导管依赖性先天性心脏病早产儿脑和内脏组织氧合的显著影响

Journal of pediatrics. Clinical practice Pub Date : 2024-09-18 eCollection Date: 2024-12-01 DOI:10.1016/j.jpedcp.2024.200126
Anastasiya Mankouski, Timothy M Bahr, Katherine L Braski, Kimberlee Weaver Lewis, Mariana C Baserga
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引用次数: 0

摘要

目的:利用近红外光谱(NIRS)研究前列腺素(PGE)依赖性先天性心脏病(CHD)早产儿脑和内脏氧合(rSO2)是否受损。研究设计:使用近红外光谱(NIRS)对出生14天的早产儿进行48小时的脑和内脏rSO2监测。混合效应模型估计冠心病和喂食对内脏和大脑近红外光谱的影响,并在喂食前后的3个不同时间(喂食前30分钟、喂食中30分钟和喂食后30分钟)对同一参与者进行多次测量。结果:24名参与者被纳入研究(10名冠心病患者和14名对照组)。最终的数据集包括来自23名参与者的897项测量结果。病例组和对照组的中位胎龄和出生体重具有可比性(34周胎龄vs 33周胎龄;平均出生体重分别为1811 g和1820 g)。对照组脑NIRS测量值平均比对照组高9.5点(P = 0.003);对照组的内脏近红外光谱测量值比对照组高13.1点(P = 0.001)。基线、饲喂时和饲喂后脑NIRS平均值分别为64.0±10.4、64.5±9.9和64.2±9.9;对照组分别为73.3±6.9、73.1±6.8、73.5±6.9。试验组在饲前、饲中、饲后的内脏近红外光谱平均值分别为34.4±15.8、37.2±14.8、38.3±16.1;对照组分别为50.7±11.0、51.6±11.1、50.6±13.5。结论:这些结果表明,与对照组相比,pge依赖性冠心病早产儿的大脑和内脏rSO2明显降低。这些数据引起了人们的关注,即未修复的紫绀型冠心病如何长期限制全身含氧血流,直接导致脑和胃肠道灌注不足和缺血,最终增加这些早产儿神经发育不良和坏死性小肠结肠炎的风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cerebral and Splanchnic Tissue Oxygenation Are Significantly Affected in Premature infants with Ductal-Dependent Congenital Heart Disease.

Objective: To determine whether premature infants with prostaglandin (PGE)-dependent congenital heart disease (CHD) have impaired cerebral and splanchnic oxygenation (rSO2) using near infrared spectroscopy (NIRS).

Study design: Cerebral and splanchnic rSO2 were monitored using NIRS for 48 hours in premature infants <36 weeks gestational age with PGE-dependent CHD and control infants (no CHD or patent ductus arteriosus). Both groups were receiving gavage enteral feedings and were >14 days of life. Mixed effects model estimated the effect of CHD and feedings on splanchnic and cerebral NIRS and accounted for multiple measurements on the same participant at 3 different times around feedings (30 minutes before, during, and 30 minutes after feedings).

Results: Twenty-four participants were enrolled in the study (10 with CHD and 14 controls). The final dataset included 897 measurements from 23 participants. The median gestational age and birthweight were comparable between case and control groups (34 vs 33 weeks gestational age; mean birthweight of 1811 g vs 1820 g, respectively). On average, cerebral NIRS measurements were 9.5 points higher in controls than cases (P = .003); and splanchnic NIRS measurements were 13.1 points higher in controls than cases (P = .001). The mean cerebral NIRS measurements at baseline, during feeding, and after feeding were 64.0 ± 10.4, 64.5 ± 9.9, and 64.2 ± 9.9 in cases, respectively; and 73.3 ± 6.9, 73.1 ± 6.8, 73.5 ± 6.9 in controls, respectively. The mean splanchnic NIRS measurements at baseline, during feeding, and after feeding were 34.4 ± 15.8, 37.2 ± 14.8, and 38.3 ± 16.1 in cases, respectively; and 50.7 ± 11.0, 51.6 ± 11.1, 50.6 ± 13.5 in controls, respectively.

Conclusions: These results demonstrate significantly lower cerebral and splanchnic rSO2 in premature infants with PGE-dependent CHD compared with control infants. These data raise concerns regarding how unrepaired cyanotic CHD can limit systemic oxygenated blood flow chronically, directly contributing to cerebral and gastrointestinal hypoperfusion and ischemia, ultimately increasing the risk for poor neurodevelopmental outcomes and necrotizing enterocolitis in these premature infants.

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