Recent evidence associated with the condition of preterm prelabour rupture of the membranes

Abstract

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.