Sullivan K M, Hawgood S, Flake A W, Harrison M R, Adzick N S
Fetal Treatment Center, University of California, San Francisco 94143-0570.
J Pediatr Surg. 1994 Aug;29(8):1020-3; discussion 1023-4. doi: 10.1016/0022-3468(94)90271-2.
The substantial morbidity and mortality of congenital diaphragmatic hernia (CDH) is attributed to the pulmonary hypoplasia caused by the presence of abdominal viscera in the chest during intrauterine life. Recent experimental studies suggest that surfactant deficiency may also contribute to CDH pathophysiology. Clinically, the amniocentesis-derived lecithin to sphingomyelin (L/S) ratio and phosphatidylglycerol (PG) data are used to assess fetal lung maturity. We have performed amniotic fluid phospholipid analyses at 33 to 38 weeks' gestation in 18 fetuses with prenatally diagnosed CDH to assess fetal lung maturity, plan optimal timing for delivery, and selectively employ prenatal glucocorticoid or postnatal surfactant therapy. Compared with published control values from uncomplicated pregnancies, there was no difference in the L/S ratio or PG in the CDH fetus. Based on amniotic fluid phospholipid data, the human CDH fetus is not surfactant-deficient.
先天性膈疝(CDH)的高发病率和死亡率归因于宫内生活期间胸腔内存在腹腔脏器导致的肺发育不全。最近的实验研究表明,表面活性剂缺乏也可能导致CDH的病理生理过程。临床上,羊水穿刺获得的卵磷脂与鞘磷脂(L/S)比值和磷脂酰甘油(PG)数据用于评估胎儿肺成熟度。我们对18例产前诊断为CDH的胎儿在妊娠33至38周时进行了羊水磷脂分析,以评估胎儿肺成熟度、规划最佳分娩时机,并选择性地采用产前糖皮质激素或产后表面活性剂治疗。与已发表的正常妊娠对照值相比,CDH胎儿的L/S比值或PG没有差异。基于羊水磷脂数据,人类CDH胎儿不存在表面活性剂缺乏。