Lamont Ronnie F
Department of Obstetrics and Gynaecology, Northwick Park & St Mark's Hospitals and Imperial College School of Medicine, London, UK.
Curr Opin Obstet Gynecol. 2003 Apr;15(2):91-9. doi: 10.1097/00001703-200304000-00002.
The published literature on preterm prelabour rupture of the membranes is voluminous yet despite advances in obstetric and neonatal care, the problem remains a major cause of perinatal mortality and morbidity. The purpose of this review is to present recent evidence pertaining to the role of inflammatory mediators such as cytokines and the tissue damage and long-term handicap they cause, the molecular biology and physiology of membrane structure, the role of host susceptibility and the genetics of preterm birth and therapeutic options for the management of preterm prelabour rupture, including antibiotics, amnioinfusion and special situations.
Neonatal morbidity from preterm prelabour rupture of the membranes is mainly related to oligohydramnios and pulmonary hypoplasia. Occupational factors have a significant effect on the occurrence and outcome following rupture. Matrix metalloproteinases control growth and remodelling of the pregnant uterus, placenta and membranes and are linked to a genetic predisposition to preterm birth through gene expression and variation. Transvaginal ultrasound scan, oncofetal fibronectin and the presence of abnormal genital tract flora (bacterial vaginosis) in pregnancy may help in the prediction of preterm birth.
Preterm prelabour membrane rupture remains a management problem, particularly at very early gestations, yet obstetric and neonatal care can make a difference to outcome. While at early gestations the prognosis is poor, it is not hopeless. Careful selection of the recent literature on the subject might interest and inform those faced regularly with the problem, prevent therapeutic nihilism, promote confidence in our ability to make a difference and realise that we are not alone when faced with the therapeutic dilemma that is this condition.
关于胎膜早破的已发表文献数量众多，然而尽管产科和新生儿护理取得了进展，但该问题仍然是围产期死亡和发病的主要原因。本综述的目的是介绍有关炎症介质（如细胞因子）的作用、它们所导致的组织损伤和长期残疾、胎膜结构的分子生物学和生理学、宿主易感性的作用以及早产的遗传学，以及胎膜早破管理的治疗选择，包括抗生素、羊膜腔灌注和特殊情况等方面的最新证据。
胎膜早破导致的新生儿发病主要与羊水过少和肺发育不全有关。职业因素对胎膜早破后的发生情况和结局有显著影响。基质金属蛋白酶控制着妊娠子宫、胎盘和胎膜的生长和重塑，并通过基因表达和变异与早产的遗传易感性相关联。经阴道超声扫描、癌胚纤维连接蛋白以及孕期异常生殖道菌群（细菌性阴道病）的存在可能有助于预测早产。
胎膜早破仍然是一个管理难题，尤其是在妊娠早期，然而产科和新生儿护理可以改善结局。虽然在妊娠早期预后较差，但并非毫无希望。精心挑选关于该主题的近期文献可能会引起那些经常面临此问题的人的兴趣并为他们提供信息，防止治疗虚无主义，增强我们有能力产生影响的信心，并意识到在面对这种情况的治疗困境时我们并不孤单。
