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本文引用的文献

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Pressor response to fluid resuscitation in endotoxic shock: involvement of vasopressin.内毒素休克中液体复苏的升压反应:血管加压素的作用
Crit Care Med. 2009 Nov;37(11):2968-72. doi: 10.1097/CCM.0b013e3181b02e3b.
2
Cerebral hemodynamic predictors of poor 6-month Glasgow Outcome Score in severe pediatric traumatic brain injury.小儿重度创伤性脑损伤6个月时格拉斯哥预后评分不良的脑血流动力学预测因素
J Neurotrauma. 2009 May;26(5):657-63. doi: 10.1089/neu.2008.0770.
3
Afferent pathways involved in cardiovascular adjustments induced by hypertonic saline resuscitation in rats submitted to hemorrhagic shock.在经历失血性休克的大鼠中,高渗盐水复苏诱导的心血管调节所涉及的传入通路。
Shock. 2009 Aug;32(2):190-3. doi: 10.1097/SHK.0b013e31819c3841.
4
Tissue oxygenation during management of cerebral perfusion pressure with phenylephrine or vasopressin.使用去氧肾上腺素或血管加压素管理脑灌注压期间的组织氧合。
Crit Care Med. 2008 Sep;36(9):2641-50. doi: 10.1097/CCM.0b013e3181847af3.
5
ICP and CPP: excellent predictors of long term outcome in severely brain injured children.颅内压和脑灌注压:重度脑损伤儿童长期预后的良好预测指标。
Childs Nerv Syst. 2008 Feb;24(2):245-51. doi: 10.1007/s00381-007-0461-z. Epub 2007 Aug 22.
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Pathophysiology of traumatic brain injury.创伤性脑损伤的病理生理学
Br J Anaesth. 2007 Jul;99(1):4-9. doi: 10.1093/bja/aem131.
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Intracranial pressure and cerebral perfusion pressure as risk factors in children with traumatic brain injuries.颅内压和脑灌注压作为创伤性脑损伤儿童的危险因素。
J Neurosurg. 2007 Jun;106(6 Suppl):463-6. doi: 10.3171/ped.2007.106.6.463.
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Guidelines for the management of severe traumatic brain injury. I. Blood pressure and oxygenation.重型颅脑损伤管理指南。I. 血压与氧合。
J Neurotrauma. 2007;24 Suppl 1:S7-13. doi: 10.1089/neu.2007.9995.
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Vasopressin mediates the pressor effect of hypertonic saline solution in endotoxic shock.血管加压素介导高渗盐溶液在内毒素休克中的升压作用。
Shock. 2007 Apr;27(4):416-21. doi: 10.1097/01.shk.0000239759.05583.fd.
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Incidence of traumatic brain injury in the United States, 2003.2003年美国创伤性脑损伤的发病率
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儿童创伤性脑损伤后血管加压药的使用和效果。

Use and effect of vasopressors after pediatric traumatic brain injury.

机构信息

Department of Pediatrics, University of Washington, Seattle, Wash., USA.

出版信息

Dev Neurosci. 2010;32(5-6):420-30. doi: 10.1159/000322083. Epub 2010 Dec 2.

DOI:10.1159/000322083
PMID:21124016
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3073759/
Abstract

BACKGROUND

Vasopressors are commonly used to increase mean arterial blood pressure (MAP) and cerebral perfusion pressure (CPP) after traumatic brain injury (TBI), but there are few data comparing vasopressor effectiveness after pediatric TBI.

OBJECTIVE

To determine which vasopressor is most effective at increasing MAP and CPP in children with moderate-to-severe TBI.

METHODS

After institutional review board approval, we performed a retrospective cohort study of children 0-17 years old admitted to a level 1 trauma center (Harborview Medical Center, Seattle, Wash., USA) between 2002 and 2007 with moderate-to-severe TBI who received a vasopressor to increase blood pressure. Baseline demographic and physiologic characteristics and hourly physiologic monitoring for 3 h after having started a vasopressor were abstracted. We evaluated differences in MAP and CPP at 3 h after initiation of therapy between phenylephrine, dopamine and norepinephrine among patients who did not require a second vasopressor during this time. Multivariate linear regression was used to adjust for age, gender, injury severity score and baseline MAP or CPP and to cluster by subject.

