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Published on: November 20, 2015
Recent evidence associated with the condition of preterm prelabour rupture of the membranes
1Department of Obstetrics and Gynaecology, Northwick Park & St Mark's Hospitals and Imperial College School of Medicine, London, UK. pauline.mills@nwlh.nhs.uk
Insights
Preterm prelabour rupture of membranes (PPROM) is a significant cause of perinatal complications. Recent evidence highlights inflammatory mediators, genetics, and predictive markers for improved management and outcomes.
Area of Science:
- Obstetrics and Gynecology
- Perinatal Medicine
- Reproductive Biology
Background:
- Preterm prelabour rupture of membranes (PPROM) remains a leading cause of perinatal mortality and morbidity despite advances in care.
- Understanding the underlying mechanisms of PPROM is crucial for improving obstetric and neonatal outcomes.
Purpose of the Study:
- To review recent evidence on PPROM, focusing on inflammatory mediators, membrane physiology, host susceptibility, and genetics.
- To explore therapeutic options including antibiotics and amnioinfusion for PPROM management.
Main Methods:
- Literature review of recent evidence on PPROM.
- Analysis of molecular and physiological factors contributing to PPROM.
- Evaluation of current and potential therapeutic interventions.
Main Results:
- Neonatal morbidity in PPROM is linked to oligohydramnios and pulmonary hypoplasia.
- Matrix metalloproteinases and genetic variations influence PPROM risk.
- Predictive markers include transvaginal ultrasound, oncofetal fibronectin, and bacterial vaginosis.
Conclusions:
- PPROM presents management challenges, especially at early gestations, but outcomes can be improved with appropriate obstetric and neonatal care.
- Despite poor prognosis at early gestations, PPROM is not a hopeless condition.
- Informing clinicians about recent advancements can enhance confidence and prevent therapeutic nihilism.
Purpose Of Review:
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.
Recent Findings:
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.
Summary:
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.

