压[MABP]、体温、随机血糖和随访格拉斯哥昏迷评分[GCS]和镇静评分）。结果分析表明，在第7天，与B组相比，A组倾向于具有较低的儿茶酚胺水平去甲肾上腺素（206.87 ± 44.44 vs. 529.33 ± 42.99 pg/ml，P = <0.001），肾上腺素水平多巴胺水平（32.90 ± 4.57 vs 78.00 ± 3.48 pg/ml，P <0.001）。第7天，A组患者的GCS改善，与B组相比具有统计学显著性（13 vs. 10，P = 0.006），四分位距百分比变化（20.0 vs. 8.33，P = 0.006）。两组血流动力学参数MABP、HR、RR和体温在第1天无统计学显著差异，而在第7天有高度统计学显著性和显著百分比变化（P < 0.001）。TBI后早期使用心得安可控制血流动力学和血糖，降低儿茶酚胺水平与GCS改善相关。
Traumatic brain injury (TBI) correlated with increased sympathetic activity on the expense of parasympathetic system due to loss of cortical control after brain injury. Manifestations of sympathetic storm include tachycardia, hypertension, tachypnea, and hyperthermia. The neuroprotective effects via reducing cerebral metabolism and lowering O2 and glucose consumption are the targets early after trauma. Beta-blockers reduce sympathetic activity. We suppose that using propranolol blunts the sympathetic storming phenomenon as it is a nonselective β inhibitor and has a lipophilic property to steadily penetrate blood–brain barrier. Sixty patients allocated randomly into two groups, each consisting of 30 patients. Group A started propranolol and Group B received placebo within first 24 h. Primary outcome was catecholamine levels on day 7, and the secondary outcomes were physiological measures (heart rate [HR], respiratory rate [RR], mean arterial blood pressure [MABP], temperature, random blood sugar, and follow-up Glasgow coma score [GCS] and sedation score). Analysis of outcomes demonstrated that Group A tended to have lower catecholamine levels in comparison to Group B in day 7 (norepinephrine 206.87 ± 44.44 vs. 529.33 ± 42.99 pg/ml, P = <0.001), epinephrine level (69.00 ± 8.66 vs. 190.73 ± 16.48 pg/ml, P < 0.001), and dopamine level (32.90 ± 4.57 vs. 78.00 ± 3.48 pg/ml P < 0.001). GCS of the patients in Group A improved and was statistically significant compared to Group B in day 7 (13 vs. 10, P = 0.006), with percent change interquartile range (20.0 vs. 8.33, P = 0.006). Regarding hemodynamic parameters between the two groups MABP, HR, RR, and temperature, there was no statistically significant difference on day 1, while on day 7, there is high statistical significance and significant percent change (P < 0.001). Early usage of propranolol after TBI controls hemodynamics and blood sugar with decreased catecholamine levels correlated with the improvement of GCS.