极早产儿和中度早产儿喂养不耐受的比较——一项前瞻性队列研究

F. Ahammad, T. Begum, JesminAkter, Evana Nasrin
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引用次数: 6

摘要

新生儿死亡在我国很高,占5岁以下儿童总死亡率的60%。1因此,要实现MDG-4,我们必须减少新生儿死亡。《柳叶刀》新生儿健康系列报道称,早产直接导致28%的新生儿死亡。2早产及其并发症是我国新生儿死亡的主要原因,约占新生儿死亡的45%。早产儿容易出现许多并发症。常见的并发症之一是喂养不耐受(FI)。喂养不耐受可归因于胃肠道运动不成熟,3,4因为早产儿的小肠运动和迁移运动复合体(MMC)的3期活动更不成熟,尤其是胎龄小于32周的早产儿。3,5胃肠道运动受胃动素的影响,十二指肠和空肠粘膜的肠嗜铬细胞产生的一种22氨基酸的肽。6胃排空尤其依赖于胃窦和十二指肠运动活动之间的协调。由于胃肠系统的机械和激素控制不成熟,早产儿通常难以耐受口服饲料。3饲料耐受需要食物的尾肠道协调运输。传播食物的3期迁移性运动复合体(MMC)集群与血浆胃动素水平增加2至4倍有关。7但早产儿胃动素、MMC与饲料耐受性之间的关系尚不清楚。尽管妊娠期小于32周的早产儿8的MMCs数量在妊娠20周时减少,但胃动素的肠道分布与成人相似。禁食早产儿的胃动素水平也与足月儿相似,足月儿很少表现出早产儿特有的进食不耐受程度。5还应注意的是,胎儿肠道在妊娠25周时结构成熟,能够消化和吸收乳汁,运动活动发展得更慢,可能会限制对肠内喂养的耐受性。9 FI通常需要延长肠外营养,这会导致医院感染、肝功能障碍和延长住院时间。10,11尽管FI是一个常见问题,但文献中几乎没有关于早产对喂养不耐受的影响的信息。关于早产儿喂养不耐受的患病率,也缺乏信息,而早产儿越频繁地出现喂养不耐受,尚待确定。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Comparison of feeding intolerance between very preterm and moderate preterm neonates – a prospective cohort study
Neonatal death is high in our country and it comprises 60% of total Under-5 mortality.1 So to achieve MDG-4 we have to reduce neonatal death. The Lancet series on neonatal health reported that preterm birth directly causes 28% of neonatal deaths.2 Prematurity and its complication is the major cause of neonatal death in our country and shares around 45% of neonatal death. Premature babies are prone to develop many complications. One of the common complications is Feeding Intolerance (FI). Feeding intolerance can be attributed to the immaturity of gastrointestinal motility,3, 4 as small intestinal motility and phase-3 activity of the migrating motor complex (MMC) are more immature in preterm infants, especially those with a gestational age of less than 32 weeks.3,5 Gastrointestinal motility is influenced by motilin, a 22 amino-acid peptide produced by the enterochromaffin cells of the duodenal and jejunal mucosa.6 Gastric emptying, in particular, is dependent on co-ordination between the motor activities of the gastric antrum and duodenum. Preterm infants often have difficulty in tolerating oral feeds due to immaturity of mechanical and hormonal control of their gastrointestinal system.3 Feed tolerance requires co-ordinated caudal intestinal transit of food. The clusters of phase 3 migrating motor complexes (MMC) that propagate food are associated with a twoto fourfold increase in plasma motilin levels.7 But the association between motilin, MMCs and feed tolerance, however, is unclear in preterm infants. Even though the numbers of MMCs are reduced in preterm infants of less than 32 wk gestation8 fetuses by week 20 of gestation, demonstrate intestinal distribution of motilin similar to that in adults. Motilin levels of fasting preterm infants are also similar to those of term infants, who rarely exhibit the degrees of feeding intolerance characteristic of premature infants.5 It is also noted that fetal intestine is structurally mature by 25 weeks of gestation and capable of digesting and absorbing milk feeds, motor activity develops more slowly and may limit the tolerance to enteral feeds.9 FI often needs prolong parenteral nutrition which predisposes nosocomial infections, hepatic dysfunction and prolong hospitalization.10,11 Though FI is a common problem, literature contain little information about the influence of prematurity on feeding intolerance. There is also scarcity of information regarding the prevalence of feeding intolerance among preterm babiesand whereas the more preterm babies develop more frequent feeding intolerance yet to be determined.
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