坏死性小肠结肠炎(NEC)是一种破坏性疾病,在患有先天性心脏病(CHD)的足月婴儿中相对频繁地被诊断,与无冠心病的足月婴儿相比,其中NEC是罕见的。NEC在足月婴儿CHD中的确切发病机制尚不清楚,但是据推测,肠道缺血起着举足轻重的作用。我们的目的是探讨(近)足月CHD婴儿,开发NEC的人,在出生后和进入新生儿重症监护病房后的最初48小时内表现出更多的缺氧/缺血和低身体灌注的临床症状,与未发生NEC的(近)足月CHD婴儿相比。
在1999年1月至2020年2月期间,本病例对照研究对956名胎龄≥35周后出生的CHD婴儿进行了回顾性分析。我们纳入了经影像学证实的肠道积气的婴儿和与CHD类型相匹配的对照组。七名婴儿被诊断为大动脉转位,6例左侧和4例右心室流出道梗阻。几个暗示(相对)缺氧/缺血的参数用于分析。
我们纳入了16名患有NEC的CHD婴儿,并选择了16名对照。两组之间没有显著的人口统计学差异。与对照婴儿(8[7-8])相比,患有NEC的婴儿在1分钟和5分钟时的Apgar得分(中位数[IQR])较低。(9[8-9])P=.011)和(8[8-9])与(9[9-10])P=.009)。分娩室中NEC婴儿需要呼吸支持的比例较高(11(69)vs.2(13)、P=.001)。入院后第二天的(中位数[IQR])舒张压(39mmHg[34-42],vs.43mmHg[37-51],P=.112)和入院后48小时内的最低(中位数[IQR])pH(7.24[7.17-7.35]vs.7.38([7.27–7.43],P=.157)在NEC婴儿中没有显着降低,但在NEC婴儿中,两者都表现出相似的(相对)缺氧/缺血方向。
我们的临床结果支持(近)足月CHD婴儿NEC的缺氧/缺血病理生理学,阿普加分数较低,产房中更多的呼吸支持,并且在发生NEC的CHD婴儿中,舒张压和pH值有降低的趋势。
Necrotizing enterocolitis (NEC) is a devastating disease that is relatively frequently diagnosed in term infants with congenital heart disease (CHD), compared with term infants without CHD, in whom NEC is rare. The exact pathogenesis of NEC in term infants with CHD is unknown, but it is hypothesized that ischemia of the intestines plays a pivotal role. We aimed to explore whether (near) term CHD infants, who develop NEC, exhibit more clinical signs of hypoxia/ischemia and low body perfusion directly after birth and during the first 48 hours after admission to the neonatal intensive care unit, when compared with (near) term CHD infants who did not develop NEC.
956 infants with CHD born after ≥ 35 weeks of gestational age were retrospectively reviewed for this
case-control study between January 1999 and February 2020. We included infants with radiographically confirmed pneumatosis intestinalis and controls matched by type of CHD. Seven infants were diagnosed with transposition of the great arteries, six with left and four with right ventricular outflow tract obstruction. Several parameters suggestive of (relative) hypoxia/ischemia were used for analyses.
We included sixteen CHD infants with NEC and selected sixteen controls. There were no significant demographic differences between both groups. Apgar score at one and five minutes (median [IQR]) were lower in infants who developed NEC compared with control infants (8 [7-8]) vs. (9 [8-9], P = .011) and (8 [8-9]) vs. (9 [9-10], P = .009). A higher proportion of infants with NEC required respiratory support in the delivery room (11(69) vs. 2(13), P = .001). The (median [IQR]) diastolic blood pressure on the second day after admission (39 mmHg [34-42], vs. 43 mmHg [37-51], P = .112) and lowest (median [IQR]) pH in the 48 hours after admission (7.24 [7.17-7.35] vs. 7.38 ([7.27-7.43], P = .157) were not significantly lower in NEC infants but both demonstrated a similar direction towards (relative) hypoxia/ischemia in NEC infants.
Our clinical results support a hypoxic/ischemic pathophysiology of NEC in (near) term CHD infants, with lower Apgar scores, more respiratory support in the delivery room and a tendency towards a lower diastolic blood pressure and pH in CHD infants who develop NEC.