Cardiovascular effects of low-dose dexamethasone in very low birth weight neonates with refractory hypotension.

Biology of the neonate Pub Date : 2006-01-01 Epub Date: 2005-09-12 DOI:10.1159/000088289
Shahab Noori, Bijan Siassi, Manuel Durand, Ruben Acherman, Smeeta Sardesai, Rangasamy Ramanathan
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引用次数: 30

Abstract

Background: Administration of hydrocortisone and relatively high doses of dexamethasone increase blood pressure in volume- and pressor-resistant hypotensive preterm infants. However, little is known about the temporal relationship of dexamethasone administration and the improvement in blood pressure and the weaning of pressors/inotropes. Furthermore, there are no sufficient data available on whether a smaller dose of dexamethasone would also be effective in treating refractory hypotension.

Objective: To study the cardiovascular responses to low-dose dexamethasone in very low birth weight neonates with volume- and pressor-resistant hypotension.

Methods: Retrospective database review. Twenty-four preterm neonates (gestational age 26 (23-34) weeks; birth weight 801 (457-1,180) g; postnatal age 2 (1-24) days, medians (ranges)) who remained hypotensive despite volume administration and combined dopamine and dobutamine treatment at >or=30 microg/kg/min received dexamethasone 0.1 mg/kg followed by 0.05 mg/kg intravenously every 12 h for 5 additional doses if still on pressors >or=8 microg/kg/min.

Results: Two hours after the first dose of dexamethasone the mean blood pressure increased from 30 +/- 5 to 34 +/- 6 mm Hg (p < 0.001) and remained elevated at 4, 6, 12, and 24 h after treatment was started (p < 0.001). Six hours after the initial dose of dexamethasone the pressor/inotrope requirement decreased from 34 +/- 9 to 24 +/- 13 microg/kg/min (p = 0.001) and continued to decrease at 12 and 24 h (p < 0.001). Urine output also increased significantly during the first 6 h after dexamethasone (p < 0.001).

Conclusions: Low-dose dexamethasone rapidly increases blood pressure and decreases pressor requirements in very low birth weight neonates with volume- and pressor-resistant hypotension.

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低剂量地塞米松对极低出生体重新生儿难治性低血压的心血管影响。
背景:给药氢化可的松和相对大剂量地塞米松增加血压容量和压力抵抗性低血压早产儿。然而,关于地塞米松给药与血压改善和停用降压药/肌力药物的时间关系知之甚少。此外,没有足够的数据表明小剂量地塞米松是否也能有效治疗难治性低血压。目的:探讨低剂量地塞米松对极低出生体重新生儿容量和血压抵抗性低血压的心血管反应。方法:回顾性数据库分析。24例早产儿(胎龄26(23-34)周);出生体重801 (457- 1180)g;出生后2(1-24)天,中位数(范围)),尽管大量给药和多巴胺和多巴酚丁胺联合治疗>或=30微克/千克/分钟,仍保持低血压,接受地塞米松0.1毫克/千克,然后每12小时静脉注射0.05毫克/千克,如果仍在使用升压>或=8微克/千克/分钟,再加5剂。结果:第一次给药后2小时,平均血压从30 +/- 5上升到34 +/- 6 mm Hg (p < 0.001),并在开始治疗后4、6、12和24小时保持升高(p < 0.001)。地塞米松初始剂量后6小时,加压/肌力需求从34 +/- 9降至24 +/- 13微克/千克/分钟(p = 0.001),并在12和24小时继续下降(p < 0.001)。在使用地塞米松后的前6小时内,尿量也显著增加(p < 0.001)。结论:低剂量地塞米松可迅速提高极低出生体重新生儿的血压,降低血压需求,并伴有容量和压力抵抗性低血压。
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