RESULTS

Eighty-two patients contributed data to the entire dataset. The most common initial medication was phenylephrine for 47 (57%). Patients receiving phenylephrine and norepinephrine tended to be older than those receiving dopamine and epinephrine. Thirteen (16%) of the patients received a second vasopressor during the first 3 h of treatment and were thus not included in the regression analyses; these patients received more fluid resuscitation and exhibited higher in-hospital mortality (77 vs. 32%; p = 0.004) compared to patients receiving a single vasopressor. The norepinephrine group exhibited a 5 mm Hg higher MAP (95% CI: -4 to 13; p = 0.31) and a 12 mm Hg higher CPP (95% CI: -2 to 26; p = 0.10) than the phenylephrine group, and a 5 mm Hg higher MAP (95% CI: -4 to 15; p = 0.27) and a 10 mm Hg higher CPP (95% CI: -5 to 25; p = 0.18) than the dopamine group. However, in post hoc analysis, after adjusting for time to start of vasopressor, hypertonic saline and pentobarbital, the effect on MAP was lost, but the CPP was 8 mm Hg higher (95% CI: -10 to 25; p = 0.39) than in the phenylephrine group, and 5 mm Hg higher (95% CI: -14 to 24; p = 0.59) than in the dopamine group.

CONCLUSIONS

Vasopressor use varied by age. While there was no statistically significant difference in MAP or CPP between vasopressor groups, norepinephrine was associated with a clinically relevant higher CPP and lower intracranial pressure at 3 h after start of vasopressor therapy compared to the other vasopressors examined.

摘要

背景

在创伤性脑损伤(TBI)后,血管加压药通常用于增加平均动脉血压(MAP)和脑灌注压(CPP),但关于儿科 TBI 后血管加压药疗效的比较数据很少。

目的

确定在患有中重度 TBI 的儿童中,哪种血管加压药最有效地增加 MAP 和 CPP。

方法

在机构审查委员会批准后,我们对 2002 年至 2007 年期间在西雅图港景医疗中心(美国华盛顿州)接受中重度 TBI 治疗并接受血管加压药以升高血压的 0-17 岁儿童进行了回顾性队列研究。从开始使用血管加压药后的 3 小时内,提取基线人口统计学和生理特征以及每小时生理监测数据。我们评估了在开始治疗后 3 小时内,未在此期间需要第二种血管加压药的患者中,去氧肾上腺素、多巴胺和去甲肾上腺素之间的 MAP 和 CPP 差异。使用多变量线性回归来调整年龄、性别、损伤严重程度评分以及基线 MAP 或 CPP,并按个体进行聚类。

结果

82 名患者提供了整个数据集的数据。最常见的初始药物是去氧肾上腺素,占 47%(57%)。接受去氧肾上腺素和去甲肾上腺素的患者比接受多巴胺和肾上腺素的患者年龄更大。在最初的 3 小时治疗中,有 13 名(16%)患者接受了第二种血管加压药,因此未纳入回归分析;这些患者接受了更多的液体复苏,院内死亡率更高(77%比 32%;p=0.004)与接受单一血管加压药的患者相比。去甲肾上腺素组的 MAP 比去氧肾上腺素组高 5mmHg(95%CI:-4 至 13;p=0.31),CPP 高 12mmHg(95%CI:-2 至 26;p=0.10),MAP 比多巴胺组高 5mmHg(95%CI:-4 至 15;p=0.27),CPP 高 10mmHg(95%CI:-5 至 25;p=0.18)。然而,在事后分析中,在校正血管加压药开始时间、高渗盐水和戊巴比妥钠后,MAP 的影响消失,但 CPP 高 8mmHg(95%CI:-10 至 25;p=0.39)比去氧肾上腺素组高,比多巴胺组高 5mmHg(95%CI:-14 至 24;p=0.59)。

结论

血管加压药的使用因年龄而异。虽然 MAP 或 CPP 之间在统计学上没有显著差异,但与其他检查的血管加压药相比,去甲肾上腺素在开始血管加压药治疗后 3 小时与 CPP 相关,具有临床相关的更高值和更低的颅内压。